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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="http://onlinelibrary.wiley.com/rss/journal/10.1002/(ISSN)1932-8737" xmlns="http://purl.org/rss/1.0/"><title>Clinical Cardiology</title><description> Wiley Online Library : Clinical Cardiology</description><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2F%28ISSN%291932-8737</link><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc</dc:publisher><dc:language xmlns:dc="http://purl.org/dc/elements/1.1/">en</dc:language><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/">Copyright ©, 2013 Wiley Periodicals, Inc.</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">0160-9289</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1932-8737</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">May 2013</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">36</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">5</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E1</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E6</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1002/clc.2013.36.issue-5/asset/cover.gif?v=1&amp;s=edd155259cf13c65a3ada38dcdfa32fbb7ca0e7c"/><items><rdf:Seq><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22139"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22141"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22137"/><rdf:li 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rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.20903"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22107"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22104"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22113"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22102"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22108"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22109"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22112"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22111"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22116"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22078"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22119"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22115"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22091"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22136"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22079"/></rdf:Seq></items></channel><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22139" xmlns="http://purl.org/rss/1.0/"><title>Response to Red Blood Cell Distribution Width Is a Predictor of Readmission in Cardiac Patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22139</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Response to Red Blood Cell Distribution Width Is a Predictor of Readmission in Cardiac Patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sevket Balta, Sait Demirkol, Omer Kurt, Hakan Sarlak, Turgay Celik, Dimitri P. Mikhailidis</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-15T13:38:36.227296-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22139</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22139</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22139</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Ephrem G. Clin Cardiol. 2013. doi: 10.1002/clc.22116</p></div>
]]></content:encoded><description>
Ephrem G. Clin Cardiol. 2013. doi: 10.1002/clc.22116
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22141" xmlns="http://purl.org/rss/1.0/"><title>Impacts of Mitral E/e′ on Myocardial Contractile Motion and Synchronicity in Heart Failure Patients With Reduced Ejection Fraction: An Exercise–Echocardiography Study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22141</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Impacts of Mitral E/e′ on Myocardial Contractile Motion and Synchronicity in Heart Failure Patients With Reduced Ejection Fraction: An Exercise–Echocardiography Study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yi-Chih Wang, Chih-Chieh Yu, Fu-Chun Chiu, Chia-Ti Tsai, Ling-Ping Lai, Juey-Jen Hwang, Jiunn-Lee Lin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T09:48:51.196411-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22141</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22141</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22141</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22141-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The association between diastolic abnormality and postexercise contractile decompensation is uncertain in heart failure (HF) patients with reduced left ventricular ejection fraction (LVEF).</p></div></div>
<div class="section" id="clc22141-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>The higher mitral E/annular early diastolic velocity (E/e′) is relevant to postexercise regional myocardial contractile maladaptation.</p></div></div>
<div class="section" id="clc22141-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Seventy HF patients with LVEF &lt;50 % (56 males, 58 ± 15 years) were studied pre- and postexercise using tissue Doppler echocardiography. We evaluated the mean and standard deviation of systolic myocardial velocity (Sm) and electromechanical delay (Ts) of 12 left ventricular segments, and further analyzed the corresponding changes of septal and posterolateral segments.</p></div></div>
<div class="section" id="clc22141-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The higher mitral E/e′ was associated with more blunted heterogeneity of Sm and greater ventricular dyssynchrony after exercise. This is due to the posterolateral wall not being able to increase Sm with exercise to the same degree as the septum (decreased posterolateral/septal Sm ratio). Furthermore, the postexercise aggravated difference of Ts between septum and posterolateral segments leads to more dyssynchronous contraction in the higher E/e′ groups. An E/e′ ≥10 predicted a postexercise posterolateral/septal Sm ≤ 1 (odds ratio [OR]: 5.8, 95% confidence interval [CI]: 1.5-22.6, <i>P</i> = 0.011), and a difference of Ts between septum and posterolateral segments &gt;65 ms (OR: 64, 95% CI: = 6–651, <i>P</i> &lt; 0.001) in HF patients with reduced LVEF in multivariate analysis.</p></div></div>
<div class="section" id="clc22141-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The higher mitral E/e′-related postexercise maladaptation of myocardial contractile motion and synchronicity suggests the involvement of systolic abnormality in exercise pathophysiology in HF patients with reduced LVEF.</p></div></div>
]]></content:encoded><description>


Background
The association between diastolic abnormality and postexercise contractile decompensation is uncertain in heart failure (HF) patients with reduced left ventricular ejection fraction (LVEF).


Hypothesis
The higher mitral E/annular early diastolic velocity (E/e′) is relevant to postexercise regional myocardial contractile maladaptation.


Methods
Seventy HF patients with LVEF &lt;50 % (56 males, 58 ± 15 years) were studied pre- and postexercise using tissue Doppler echocardiography. We evaluated the mean and standard deviation of systolic myocardial velocity (Sm) and electromechanical delay (Ts) of 12 left ventricular segments, and further analyzed the corresponding changes of septal and posterolateral segments.


Results
The higher mitral E/e′ was associated with more blunted heterogeneity of Sm and greater ventricular dyssynchrony after exercise. This is due to the posterolateral wall not being able to increase Sm with exercise to the same degree as the septum (decreased posterolateral/septal Sm ratio). Furthermore, the postexercise aggravated difference of Ts between septum and posterolateral segments leads to more dyssynchronous contraction in the higher E/e′ groups. An E/e′ ≥10 predicted a postexercise posterolateral/septal Sm ≤ 1 (odds ratio [OR]: 5.8, 95% confidence interval [CI]: 1.5-22.6, P = 0.011), and a difference of Ts between septum and posterolateral segments &gt;65 ms (OR: 64, 95% CI: = 6–651, P &lt; 0.001) in HF patients with reduced LVEF in multivariate analysis.


Conclusions
The higher mitral E/e′-related postexercise maladaptation of myocardial contractile motion and synchronicity suggests the involvement of systolic abnormality in exercise pathophysiology in HF patients with reduced LVEF.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22137" xmlns="http://purl.org/rss/1.0/"><title>A Clinician's Guide to the ABCs of Cardiovascular Disease Prevention: The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease and American College of Cardiology Cardiosource Approach to the Million Hearts Initiative</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22137</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A Clinician's Guide to the ABCs of Cardiovascular Disease Prevention: The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease and American College of Cardiology Cardiosource Approach to the Million Hearts Initiative</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Steven Hsu, Van-Khue Ton, M. Dominique Ashen, Seth S. Martin, Ty J. Gluckman, Payal Kohli, Stephen D. Sisson, Roger S. Blumenthal, Michael J. Blaha</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T09:45:52.308734-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22137</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22137</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22137</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Atherosclerotic cardiovascular disease (CVD) is the leading cause of death in the United States and worldwide. Fortunately, it is often preventable with early adoption of lifestyle modification, prevention of risk factor onset, and aggressive treatment of existing risk factors. The Million Hearts Initiative is an effort by the Centers for Disease Control that aims to prevent 1 million myocardial infarctions and strokes over the next 5 years. As part of this initiative, we present a simply organized “ABCDE” approach for guiding a consistent comprehensive approach to managing cardiovascular risk in daily clinical practice. ABCDE stands for assessment of risk, antiplatelet therapy, blood pressure management, cholesterol management, cigarette/tobacco cessation, diet and weight management, diabetes prevention and treatment, and exercise, interventions regularly used to reduce cardiovascular (CV) risk. Throughout this article we summarize recommendations related to each topic and reference landmark trials and data that support our approach. We believe that the ABCDE approach will be the core framework for addressing CV risk in our effort to prevent CVD.</p></div>
]]></content:encoded><description>

Atherosclerotic cardiovascular disease (CVD) is the leading cause of death in the United States and worldwide. Fortunately, it is often preventable with early adoption of lifestyle modification, prevention of risk factor onset, and aggressive treatment of existing risk factors. The Million Hearts Initiative is an effort by the Centers for Disease Control that aims to prevent 1 million myocardial infarctions and strokes over the next 5 years. As part of this initiative, we present a simply organized “ABCDE” approach for guiding a consistent comprehensive approach to managing cardiovascular risk in daily clinical practice. ABCDE stands for assessment of risk, antiplatelet therapy, blood pressure management, cholesterol management, cigarette/tobacco cessation, diet and weight management, diabetes prevention and treatment, and exercise, interventions regularly used to reduce cardiovascular (CV) risk. Throughout this article we summarize recommendations related to each topic and reference landmark trials and data that support our approach. We believe that the ABCDE approach will be the core framework for addressing CV risk in our effort to prevent CVD.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22134" xmlns="http://purl.org/rss/1.0/"><title>Impact of Smoking Status on Cardiovascular Outcomes Following Percutaneous Coronary Intervention</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22134</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Impact of Smoking Status on Cardiovascular Outcomes Following Percutaneous Coronary Intervention</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Burhan Mohamedali, Adhir Shroff</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T09:45:46.748895-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22134</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22134</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22134</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Quality and Outcomes</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22134-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Many military veterans in the United States with coronary artery disease continue to smoke despite undergoing percutaneous coronary intervention (PCI). Previous studies have described improved cardiovascular outcomes in smokers, the so-called “smokers' paradox.” In this study, we examined the effects of smoking on cardiovascular outcomes following PCI.</p></div></div>
<div class="section" id="clc22134-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Do patients who smoke have different post-PCI outcomes than nonsmokers?</p></div></div>
<div class="section" id="clc22134-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>All patients who underwent PCI at a single US Veterans Administration hospital from 2004 to 2009 were followed. Outcomes of interest included myocardial infarction, unplanned coronary intervention, unplanned cardiac hospitalization, death, and a composite of events for 6 months after PCI. Changes in traditional risk factors were also assessed.</p></div></div>
<div class="section" id="clc22134-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Unadjusted analysis revealed that in almost all categories, smokers had lower incidence of adverse events than nonsmokers. However, after adjusting for the older age of the nonsmokers, no favorable statistical trend toward smokers was seen. Significant improvement in blood pressure and lipid levels were seen in both groups.</p></div></div>
<div class="section" id="clc22134-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>After adjusting for differences in age, there did not appear to be any protective effect of smoking on cardiovascular outcomes following PCI. Smokers achieved similar degrees of risk factor optimization during the follow-up period as their nonsmoker counterparts. Aggressive efforts to decrease the prevalence of smoking must be maintained.</p></div></div>
]]></content:encoded><description>


Background
Many military veterans in the United States with coronary artery disease continue to smoke despite undergoing percutaneous coronary intervention (PCI). Previous studies have described improved cardiovascular outcomes in smokers, the so-called “smokers' paradox.” In this study, we examined the effects of smoking on cardiovascular outcomes following PCI.


Hypothesis
Do patients who smoke have different post-PCI outcomes than nonsmokers?

Methods
All patients who underwent PCI at a single US Veterans Administration hospital from 2004 to 2009 were followed. Outcomes of interest included myocardial infarction, unplanned coronary intervention, unplanned cardiac hospitalization, death, and a composite of events for 6 months after PCI. Changes in traditional risk factors were also assessed.


Results
Unadjusted analysis revealed that in almost all categories, smokers had lower incidence of adverse events than nonsmokers. However, after adjusting for the older age of the nonsmokers, no favorable statistical trend toward smokers was seen. Significant improvement in blood pressure and lipid levels were seen in both groups.


Conclusions
After adjusting for differences in age, there did not appear to be any protective effect of smoking on cardiovascular outcomes following PCI. Smokers achieved similar degrees of risk factor optimization during the follow-up period as their nonsmoker counterparts. Aggressive efforts to decrease the prevalence of smoking must be maintained.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22132" xmlns="http://purl.org/rss/1.0/"><title>A Prospective Randomized Study Comparing Isolation of the Arrhythmogenic Vein Versus All Veins in Paroxysmal Atrial Fibrillation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22132</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A Prospective Randomized Study Comparing Isolation of the Arrhythmogenic Vein Versus All Veins in Paroxysmal Atrial Fibrillation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Stephanie Fichtner, Gabriele Hessling, Sonia Ammar, Tilko Reents, Heidi L. Estner, Clemens Jilek, Susanne Kathan, Michael Büchner, Roger Dillier, Isabel Deisenhofer</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T08:55:52.388206-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22132</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22132</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22132</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22132-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Ablation procedures in patients with paroxysmal atrial fibrillation (PAF) includes isolation of all pulmonary veins (PVs). We hypothesized that an approach using an algorithm to detect arrhythmogenic PVs (aPVs) might lead to shorter procedure duration (PD) and fewer proarrhythmic effects (PE).</p></div></div>
<div class="section" id="clc22132-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Isolation of the aPVs only leads to a reduced PD, reduced PEs, and fewer adverse events, with a success rate comparable to the standard all-PV approach.</p></div></div>
<div class="section" id="clc22132-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>In this prospective trial, 207 patients with PAF were randomized to undergo isolation of the aPV (AG group, n = 105) or isolation of all PVs (VG group, n = 102). The aPV was identified by atrial fibrillation (AF) induction, focal discharge, or short local PV decremental conduction during PV pacing. Patients were followed with repetitive 7-day Holter electrocardiograms (ECGs) after 3, 6, and 12 months in our arrhythmia clinic.</p></div></div>
<div class="section" id="clc22132-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In 97% of patients, at least 1 aPV was identified (mean, 2.1). PD did not differ significantly (152.3 ± 57.1 minutes vs 162 ± 68 minutes, <i>P</i> = 0.27) between the groups, but the number of radiofrequency (RF) applications and fluoroscopy time (FT) and dose were significantly lower in the AG group than in the VG group. The occurrence of PE (new-onset atrial tachycardia) and adverse events (AE) did not differ between the 2 groups (<i>P</i> = 0.1). Sinus rhythm off antiarrhythmic medication (documented on 7-day Holter ECGs) 12 months after a single procedure was achieved in 53% in the AG group and 59% in the VG group (<i>P</i> = 0.51).</p></div></div>
<div class="section" id="clc22132-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Isolation of the aPVs detected by a straightforward algorithm leads to similar success rates compared to a standard all-PV approach with regard to PD, AE, or PE and is associated with less RF and a shorter FT.</p></div></div>
]]></content:encoded><description>


Background
Ablation procedures in patients with paroxysmal atrial fibrillation (PAF) includes isolation of all pulmonary veins (PVs). We hypothesized that an approach using an algorithm to detect arrhythmogenic PVs (aPVs) might lead to shorter procedure duration (PD) and fewer proarrhythmic effects (PE).


Hypothesis
Isolation of the aPVs only leads to a reduced PD, reduced PEs, and fewer adverse events, with a success rate comparable to the standard all-PV approach.


Methods
In this prospective trial, 207 patients with PAF were randomized to undergo isolation of the aPV (AG group, n = 105) or isolation of all PVs (VG group, n = 102). The aPV was identified by atrial fibrillation (AF) induction, focal discharge, or short local PV decremental conduction during PV pacing. Patients were followed with repetitive 7-day Holter electrocardiograms (ECGs) after 3, 6, and 12 months in our arrhythmia clinic.


Results
In 97% of patients, at least 1 aPV was identified (mean, 2.1). PD did not differ significantly (152.3 ± 57.1 minutes vs 162 ± 68 minutes, P = 0.27) between the groups, but the number of radiofrequency (RF) applications and fluoroscopy time (FT) and dose were significantly lower in the AG group than in the VG group. The occurrence of PE (new-onset atrial tachycardia) and adverse events (AE) did not differ between the 2 groups (P = 0.1). Sinus rhythm off antiarrhythmic medication (documented on 7-day Holter ECGs) 12 months after a single procedure was achieved in 53% in the AG group and 59% in the VG group (P = 0.51).


Conclusions
Isolation of the aPVs detected by a straightforward algorithm leads to similar success rates compared to a standard all-PV approach with regard to PD, AE, or PE and is associated with less RF and a shorter FT.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22133" xmlns="http://purl.org/rss/1.0/"><title>Guideline Adherence of Antithrombotic Treatment Initiated by General Practitioners in Patients With Nonvalvular Atrial Fibrillation: A Danish Survey</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22133</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Guideline Adherence of Antithrombotic Treatment Initiated by General Practitioners in Patients With Nonvalvular Atrial Fibrillation: A Danish Survey</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Axel Brandes, Mikkel Overgaard, Liane Plauborg, Christian Dehlendorff, Frede Lyck, Jørgen Peulicke, Søren Vinther Poulsen, Steen Husted</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T08:51:14.665228-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22133</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22133</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22133</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22133-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The aim of this prospective survey was to describe the demographics, stroke risk profile, and the guideline adherence of antithrombotic treatment in a Danish primary care population of patients with nonvalvular atrial fibrillation (AF).</p></div></div>
<div class="section" id="clc22133-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>We hypothesized that a significant proportion of patients with nonvalvular AF do not receive guideline-adherent antithrombotic treatment in primary care.</p></div></div>
<div class="section" id="clc22133-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We performed a cross-sectional survey of antithrombotic treatment using data of AF patients from general practices.</p></div></div>
<div class="section" id="clc22133-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Sixty-four general practitioners enrolled 1743 patients with a mean age of 74.8 ± 11.2 years. The mean CHADS<sub>2</sub> and CHA<sub>2</sub>DS<sub>2</sub>-VASc scores were 1.9 ± 1.3 and 3.5 ± 1.8, respectively. Of the patients, 12.4% and 4.04%, respectively, were at truly low risk, with a CHADS<sub>2</sub> and CHA<sub>2</sub>DS<sub>2</sub>-VASc score 0 (<i>P</i> &lt; 0.001). A score of 1 was seen in 28.0% vs 9.0% (<i>P</i> &lt; 0.001) of the patients. Of all patients, 66.3% were treated with oral anticoagulants, 18.7% with antiplatelet drugs only, and 15% received no antithrombotic therapy. Based on the CHADS<sub>2</sub> score, 75.7% of the patients were treated in adherence with the guidelines, 16% were undertreated, and 8.4% overtreated. The corresponding numbers for the CHA<sub>2</sub>DS<sub>2</sub>-VASc score were 75.4%, 22.7%, and 1.8%, respectively. The differences in guideline adherence applying the 2 scores were significant (<i>P</i> &lt; 0.001). Of patients receiving no antithrombotic therapy, 64.1% were treated in adherence to the guidelines according to the CHADS<sub>2</sub> score. Applying the CHA<sub>2</sub>DS<sub>2</sub>-VASc score, this proportion was only 53.4%. Antiplatelet drug treatment was in adherence to the guidelines (CHADS<sub>2</sub> and CHA<sub>2</sub>DS<sub>2</sub>-VASc score of 1) in only 31% and 12% of the patients, respectively.</p></div></div>
<div class="section" id="clc22133-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Antithrombotic treatment of AF patients is in general well performed in primary care in Denmark. Further improvements may be achieved by thorough stroke risk stratification on the basis of current evidence-based guidelines.</p></div></div>
]]></content:encoded><description>


Background
The aim of this prospective survey was to describe the demographics, stroke risk profile, and the guideline adherence of antithrombotic treatment in a Danish primary care population of patients with nonvalvular atrial fibrillation (AF).


Hypothesis
We hypothesized that a significant proportion of patients with nonvalvular AF do not receive guideline-adherent antithrombotic treatment in primary care.


Methods
We performed a cross-sectional survey of antithrombotic treatment using data of AF patients from general practices.


Results
Sixty-four general practitioners enrolled 1743 patients with a mean age of 74.8 ± 11.2 years. The mean CHADS2 and CHA2DS2-VASc scores were 1.9 ± 1.3 and 3.5 ± 1.8, respectively. Of the patients, 12.4% and 4.04%, respectively, were at truly low risk, with a CHADS2 and CHA2DS2-VASc score 0 (P &lt; 0.001). A score of 1 was seen in 28.0% vs 9.0% (P &lt; 0.001) of the patients. Of all patients, 66.3% were treated with oral anticoagulants, 18.7% with antiplatelet drugs only, and 15% received no antithrombotic therapy. Based on the CHADS2 score, 75.7% of the patients were treated in adherence with the guidelines, 16% were undertreated, and 8.4% overtreated. The corresponding numbers for the CHA2DS2-VASc score were 75.4%, 22.7%, and 1.8%, respectively. The differences in guideline adherence applying the 2 scores were significant (P &lt; 0.001). Of patients receiving no antithrombotic therapy, 64.1% were treated in adherence to the guidelines according to the CHADS2 score. Applying the CHA2DS2-VASc score, this proportion was only 53.4%. Antiplatelet drug treatment was in adherence to the guidelines (CHADS2 and CHA2DS2-VASc score of 1) in only 31% and 12% of the patients, respectively.


Conclusions
Antithrombotic treatment of AF patients is in general well performed in primary care in Denmark. Further improvements may be achieved by thorough stroke risk stratification on the basis of current evidence-based guidelines.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22135" xmlns="http://purl.org/rss/1.0/"><title>Statin Therapy in the Reduction of Cardiovascular Events in Patients Undergoing Intermediate-Risk Noncardiac, Nonvascular Surgery</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22135</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Statin Therapy in the Reduction of Cardiovascular Events in Patients Undergoing Intermediate-Risk Noncardiac, Nonvascular Surgery</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Manjunath G. Raju, Ajay Pachika, Sujeeth R. Punnam, Joseph C. Gardiner, Mehdi H. Shishehbor, Samir R. Kapadia, George S. Abela</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T08:50:39.55277-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22135</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22135</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22135</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22135-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) reduce perioperative cardiac events in high-risk patients undergoing cardiovascular surgery. However, there is paucity of data on the role of statins in patients undergoing intermediate-risk noncardiac, nonvascular surgery (NCNVS).</p></div></div>
<div class="section" id="clc22135-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Statins are cardioprotective in intermediate-risk NCNVS.</p></div></div>
<div class="section" id="clc22135-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We identified a retrospective cohort of patients undergoing intermediate risk NCNVS. Our composite end point (CEP) included 30-day all-cause mortality, atrial fibrillation (AF), and nonfatal myocardial infarction (MI). A stepwise logistic regression with adjustment using propensity scores was performed to determine if statin therapy was independently associated with the risk reduction of adverse postoperative cardiovascular outcomes.</p></div></div>
<div class="section" id="clc22135-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We identified 752 patients. Seventy-five of them (9.97%) developed composite end points; 10 (1.33%) had in-hospital nonfatal MI, 44 (5.85%) developed AF, and 35 (4.65%) died within 30 days. The 30-day all-cause mortality was 31/478 (6.48%) among statin nonusers vs 4/274 (1.45%) for statin users (<i>P</i> &lt; 0.002). As compared with nonusers, patients on statin therapy had a 5-fold reduced risk of 30-day all-cause mortality. Statin therapy was associated with decreased CEP after adjusting for baseline characteristics, with a propensity score to predict use of statins (odds ratio [OR]: 0.54, 95% confidence interval [CI]: 0.30–0.97, <i>P</i> = 0.039). After further adjustment for propensity score, diabetes mellitus, percutaneous coronary intervention, and prior coronary artery bypass grafting, statin therapy proved beneficial (OR: 0.51, 95% CI: 0.28–0.92, <i>P</i> = 0.026).</p></div></div>
<div class="section" id="clc22135-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Statin use in the perioperative period was associated with a reduction in cardiovascular adverse events and 30-day all-cause mortality in patients undergoing intermediate-risk NCNVS.</p></div></div>
]]></content:encoded><description>


Background
Hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) reduce perioperative cardiac events in high-risk patients undergoing cardiovascular surgery. However, there is paucity of data on the role of statins in patients undergoing intermediate-risk noncardiac, nonvascular surgery (NCNVS).


Hypothesis
Statins are cardioprotective in intermediate-risk NCNVS.


Methods
We identified a retrospective cohort of patients undergoing intermediate risk NCNVS. Our composite end point (CEP) included 30-day all-cause mortality, atrial fibrillation (AF), and nonfatal myocardial infarction (MI). A stepwise logistic regression with adjustment using propensity scores was performed to determine if statin therapy was independently associated with the risk reduction of adverse postoperative cardiovascular outcomes.


Results
We identified 752 patients. Seventy-five of them (9.97%) developed composite end points; 10 (1.33%) had in-hospital nonfatal MI, 44 (5.85%) developed AF, and 35 (4.65%) died within 30 days. The 30-day all-cause mortality was 31/478 (6.48%) among statin nonusers vs 4/274 (1.45%) for statin users (P &lt; 0.002). As compared with nonusers, patients on statin therapy had a 5-fold reduced risk of 30-day all-cause mortality. Statin therapy was associated with decreased CEP after adjusting for baseline characteristics, with a propensity score to predict use of statins (odds ratio [OR]: 0.54, 95% confidence interval [CI]: 0.30–0.97, P = 0.039). After further adjustment for propensity score, diabetes mellitus, percutaneous coronary intervention, and prior coronary artery bypass grafting, statin therapy proved beneficial (OR: 0.51, 95% CI: 0.28–0.92, P = 0.026).


Conclusions
Statin use in the perioperative period was associated with a reduction in cardiovascular adverse events and 30-day all-cause mortality in patients undergoing intermediate-risk NCNVS.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22140" xmlns="http://purl.org/rss/1.0/"><title>Can Statins Improve Outcomes After Isolated Cardiac Valve Surgery? A Systematic Literature Review</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22140</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Can Statins Improve Outcomes After Isolated Cardiac Valve Surgery? A Systematic Literature Review</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jacob Chacko, Leanne Harling, Hutan Ashrafian, Thanos Athanasiou</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T08:47:01.439954-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22140</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22140</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22140</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22140-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors, or statins, have been associated with an improvement in outcomes after coronary artery surgery for some time; however, their role in isolated valve surgery (IVS) remains undetermined.</p></div></div>
<div class="section" id="clc22140-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>The pleiotropic effects of statins may produce similar beneficial effects on outcomes after IVS.</p></div></div>
<div class="section" id="clc22140-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A systematic review of the literature was performed investigating the role of statins in bioprosthetic valve replacement.</p></div></div>
<div class="section" id="clc22140-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Nine observational studies (7 retrospective, 2 prospective) incorporating a total of 18 154 patients were found investigating the role of statin therapy in bioprosthetic valve replacement.</p></div></div>
<div class="section" id="clc22140-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>There is presently insufficient evidence to recommend routine statin therapy in IVS, unless concomitant hypercholesterolemia or coronary artery disease is present. A prospective study clearly defining the dose, type, and duration of therapy is now required to finally clarify whether statins alone confer a postoperative benefit in these patients.</p></div></div>
]]></content:encoded><description>


Background
HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors, or statins, have been associated with an improvement in outcomes after coronary artery surgery for some time; however, their role in isolated valve surgery (IVS) remains undetermined.


Hypothesis
The pleiotropic effects of statins may produce similar beneficial effects on outcomes after IVS.


Methods
A systematic review of the literature was performed investigating the role of statins in bioprosthetic valve replacement.


Results
Nine observational studies (7 retrospective, 2 prospective) incorporating a total of 18 154 patients were found investigating the role of statin therapy in bioprosthetic valve replacement.


Conclusions
There is presently insufficient evidence to recommend routine statin therapy in IVS, unless concomitant hypercholesterolemia or coronary artery disease is present. A prospective study clearly defining the dose, type, and duration of therapy is now required to finally clarify whether statins alone confer a postoperative benefit in these patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22138" xmlns="http://purl.org/rss/1.0/"><title>Letters to the Editor</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22138</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Letters to the Editor</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Georges Ephrem</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-08T11:38:31.142953-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22138</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22138</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22138</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letters to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22123" xmlns="http://purl.org/rss/1.0/"><title>Response to Immediate and Long-Term Results Following Balloon Mitral Valvotomy in Patients With Atrial Fibrillation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22123</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Response to Immediate and Long-Term Results Following Balloon Mitral Valvotomy in Patients With Atrial Fibrillation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Vecih Oduncu</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-08T11:38:22.554103-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22123</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22123</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22123</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Mohanan Nair KK et al. Clin Cardiol. 2012;35:35–39</p></div>
]]></content:encoded><description>
Mohanan Nair KK et al. Clin Cardiol. 2012;35:35–39
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22131" xmlns="http://purl.org/rss/1.0/"><title>Mild Therapeutic Hypothermia After Out-Of-Hospital Cardiac Arrest Complicating ST-Elevation Myocardial Infarction: Long-term Results in Clinical Practice</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22131</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Mild Therapeutic Hypothermia After Out-Of-Hospital Cardiac Arrest Complicating ST-Elevation Myocardial Infarction: Long-term Results in Clinical Practice</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Stefan Zimmermann, Frank A. Flachskampf, Reinhard Schneider, Katharina Dechant, Anna Alff, Lutz Klinghammer, Harald Rittger, Stephan Achenbach</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T12:10:27.458503-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22131</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22131</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22131</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22131-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Recently, mild therapeutic hypothermia (MTH) has been integrated into the European resuscitation guidelines to improve outcomes after out-of-hospital cardiac arrest (OHCA). Data on long-term results are limited, especially in patients with acute ST-elevation myocardial infarction (STEMI).</p></div></div>
<div class="section" id="clc22131-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Invasive MTH influences long-term prognosis after OHCA due to STEMI.</p></div></div>
<div class="section" id="clc22131-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We analyzed 48 patients who underwent emergency coronary angiography for STEMI after witnessed OHCA. In 24 consecutive patients, MTH was performed via intravascular cooling (CoolGard System, 34°C maintained for 24 hours) after initialization by rapid infusion of cold saline. Clinical, procedural, and mortality data were compared to 24 historical controls. Neurological recovery was assessed using the Cerebral Performance Category score (CPC) at 30-day and 1-year follow-up.</p></div></div>
<div class="section" id="clc22131-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Median time delay until arrival of emergency medical service was 6 minutes (MTH group) vs 6.5 minutes (controls) (<i>P</i> = 0.16). Initial rhythm was ventricular fibrillation in 75% vs 66.7% (<i>P</i> = 0.75). There were no differences regarding baseline characteristics, angiographic findings, and success of cardiac catheterization procedures. MTH was not associated with a higher frequency of bleeding complications or of pneumonia. Thirty-day mortality was 33.3% in both groups. One-year mortality was 37.5% (MTH group) vs 50% (controls) (<i>P</i> = 0.56). At 1 year, favorable neurological outcome (CPC ≤2) was significantly more frequent in the MTH group (58.3% vs 20.8%, <i>P</i> = 0.017). Multivariate analysis identified MTH as independent predictor of favorable neurological outcome (<i>P</i> &lt; 0.02, odds ratio: 12.73).</p></div></div>
<div class="section" id="clc22131-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>MTH via intravascular cooling improves neurological long-term prognosis after OHCA due to STEMI and is safe in clinical practice.</p></div></div>
]]></content:encoded><description>


Background
Recently, mild therapeutic hypothermia (MTH) has been integrated into the European resuscitation guidelines to improve outcomes after out-of-hospital cardiac arrest (OHCA). Data on long-term results are limited, especially in patients with acute ST-elevation myocardial infarction (STEMI).


Hypothesis
Invasive MTH influences long-term prognosis after OHCA due to STEMI.


Methods
We analyzed 48 patients who underwent emergency coronary angiography for STEMI after witnessed OHCA. In 24 consecutive patients, MTH was performed via intravascular cooling (CoolGard System, 34°C maintained for 24 hours) after initialization by rapid infusion of cold saline. Clinical, procedural, and mortality data were compared to 24 historical controls. Neurological recovery was assessed using the Cerebral Performance Category score (CPC) at 30-day and 1-year follow-up.


Results
Median time delay until arrival of emergency medical service was 6 minutes (MTH group) vs 6.5 minutes (controls) (P = 0.16). Initial rhythm was ventricular fibrillation in 75% vs 66.7% (P = 0.75). There were no differences regarding baseline characteristics, angiographic findings, and success of cardiac catheterization procedures. MTH was not associated with a higher frequency of bleeding complications or of pneumonia. Thirty-day mortality was 33.3% in both groups. One-year mortality was 37.5% (MTH group) vs 50% (controls) (P = 0.56). At 1 year, favorable neurological outcome (CPC ≤2) was significantly more frequent in the MTH group (58.3% vs 20.8%, P = 0.017). Multivariate analysis identified MTH as independent predictor of favorable neurological outcome (P &lt; 0.02, odds ratio: 12.73).


Conclusions
MTH via intravascular cooling improves neurological long-term prognosis after OHCA due to STEMI and is safe in clinical practice.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22126" xmlns="http://purl.org/rss/1.0/"><title>Physician Factors Affecting Cardiac Rehabilitation Referral and Patient Enrollment: A Systematic Review</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22126</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Physician Factors Affecting Cardiac Rehabilitation Referral and Patient Enrollment: A Systematic Review</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gabriela L. M. Ghisi, Peter Polyzotis, Paul Oh, Maureen Pakosh, Sherry L. Grace</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-03T01:53:11.110863-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22126</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22126</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22126</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Physicians play an important role in CR referral and enrollment. Despite established benefits and recommendations, cardiac rehabilitation (CR) enrollment rates are pervasively low. The reasons cardiac patients are missing from CR programs are multifactorial and include provider factors. A number of studies have now investigated physician factors associated with referral to CR programs and patient enrollment. The objective of this study was to qualitatively and systematically review this literature. A literature search of MEDLINE, PsycINFO, CINAHL, Embase, and EBM was conducted for published articles from database inception to October 2011. Overall, 17 articles were included following a process of independent review of each article by 2 authors. Seven (41.2%) were graded as good quality according to Downs and Black criteria. There were no randomized controlled trials. Results showed that medical specialty (ie, cardiac specialists more likely to refer; n = 8 studies) and other physician-reported reasons (eg, physician report of their reasons for CR referral and physician sex) were related to referral. Physician factors related to patient enrollment in CR were physician endorsement, medical specialty, being referred, and physician attitudes toward CR. Physician factors are consistently related to CR referral and enrollment. The role of physician endorsements in promoting patient enrollment should be optimized and exploited.</p></div>
]]></content:encoded><description>

Physicians play an important role in CR referral and enrollment. Despite established benefits and recommendations, cardiac rehabilitation (CR) enrollment rates are pervasively low. The reasons cardiac patients are missing from CR programs are multifactorial and include provider factors. A number of studies have now investigated physician factors associated with referral to CR programs and patient enrollment. The objective of this study was to qualitatively and systematically review this literature. A literature search of MEDLINE, PsycINFO, CINAHL, Embase, and EBM was conducted for published articles from database inception to October 2011. Overall, 17 articles were included following a process of independent review of each article by 2 authors. Seven (41.2%) were graded as good quality according to Downs and Black criteria. There were no randomized controlled trials. Results showed that medical specialty (ie, cardiac specialists more likely to refer; n = 8 studies) and other physician-reported reasons (eg, physician report of their reasons for CR referral and physician sex) were related to referral. Physician factors related to patient enrollment in CR were physician endorsement, medical specialty, being referred, and physician attitudes toward CR. Physician factors are consistently related to CR referral and enrollment. The role of physician endorsements in promoting patient enrollment should be optimized and exploited.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22125" xmlns="http://purl.org/rss/1.0/"><title>Study Design and Rationale of a Dose-Ranging Trial of LX4211, a Dual Inhibitor of SGLT1 and SGLT2, in Type 2 Diabetes Inadequately Controlled on Metformin Monotherapy</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22125</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Study Design and Rationale of a Dose-Ranging Trial of LX4211, a Dual Inhibitor of SGLT1 and SGLT2, in Type 2 Diabetes Inadequately Controlled on Metformin Monotherapy</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Pablo Lapuerta, Julio Rosenstock, Brian Zambrowicz, David R. Powell, Ike Ogbaa, Joel Freiman, William T. Cefalu, Phillip Banks, Kenny Frazier, Mike Kelly, Arthur Sands</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-29T08:33:43.715539-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22125</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22125</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22125</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Trial Designs</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">ABSTRACT</h3>
<div class="section" id="clc22125-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><div class="para"><p>Sodium-glucose cotransporters 1 (SGLT1) and 2 (SGLT2) are the major cellular transporters responsible for gastrointestinal (GI) glucose absorption and renal glucose reabsorption, respectively. LX4211, a dual inhibitor of SGLT1 and SGLT2, reduces glucose absorption from the GI tract and enhances urinary glucose excretion. Although several SGLT2-selective inhibitors have been tested in large phase 2 studies, dual inhibition of SGLT1 and SGLT2 is novel at this stage of drug development, and it has implications for clinical-trial design. In this article, we describe the design and rationale of a phase 2, multicenter, randomized, double-blind, placebo-controlled, parallel group study to evaluate the safety and efficacy of LX4211 in subjects with type 2 diabetes mellitus who have inadequate glycemic control on metformin monotherapy. The primary endpoint is the change in glycated hemoglobin A<sub>1c</sub> from baseline to week 12. Secondary endpoints include the proportion of subjects achieving a glycated hemoglobin A<sub>1c</sub> value of &lt;7%, change from baseline in fasting plasma glucose and postprandial glucose (as part of an oral glucose tolerance test), body weight, and blood pressure. Safety is evaluated with particular focus on hypoglycemia, GI symptoms, and incidence of genitourinary tract infections.</p></div></div>
]]></content:encoded><description>

Sodium-glucose cotransporters 1 (SGLT1) and 2 (SGLT2) are the major cellular transporters responsible for gastrointestinal (GI) glucose absorption and renal glucose reabsorption, respectively. LX4211, a dual inhibitor of SGLT1 and SGLT2, reduces glucose absorption from the GI tract and enhances urinary glucose excretion. Although several SGLT2-selective inhibitors have been tested in large phase 2 studies, dual inhibition of SGLT1 and SGLT2 is novel at this stage of drug development, and it has implications for clinical-trial design. In this article, we describe the design and rationale of a phase 2, multicenter, randomized, double-blind, placebo-controlled, parallel group study to evaluate the safety and efficacy of LX4211 in subjects with type 2 diabetes mellitus who have inadequate glycemic control on metformin monotherapy. The primary endpoint is the change in glycated hemoglobin A1c from baseline to week 12. Secondary endpoints include the proportion of subjects achieving a glycated hemoglobin A1c value of &lt;7%, change from baseline in fasting plasma glucose and postprandial glucose (as part of an oral glucose tolerance test), body weight, and blood pressure. Safety is evaluated with particular focus on hypoglycemia, GI symptoms, and incidence of genitourinary tract infections.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22117" xmlns="http://purl.org/rss/1.0/"><title>Platelet Inhibitory Effect of Clopidogrel in Patients Treated With Omeprazole, Pantoprazole, and Famotidine: A Prospective, Randomized, Crossover Study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22117</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Platelet Inhibitory Effect of Clopidogrel in Patients Treated With Omeprazole, Pantoprazole, and Famotidine: A Prospective, Randomized, Crossover Study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yaron Arbel, Edo Y. Birati, Ariel Finkelstein, Amir Halkin, Hanna Kletzel, Yigal Abramowitz, Shlomo Berliner, Varda Deutsch, Itzhak Herz, Gad Keren, Shmuel Banai</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-29T08:33:38.913563-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22117</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22117</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22117</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22117-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Concerns about an inhibitory effect of proton pump inhibitors (PPIs) on clopidogrel metabolism have been raised. Because the pharmacological effect of clopidogrel is dependent on genetically determined activity of the hepatic cytochrome P450 isoenzymes system, it is important to examine the interaction between different PPIs and high on-treatment platelet reactivity (HPR) after controlling for genetic variability. The aim of the study was to assess the effect of 2 PPIs and a histamine-2 (H2) receptor-blocker on platelet reactivity in a crossover trial where each patient was alternately treated with each drug.</p></div></div>
<div class="section" id="clc22117-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Omeprazole reduces HPR more than other PPI or H<sub>2</sub> blockers.</p></div></div>
<div class="section" id="clc22117-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Patients treated with aspirin and clopidogrel for at least 1 month were assigned to 3 consecutive 1-month treatment periods during which they were treated with each of the 3 study medications twice daily: omeprazole 20 mg, famotidine 40 mg, and pantoprazole 20 mg. At the end of each treatment phase, platelet function was evaluated with the Verify Now system using 2 cutoff values (&gt;208 P2Y12 reaction units [PRUs] and &gt;230 PRUs) for the definition of HPR.</p></div></div>
<div class="section" id="clc22117-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Patients with HPR were older than those without HPR (62 ± 10 vs 55 ± 8 years, respectively, P = 0.03). HPR was more prevalent during omeprazole therapy compared to famotidine or pantoprazole (48%, 33%, and 31%, respectively, for the 208 PRU cutoff, P= 0.04; and 37%, 17%, and 23%, respectively, for the 230 PRU cutoff, P= 0.003).</p></div></div>
<div class="section" id="clc22117-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>After eliminating the effects of interindividual variability in clopidogrel metabolism, omeprazole therapy was associated with substantially more HPR than famotidine or pantoprazole.</p></div></div>
]]></content:encoded><description>


Background
Concerns about an inhibitory effect of proton pump inhibitors (PPIs) on clopidogrel metabolism have been raised. Because the pharmacological effect of clopidogrel is dependent on genetically determined activity of the hepatic cytochrome P450 isoenzymes system, it is important to examine the interaction between different PPIs and high on-treatment platelet reactivity (HPR) after controlling for genetic variability. The aim of the study was to assess the effect of 2 PPIs and a histamine-2 (H2) receptor-blocker on platelet reactivity in a crossover trial where each patient was alternately treated with each drug.


Hypothesis
Omeprazole reduces HPR more than other PPI or H2 blockers.


Methods
Patients treated with aspirin and clopidogrel for at least 1 month were assigned to 3 consecutive 1-month treatment periods during which they were treated with each of the 3 study medications twice daily: omeprazole 20 mg, famotidine 40 mg, and pantoprazole 20 mg. At the end of each treatment phase, platelet function was evaluated with the Verify Now system using 2 cutoff values (&gt;208 P2Y12 reaction units [PRUs] and &gt;230 PRUs) for the definition of HPR.


Results
Patients with HPR were older than those without HPR (62 ± 10 vs 55 ± 8 years, respectively, P = 0.03). HPR was more prevalent during omeprazole therapy compared to famotidine or pantoprazole (48%, 33%, and 31%, respectively, for the 208 PRU cutoff, P= 0.04; and 37%, 17%, and 23%, respectively, for the 230 PRU cutoff, P= 0.003).


Conclusions
After eliminating the effects of interindividual variability in clopidogrel metabolism, omeprazole therapy was associated with substantially more HPR than famotidine or pantoprazole.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22124" xmlns="http://purl.org/rss/1.0/"><title>Heart Transplantation and Left Ventricular Assist Device Therapy: Two Comparable Options in End-Stage Heart Failure?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22124</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Heart Transplantation and Left Ventricular Assist Device Therapy: Two Comparable Options in End-Stage Heart Failure?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jens Garbade, Markus J. Barten, Hartmuth B. Bittner, Friedrich-Wilhelm Mohr</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-17T17:34:10.456065-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22124</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22124</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22124</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Heart transplantation is the only curative therapy for chronic heart failure, and it plays an important role in the treatment of chronic heart failure with a survival rate of approximately 50% of all patients after 10 years. This has to be kept in mind when alternative therapies enter into our daily routine in treating this patient population. However, the shortage of appropriate donor organs and the expanding pool of patients waiting for heart transplantation have led to growing interest in alternative strategies, particularly in left ventricular assist device (LVAD) therapy. With growing clinical experience and continued technical advances, continuous-flow pumps are evolving as a bridge to transplantation or as a destination therapy for advanced heart failure. Nevertheless, the importance of this new indication of chronic cardiac support compared to heart transplantation is still completely open and the object of controversial ongoing discussion. This review (1) describes the clinical use and long-term outcome of a currently available miniaturized LVAD in the context to the standard of care—heart transplantation, (2) provides an outlook of the ongoing process of further optimization of LVADs, and (3) comments on the challenges with assist devices as alternatives to transplantation with a 5-year outlook.</p></div>
]]></content:encoded><description>

Heart transplantation is the only curative therapy for chronic heart failure, and it plays an important role in the treatment of chronic heart failure with a survival rate of approximately 50% of all patients after 10 years. This has to be kept in mind when alternative therapies enter into our daily routine in treating this patient population. However, the shortage of appropriate donor organs and the expanding pool of patients waiting for heart transplantation have led to growing interest in alternative strategies, particularly in left ventricular assist device (LVAD) therapy. With growing clinical experience and continued technical advances, continuous-flow pumps are evolving as a bridge to transplantation or as a destination therapy for advanced heart failure. Nevertheless, the importance of this new indication of chronic cardiac support compared to heart transplantation is still completely open and the object of controversial ongoing discussion. This review (1) describes the clinical use and long-term outcome of a currently available miniaturized LVAD in the context to the standard of care—heart transplantation, (2) provides an outlook of the ongoing process of further optimization of LVADs, and (3) comments on the challenges with assist devices as alternatives to transplantation with a 5-year outlook.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22130" xmlns="http://purl.org/rss/1.0/"><title>Cost-Effectiveness of Paclitaxel-Coated Balloon Angioplasty in Patients With Drug-Eluting Stent Restenosis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22130</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cost-Effectiveness of Paclitaxel-Coated Balloon Angioplasty in Patients With Drug-Eluting Stent Restenosis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Marc Dorenkamp, Julia Boldt, Alexander W. Leber, Christian Sohns, Mattias Roser, Leif-Hendrik Boldt, Wilhelm Haverkamp, Klaus Bonaventura</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-17T17:34:00.557446-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22130</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22130</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22130</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22130-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The economic impact of drug-eluting stent (DES) in-stent restenosis (ISR) is substantial, highlighting the need for cost-effective treatment strategies.</p></div></div>
<div class="section" id="clc22130-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Compared to plain old balloon angioplasty (POBA) or repeat DES implantation, drug-coated balloon (DCB) angioplasty is a cost-effective therapy for DES-ISR.</p></div></div>
<div class="section" id="clc22130-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A Markov state-transition model was used to compare DCB angioplasty with POBA and repeat DES implantation. Model input parameters were obtained from the literature, and the cost analysis was conducted from a German healthcare payer's perspective. Extensive sensitivity analyses were performed.</p></div></div>
<div class="section" id="clc22130-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Initial procedure costs amounted to €3488 for DCB angioplasty and to €2782 for POBA. Over a 6-month time horizon, the DCB strategy was less costly (€4028 vs €4169) and more effective in terms of life-years (LYs) gained (0.497 versus 0.489) than POBA. The DES strategy incurred initial costs of €3167 and resulted in 0.494 LYs gained, at total costs of €4101 after a 6-month follow-up. Thus, DCB angioplasty was the least costly and most effective strategy. Base-case results were influenced mostly by initial procedure costs, target lesion revascularization rates, and the costs of dual antiplatelet therapy.</p></div></div>
<div class="section" id="clc22130-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>DCB angioplasty is a cost-effective treatment option for coronary DES-ISR. The higher initial costs of the DCB strategy compared to POBA or repeat DES implantation are offset by later cost savings.</p></div></div>
]]></content:encoded><description>


Background
The economic impact of drug-eluting stent (DES) in-stent restenosis (ISR) is substantial, highlighting the need for cost-effective treatment strategies.


Hypothesis
Compared to plain old balloon angioplasty (POBA) or repeat DES implantation, drug-coated balloon (DCB) angioplasty is a cost-effective therapy for DES-ISR.


Methods
A Markov state-transition model was used to compare DCB angioplasty with POBA and repeat DES implantation. Model input parameters were obtained from the literature, and the cost analysis was conducted from a German healthcare payer's perspective. Extensive sensitivity analyses were performed.


Results
Initial procedure costs amounted to €3488 for DCB angioplasty and to €2782 for POBA. Over a 6-month time horizon, the DCB strategy was less costly (€4028 vs €4169) and more effective in terms of life-years (LYs) gained (0.497 versus 0.489) than POBA. The DES strategy incurred initial costs of €3167 and resulted in 0.494 LYs gained, at total costs of €4101 after a 6-month follow-up. Thus, DCB angioplasty was the least costly and most effective strategy. Base-case results were influenced mostly by initial procedure costs, target lesion revascularization rates, and the costs of dual antiplatelet therapy.


Conclusions
DCB angioplasty is a cost-effective treatment option for coronary DES-ISR. The higher initial costs of the DCB strategy compared to POBA or repeat DES implantation are offset by later cost savings.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22127" xmlns="http://purl.org/rss/1.0/"><title>Improvement of Arterial Stiffness in the Transition From Acute Decompensated Heart Failure to Chronic Compensated Heart Failure</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22127</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Improvement of Arterial Stiffness in the Transition From Acute Decompensated Heart Failure to Chronic Compensated Heart Failure</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dong-Bin Kim, Sang Hong Baek, Sung Won Jang, Sung-Ho Her, Dong-Il Shin, Chan Seok Park, Hoon Joon Park, Pum Joon Kim, Hae Ok Jung, Ki Bae Seung</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-12T15:09:51.370654-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22127</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22127</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22127</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22127-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Pulse wave velocity (PWV) is a well-established marker for aortic stiffness and may be a prognostic factor in heart failure (HF). This study investigates whether PWV changes as patients transition from acute decompensated heart failure (ADHF) to chronic compensated heart failure (CCHF).</p></div></div>
<div class="section" id="clc22127-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Arterial stiffness is related with the development of HF.</p></div></div>
<div class="section" id="clc22127-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Regional PWV was prospectively measured using noninvasive applanation tonometry in consecutive ADHF patients (n = 55). PWV measurements of 45 patients were taken at admission and 3-month follow-up (F/U).</p></div></div>
<div class="section" id="clc22127-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Central and upper-extremity PWV, but not lower-extremity PWVs, were found to have improved after 3 months compared with the admission PWV (central: 8.73 ± 1.17 vs 8.39 ± 0.99 m/s, <i>P =</i> 0.018; upper extremity: 8.59 ± 0.84 vs 8.33 ± 0.82 m/s, <i>P</i> = 0.028). Multivariate logistic regression analyses revealed that low-density lipoprotein cholesterol was significantly associated with the change of PWV in HF (odds ratio: 1.037, 95% confidence interval: 1.003-1.071, <i>P</i> = 0.030). In preserved left ventricular ejection fraction patients (n = 26) and ischemic patients (n = 31), central and upper-extremity PWVs improved over the admission PWV at 3-month F/U.</p></div></div>
<div class="section" id="clc22127-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The present results indicate that central and upper-extremity PWVs, but not lower-extremity PWV, are increased in ADHF and improve as patients transition from ADHF to CCHF.</p></div></div>
]]></content:encoded><description>


Background
Pulse wave velocity (PWV) is a well-established marker for aortic stiffness and may be a prognostic factor in heart failure (HF). This study investigates whether PWV changes as patients transition from acute decompensated heart failure (ADHF) to chronic compensated heart failure (CCHF).


Hypothesis
Arterial stiffness is related with the development of HF.


Methods
Regional PWV was prospectively measured using noninvasive applanation tonometry in consecutive ADHF patients (n = 55). PWV measurements of 45 patients were taken at admission and 3-month follow-up (F/U).


Results
Central and upper-extremity PWV, but not lower-extremity PWVs, were found to have improved after 3 months compared with the admission PWV (central: 8.73 ± 1.17 vs 8.39 ± 0.99 m/s, P = 0.018; upper extremity: 8.59 ± 0.84 vs 8.33 ± 0.82 m/s, P = 0.028). Multivariate logistic regression analyses revealed that low-density lipoprotein cholesterol was significantly associated with the change of PWV in HF (odds ratio: 1.037, 95% confidence interval: 1.003-1.071, P = 0.030). In preserved left ventricular ejection fraction patients (n = 26) and ischemic patients (n = 31), central and upper-extremity PWVs improved over the admission PWV at 3-month F/U.


Conclusions
The present results indicate that central and upper-extremity PWVs, but not lower-extremity PWV, are increased in ADHF and improve as patients transition from ADHF to CCHF.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22129" xmlns="http://purl.org/rss/1.0/"><title>Dissociation Between Severity of Takotsubo Cardiomyopathy and Presentation With Shock or Hypotension</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22129</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Dissociation Between Severity of Takotsubo Cardiomyopathy and Presentation With Shock or Hypotension</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Cher-Rin Chong, Christopher J. Neil, Thanh H. Nguyen, Jeanette Stansborough, Gin Way Law, Kuljit Singh, John D. Horowitz</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-12T15:08:51.32933-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22129</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22129</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22129</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22129-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Takotsubo cardiomyopathy (TTC) is increasingly well-recognized as a cause of chest-pain syndromes, especially in aging females. The most common complications of TTC occur in the first 24 hours post onset of symptoms and include shock and/or arrhythmias.</p></div></div>
<div class="section" id="clc22129-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>We tested the hypothesis that the severity of early hypotension in TTC reflects the extent of myocardial involvement and dysfunction.</p></div></div>
<div class="section" id="clc22129-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>In 80 consecutive TTC patients, correlates of blood pressure on the day of admission were sought via univariate followed by multivariate analysis.</p></div></div>
<div class="section" id="clc22129-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Mean systolic blood pressure (SBP) on day 1 was 120 ± 24 (SD) mm Hg. During the first 3 days of admission, 39% of patients had SBP &lt;90 mm Hg, and 9% died and/or required intra-aortic balloon pump insertion. The extent of release of N-terminal pro-brain natriuretic peptide, with its potential correlate of associated vasodilator activity, varied inversely with pulmonary-artery saturation, a measure of cardiac output. However, there was no significant relationship between normetanephrine release and SBP. On multivariate analyses there was no significant relationship between SBP and (1) wall-motion score index (as an index of left-ventricular systolic dysfunction) or (2) T<sub>2</sub> enhancement on cardiac magnetic resonance imaging and peak N-terminal pro-brain natriuretic peptide (as indices of myocardial inflammation).</p></div></div>
<div class="section" id="clc22129-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Although severe hypotension and shock occur commonly during acute stages of TTC, these complications are multifactorial in origin, probably representing a combination of impaired inotropic state and vasodilatation. Importantly, initial hypotension does not imply severe left ventricular inflammation or systolic dysfunction.</p></div></div>
]]></content:encoded><description>


Background
Takotsubo cardiomyopathy (TTC) is increasingly well-recognized as a cause of chest-pain syndromes, especially in aging females. The most common complications of TTC occur in the first 24 hours post onset of symptoms and include shock and/or arrhythmias.


Hypothesis
We tested the hypothesis that the severity of early hypotension in TTC reflects the extent of myocardial involvement and dysfunction.


Methods
In 80 consecutive TTC patients, correlates of blood pressure on the day of admission were sought via univariate followed by multivariate analysis.


Results
Mean systolic blood pressure (SBP) on day 1 was 120 ± 24 (SD) mm Hg. During the first 3 days of admission, 39% of patients had SBP &lt;90 mm Hg, and 9% died and/or required intra-aortic balloon pump insertion. The extent of release of N-terminal pro-brain natriuretic peptide, with its potential correlate of associated vasodilator activity, varied inversely with pulmonary-artery saturation, a measure of cardiac output. However, there was no significant relationship between normetanephrine release and SBP. On multivariate analyses there was no significant relationship between SBP and (1) wall-motion score index (as an index of left-ventricular systolic dysfunction) or (2) T2 enhancement on cardiac magnetic resonance imaging and peak N-terminal pro-brain natriuretic peptide (as indices of myocardial inflammation).


Conclusions
Although severe hypotension and shock occur commonly during acute stages of TTC, these complications are multifactorial in origin, probably representing a combination of impaired inotropic state and vasodilatation. Importantly, initial hypotension does not imply severe left ventricular inflammation or systolic dysfunction.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22121" xmlns="http://purl.org/rss/1.0/"><title>Impact of Concomitant Coronary Artery Disease on Atherosclerotic Plaques in the Aortic Arch in Patients With Severe Aortic Stenosis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22121</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Impact of Concomitant Coronary Artery Disease on Atherosclerotic Plaques in the Aortic Arch in Patients With Severe Aortic Stenosis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Suwako Fujita, Kenichi Sugioka, Yoshiki Matsumura, Asahiro Ito, Takeshi Hozumi, Takao Hasegawa, Akihisa Hanatani, Takahiko Naruko, Makiko Ueda, Minoru Yoshiyama</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-12T14:05:25.160187-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22121</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22121</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22121</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22121-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Coronary artery disease (CAD) often occurs concurrently in patients with severe aortic stenosis (AS). However, the influence of concomitant CAD on the presence of atherosclerotic complex plaques in the aortic arch, which is associated with increased stroke risk, has not been fully assessed in patients with severe AS.</p></div></div>
<div class="section" id="clc22121-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>We hypothesized that concomitant CAD would be associated with the presence of complex arch plaques in patients with severe AS.</p></div></div>
<div class="section" id="clc22121-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The study population consisted of 154 patients with severe AS who had undergone transesophageal echocardiography (TEE) and coronary angiography (71 male; mean age, 72 ± 8 years; mean aortic valve area, 0.67 ± 0.15 cm<sup>2</sup>). Aortic arch plaques were assessed using TEE, and complex arch plaques were defined as large plaques (≥4 mm), ulcerated plaques, or mobile plaques.</p></div></div>
<div class="section" id="clc22121-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The prevalence of aortic arch plaques (87% vs 70%; P = 0.03) and complex arch plaques (48% vs 20%; P &lt; 0.001) was significantly greater in AS patients with CAD than in those without CAD. After adjustment for traditional atherosclerotic risk factors, we found that concomitant CAD was independently associated with the presence of complex arch plaques (odds ratio: 2.86, 95% confidence interval: 1.23-6.68, P = 0.01).</p></div></div>
<div class="section" id="clc22121-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In patients with severe AS, concomitant CAD is associated with severe atherosclerotic burden in the aortic arch. This observation suggests that AS patients with concomitant CAD are at a higher risk for stroke, and that careful evaluation of complex arch plaques by TEE is needed for the risk stratification of stroke in these patients.</p></div></div>
]]></content:encoded><description>


Background
Coronary artery disease (CAD) often occurs concurrently in patients with severe aortic stenosis (AS). However, the influence of concomitant CAD on the presence of atherosclerotic complex plaques in the aortic arch, which is associated with increased stroke risk, has not been fully assessed in patients with severe AS.


Hypothesis
We hypothesized that concomitant CAD would be associated with the presence of complex arch plaques in patients with severe AS.


Methods
The study population consisted of 154 patients with severe AS who had undergone transesophageal echocardiography (TEE) and coronary angiography (71 male; mean age, 72 ± 8 years; mean aortic valve area, 0.67 ± 0.15 cm2). Aortic arch plaques were assessed using TEE, and complex arch plaques were defined as large plaques (≥4 mm), ulcerated plaques, or mobile plaques.


Results
The prevalence of aortic arch plaques (87% vs 70%; P = 0.03) and complex arch plaques (48% vs 20%; P &lt; 0.001) was significantly greater in AS patients with CAD than in those without CAD. After adjustment for traditional atherosclerotic risk factors, we found that concomitant CAD was independently associated with the presence of complex arch plaques (odds ratio: 2.86, 95% confidence interval: 1.23-6.68, P = 0.01).


Conclusions
In patients with severe AS, concomitant CAD is associated with severe atherosclerotic burden in the aortic arch. This observation suggests that AS patients with concomitant CAD are at a higher risk for stroke, and that careful evaluation of complex arch plaques by TEE is needed for the risk stratification of stroke in these patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22128" xmlns="http://purl.org/rss/1.0/"><title>Reduced Diurnal Variation of Heart Rate is Associated With Increased Plasma B-Type Natriuretic Peptide Level in Patients With Atrial Fibrillation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22128</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Reduced Diurnal Variation of Heart Rate is Associated With Increased Plasma B-Type Natriuretic Peptide Level in Patients With Atrial Fibrillation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shigeshi Kamikawa, Toru Miyoshi, Masayuki Doi, Naoko Orita, Mutsuko Sangawa, Takaaki Nakatsu, Youko Noguchi, Satoshi Hirohata, Shozo Kusachi, Kazufumi Nakamura, Hiroshi Ito</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-12T14:03:10.910788-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22128</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22128</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22128</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22128-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The plasma B-type natriuretic peptide (BNP) level has been shown to be increased in patients with chronic atrial fibrillation (AF) independent of left ventricular ejection fraction (LVEF). The purpose of this study is to evaluate the relationship between the plasma BNP level and heart rate variation in patients with AF.</p></div></div>
<div class="section" id="clc22128-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>The plasma BNP level is associated with heart rate variation in patients with AF.</p></div></div>
<div class="section" id="clc22128-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A total  of 102 patients with AF and preserved LVEF were included from 2 hospitals. The ambulatory electrocardiographic recording and measurement of plasma BNP levels were performed simultaneously. Echo-Doppler parameters were measured as the average of 10 consecutive cardiac cycles.</p></div></div>
<div class="section" id="clc22128-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>A difference in the mean heart rate between night and day (DIFF) and the standard deviation of the 5-miniute mean R-R interval (SDARR) were significantly associated with log-transformed BNP levels (<i>r</i> = −0.411, <i>P</i> &lt; 0.001 and <i>r</i> = −0.243, <i>P</i> = 0.049, respectively). In echocardiography, the ratio of E velocity to early diastolic velocity, which reflects left ventricular (LV) filling pressure, was significantly correlated with the DIFF and SDARR, along with the log-transformed BNP level. Stepwise multiple linear regression analysis revealed that the DIFF and age were independent factors related with the BNP level (<i>P</i> &lt; 0.01).</p></div></div>
<div class="section" id="clc22128-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The reduced diurnal variation of heart rate was significantly associated with increased BNP, which is linked to LV diastolic dysfunction in patients with AF.</p></div></div>
]]></content:encoded><description>


Background
The plasma B-type natriuretic peptide (BNP) level has been shown to be increased in patients with chronic atrial fibrillation (AF) independent of left ventricular ejection fraction (LVEF). The purpose of this study is to evaluate the relationship between the plasma BNP level and heart rate variation in patients with AF.


Hypothesis
The plasma BNP level is associated with heart rate variation in patients with AF.


Methods
A total  of 102 patients with AF and preserved LVEF were included from 2 hospitals. The ambulatory electrocardiographic recording and measurement of plasma BNP levels were performed simultaneously. Echo-Doppler parameters were measured as the average of 10 consecutive cardiac cycles.


Results
A difference in the mean heart rate between night and day (DIFF) and the standard deviation of the 5-miniute mean R-R interval (SDARR) were significantly associated with log-transformed BNP levels (r = −0.411, P &lt; 0.001 and r = −0.243, P = 0.049, respectively). In echocardiography, the ratio of E velocity to early diastolic velocity, which reflects left ventricular (LV) filling pressure, was significantly correlated with the DIFF and SDARR, along with the log-transformed BNP level. Stepwise multiple linear regression analysis revealed that the DIFF and age were independent factors related with the BNP level (P &lt; 0.01).


Conclusions
The reduced diurnal variation of heart rate was significantly associated with increased BNP, which is linked to LV diastolic dysfunction in patients with AF.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22122" xmlns="http://purl.org/rss/1.0/"><title>Advances in Stroke Prevention in Atrial Fibrillation: Enhanced Risk Stratification Combined With the Newer Oral Anticoagulants</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22122</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Advances in Stroke Prevention in Atrial Fibrillation: Enhanced Risk Stratification Combined With the Newer Oral Anticoagulants</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Freek W. A. Verheugt</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-08T09:42:25.834873-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22122</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22122</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22122</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Patients with atrial fibrillation (AF) have an increased stroke risk compared with those in sinus rhythm, although the absolute risk for individual patients is modulated by the presence of various additional risk factors. Patient selection for oral anticoagulation for stroke prevention is based on risks of stroke and bleeding. Although CHADS<sub>2</sub> (congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, stroke or transient ischemic attack) is the most widely used scheme for evaluating stroke risk in patients with AF, several other stroke risk factors are not included; therefore, many patients' stroke risk may be underestimated, contributing to the underuse of anticoagulants. Furthermore, a substantial proportion of patients are categorized as being at moderate risk (CHADS<sub>2</sub> = 1), and there has been some ambiguity regarding optimum thromboprophylaxis in this group. The refinement of CHADS<sub>2</sub>, CHA<sub>2</sub>DS<sub>2</sub>-VASc (Congestive heart failure, Hypertension, Age 75 years [2 points], Diabetes mellitus, Stroke or transient ischemic attack [2 points], Vascular disease, Age 65 to 74 years, Sex category [female]), considers additional risk factors. Its main advantage is its ability to identify patients truly at low risk of thromboembolism (CHA<sub>2</sub>DS<sub>2</sub>-VASc = 0), who are unlikely to benefit from antithrombotic therapy. For all others, an oral anticoagulant may be the preferred approach, simplifying clinical decision making. Implementation of CHA<sub>2</sub>DS<sub>2</sub>-VASc may also result in an increased proportion of patients receiving anticoagulation. The emergence of newer oral anticoagulants that can be given without routine coagulation monitoring, with improved benefit–risk profiles vs vitamin K antagonists, promises to simplify therapy for patients with AF at risk of stroke. This, coupled with advances in stroke risk stratification, is expected to improve patient outcomes and reduce the burden of AF-related stroke.</p></div>
]]></content:encoded><description>

Patients with atrial fibrillation (AF) have an increased stroke risk compared with those in sinus rhythm, although the absolute risk for individual patients is modulated by the presence of various additional risk factors. Patient selection for oral anticoagulation for stroke prevention is based on risks of stroke and bleeding. Although CHADS2 (congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, stroke or transient ischemic attack) is the most widely used scheme for evaluating stroke risk in patients with AF, several other stroke risk factors are not included; therefore, many patients' stroke risk may be underestimated, contributing to the underuse of anticoagulants. Furthermore, a substantial proportion of patients are categorized as being at moderate risk (CHADS2 = 1), and there has been some ambiguity regarding optimum thromboprophylaxis in this group. The refinement of CHADS2, CHA2DS2-VASc (Congestive heart failure, Hypertension, Age 75 years [2 points], Diabetes mellitus, Stroke or transient ischemic attack [2 points], Vascular disease, Age 65 to 74 years, Sex category [female]), considers additional risk factors. Its main advantage is its ability to identify patients truly at low risk of thromboembolism (CHA2DS2-VASc = 0), who are unlikely to benefit from antithrombotic therapy. For all others, an oral anticoagulant may be the preferred approach, simplifying clinical decision making. Implementation of CHA2DS2-VASc may also result in an increased proportion of patients receiving anticoagulation. The emergence of newer oral anticoagulants that can be given without routine coagulation monitoring, with improved benefit–risk profiles vs vitamin K antagonists, promises to simplify therapy for patients with AF at risk of stroke. This, coupled with advances in stroke risk stratification, is expected to improve patient outcomes and reduce the burden of AF-related stroke.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22114" xmlns="http://purl.org/rss/1.0/"><title>Incremental Predictive Value of Red Cell Distribution Width for 12-Month Clinical Outcome After Acute Myocardial Infarction</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22114</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Incremental Predictive Value of Red Cell Distribution Width for 12-Month Clinical Outcome After Acute Myocardial Infarction</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jang Hoon Lee, Dong Heon Yang, Se Yong Jang, Won Suk Choi, Kyun Hee Kim, Won Kee Lee, Myung Hwan Bae, Hun Sik Park, Yongkeun Cho, Shung Chull Chae</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-08T09:42:11.353223-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22114</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22114</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22114</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22114-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The incremental predictive value of red cell distribution width (RDW) for major adverse cardiac events (MACEs) has not been fully investigated in patients with acute myocardial infarction (AMI).</p></div></div>
<div class="section" id="clc22114-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>The aim of this study was to determine the incremental value of RDW to the established risk factors in predicting clinical outcomes after AMI.</p></div></div>
<div class="section" id="clc22114-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Between November 2005 and January 2010, 1596 patients with AMI (1070 male; mean age, 64.5 ± 11.9 years) were analyzed in this study. Baseline levels of RDW were measured at the time of admission. The 12-month MACEs were defined as death and nonfatal MI.</p></div></div>
<div class="section" id="clc22114-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The RDW levels were significantly higher in patients with 12-month MACEs (13.8 ± 1.3% vs 13.3 ± 1.2%, <i>P</i> &lt; 0.001). In a Cox proportional hazards model, RDW (hazard ratio [HR]: 1.19, <i>P</i> = 0.016) was an independent predictor for 12-month MACEs. Adding RDW to established risk factors and hemoglobin levels significantly improved prediction for 12-month MACEs, as shown by the net reclassification improvement (0.297; <i>P</i> = 0.012) and integrated discrimination improvement (0.0143; <i>P</i> = 0.042). The likelihood ratio test showed that RDW added incremental predictive value to the combination of hemoglobin and established risk factors (<i>P</i> = 0.005). Patients were categorized into 4 groups according to quartiles of RDW at baseline. Adjusted HRs for 12-month MACEs were 1 (RDW ≤12.6%, reference), 4.24 (RDW 12.7%–13.1%, <i>P</i> = 0.01), 4.36 (RDW 13.2%–13.9%, <i>P</i> = 0.008), and 6.18 (RDW 13.2%–13.9%, <i>P</i> = 0.001), respectively.</p></div></div>
<div class="section" id="clc22114-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In post-myocardial infarction patients, baseline RDW levels at admission could provide incremental predictive value to established risk factors for predicting 12-month MACEs.</p></div></div>
]]></content:encoded><description>


Background
The incremental predictive value of red cell distribution width (RDW) for major adverse cardiac events (MACEs) has not been fully investigated in patients with acute myocardial infarction (AMI).


Hypothesis
The aim of this study was to determine the incremental value of RDW to the established risk factors in predicting clinical outcomes after AMI.


Methods
Between November 2005 and January 2010, 1596 patients with AMI (1070 male; mean age, 64.5 ± 11.9 years) were analyzed in this study. Baseline levels of RDW were measured at the time of admission. The 12-month MACEs were defined as death and nonfatal MI.


Results
The RDW levels were significantly higher in patients with 12-month MACEs (13.8 ± 1.3% vs 13.3 ± 1.2%, P &lt; 0.001). In a Cox proportional hazards model, RDW (hazard ratio [HR]: 1.19, P = 0.016) was an independent predictor for 12-month MACEs. Adding RDW to established risk factors and hemoglobin levels significantly improved prediction for 12-month MACEs, as shown by the net reclassification improvement (0.297; P = 0.012) and integrated discrimination improvement (0.0143; P = 0.042). The likelihood ratio test showed that RDW added incremental predictive value to the combination of hemoglobin and established risk factors (P = 0.005). Patients were categorized into 4 groups according to quartiles of RDW at baseline. Adjusted HRs for 12-month MACEs were 1 (RDW ≤12.6%, reference), 4.24 (RDW 12.7%–13.1%, P = 0.01), 4.36 (RDW 13.2%–13.9%, P = 0.008), and 6.18 (RDW 13.2%–13.9%, P = 0.001), respectively.


Conclusions
In post-myocardial infarction patients, baseline RDW levels at admission could provide incremental predictive value to established risk factors for predicting 12-month MACEs.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22120" xmlns="http://purl.org/rss/1.0/"><title>Letters to the Editor</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22120</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Letters to the Editor</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Krishna Kumar Mohanan Nair, Harikrishnan Sivadasan Pillai, Jaganmohan Tharakan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-01T09:27:12.05507-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22120</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22120</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22120</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letters to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22118" xmlns="http://purl.org/rss/1.0/"><title>Elevated Rho-Kinase Activity as a Marker Indicating Atherosclerosis and Inflammation Burden in Polyvascular Disease Patients With Concomitant Coronary and Peripheral Arterial Disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22118</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Elevated Rho-Kinase Activity as a Marker Indicating Atherosclerosis and Inflammation Burden in Polyvascular Disease Patients With Concomitant Coronary and Peripheral Arterial Disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ming Dong, Xin Jiang, James K. Liao, Bryan P. Yan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-28T09:20:49.771901-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22118</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22118</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22118</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22118-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Recent evidence suggests that Rho-kinase (ROCK) plays an important role in the pathogenesis of atherosclerosis and a marker of atherosclerotic burden. Polyvascular disease with concomitant peripheral arterial disease (PAD) and coronary artery disease (CAD) is common and associated with a worse prognosis. The aim of this study was to evaluate ROCK activity as a marker of polyvascular disease.</p></div></div>
<div class="section" id="clc22118-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4></div>
<div class="section" id="clc22118-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We retrospectively analyzed patients undergoing coronary angiography at our institution between February 2009 and May 2009. Patients with only CAD (n = 40) defined by coronary artery stenosis of ≥50% by angiography, only PAD (n = 40) defined by an ankle brachial index (ABI) &lt;0.9, and combined CAD/PAD (n = 40) were matched by age and sex to control patients (n = 40) without CAD or PAD. ROCK activity was determined by phosphorylation of the myosin binding subunit in leukocytes and then compared between each group. Multivariate analysis was used to determine independent predictors of polyvascular disease. Discriminative ability of elevated ROCK activity was assessed using receiver operator characteristics (ROC) curves.</p></div></div>
<div class="section" id="clc22118-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Patients (age 68 ± 12 years, 79% male) with CAD, PAD, and CAD/PAD had a mean ABI of 1.08, 0.62, and 0.65, respectively, compared to 1.08 in the control group. There was an incremental increase in ROCK activity in patients with CAD (4.61 ± 2.11), PAD (4.27 ± 1.39), and CAD/PAD (5.96 ± 1.94) compared to control (2.40 ± 0.43) (all P &lt; 0.05). ROCK activity (odds ratio: 4.53, 95% confidence interval: 1.26-6.30) was an independent predictor of polyvascular disease. The ROCK cutoff value of 4.85 had a sensitivity of 72.7% and a specificity of 65.7%, with an area under ROC curve of 0.71 for polyvascular disease.</p></div></div>
<div class="section" id="clc22118-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Patients with concomitant peripheral and coronary arterial disease are associated with increased Rho-kinase activity. Rho-kinase activity may be a potential marker of atherosclerotic burden for patients with polyvascular disease.</p></div></div>
]]></content:encoded><description>


Background
Recent evidence suggests that Rho-kinase (ROCK) plays an important role in the pathogenesis of atherosclerosis and a marker of atherosclerotic burden. Polyvascular disease with concomitant peripheral arterial disease (PAD) and coronary artery disease (CAD) is common and associated with a worse prognosis. The aim of this study was to evaluate ROCK activity as a marker of polyvascular disease.


Hypothesis


Methods
We retrospectively analyzed patients undergoing coronary angiography at our institution between February 2009 and May 2009. Patients with only CAD (n = 40) defined by coronary artery stenosis of ≥50% by angiography, only PAD (n = 40) defined by an ankle brachial index (ABI) &lt;0.9, and combined CAD/PAD (n = 40) were matched by age and sex to control patients (n = 40) without CAD or PAD. ROCK activity was determined by phosphorylation of the myosin binding subunit in leukocytes and then compared between each group. Multivariate analysis was used to determine independent predictors of polyvascular disease. Discriminative ability of elevated ROCK activity was assessed using receiver operator characteristics (ROC) curves.


Results
Patients (age 68 ± 12 years, 79% male) with CAD, PAD, and CAD/PAD had a mean ABI of 1.08, 0.62, and 0.65, respectively, compared to 1.08 in the control group. There was an incremental increase in ROCK activity in patients with CAD (4.61 ± 2.11), PAD (4.27 ± 1.39), and CAD/PAD (5.96 ± 1.94) compared to control (2.40 ± 0.43) (all P &lt; 0.05). ROCK activity (odds ratio: 4.53, 95% confidence interval: 1.26-6.30) was an independent predictor of polyvascular disease. The ROCK cutoff value of 4.85 had a sensitivity of 72.7% and a specificity of 65.7%, with an area under ROC curve of 0.71 for polyvascular disease.


Conclusions
Patients with concomitant peripheral and coronary arterial disease are associated with increased Rho-kinase activity. Rho-kinase activity may be a potential marker of atherosclerotic burden for patients with polyvascular disease.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22110" xmlns="http://purl.org/rss/1.0/"><title>Cholesterol Levels and the Association of Statins With In-Hospital Mortality of Myocardial Infarction Patients Insights From a Chilean Registry of Myocardial Infarction</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22110</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cholesterol Levels and the Association of Statins With In-Hospital Mortality of Myocardial Infarction Patients Insights From a Chilean Registry of Myocardial Infarction</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gonzalo Martínez, Attilio Rigotti, Mónica Acevedo, Carlos Navarrete, Juanita Rosales, Robert P. Giugliano, Ramón Corbalán</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-14T10:58:52.703582-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22110</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22110</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22110</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Quality and Outcomes</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22110-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Hypercholesterolemia is a strong risk factor for myocardial infarction (MI). There is scarce information regarding lipoprotein levels among patients with MI in Latin America as well as about the association of very early statin therapy during the course of acute MI.</p></div></div>
<div class="section" id="clc22110-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Very early statin prescription might be associated with a reduction on in-hospital mortality in MI patients with nearly normal lipid levels.</p></div></div>
<div class="section" id="clc22110-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Prospective registry database analysis of MI patients admitted between 2001 and 2007 at a single university hospital from which demographics, treatments, clinical variables, and mortality were assessed. Patients naïve to statin therapy were divided in 2 groups, according to whether they received (group A) or did not receive (group B) statins during the first 24 hours after admission.</p></div></div>
<div class="section" id="clc22110-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In the 1465 patients analyzed, mean plasma levels of total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol (HDL-C) were 197, 117, and 44 mg/dL, respectively, and 41.8% had HDL-C ≤40 mg/dL. Among statin naïve patients (n = 1272), 67% were classified in group A and 33% in group B. Overall in-hospital mortality was 4.1%: 1.8% in group A and 8.5% in group B. In the multivariate analysis, including propensity score for statin prescription, the odds ratio for in-hospital mortality for group A was 0.971 (95% confidence interval: 0.944-0.999, <i>P</i> = 0.04).</p></div></div>
<div class="section" id="clc22110-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In the Chilean registry of MI patients, low HDL-C was the main lipid disturbance. Very early statin use after MI appears to be associated with a borderline significant and independent reduction of in-hospital mortality.</p></div></div>
]]></content:encoded><description>


Background
Hypercholesterolemia is a strong risk factor for myocardial infarction (MI). There is scarce information regarding lipoprotein levels among patients with MI in Latin America as well as about the association of very early statin therapy during the course of acute MI.


Hypothesis
Very early statin prescription might be associated with a reduction on in-hospital mortality in MI patients with nearly normal lipid levels.


Methods
Prospective registry database analysis of MI patients admitted between 2001 and 2007 at a single university hospital from which demographics, treatments, clinical variables, and mortality were assessed. Patients naïve to statin therapy were divided in 2 groups, according to whether they received (group A) or did not receive (group B) statins during the first 24 hours after admission.


Results
In the 1465 patients analyzed, mean plasma levels of total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol (HDL-C) were 197, 117, and 44 mg/dL, respectively, and 41.8% had HDL-C ≤40 mg/dL. Among statin naïve patients (n = 1272), 67% were classified in group A and 33% in group B. Overall in-hospital mortality was 4.1%: 1.8% in group A and 8.5% in group B. In the multivariate analysis, including propensity score for statin prescription, the odds ratio for in-hospital mortality for group A was 0.971 (95% confidence interval: 0.944-0.999, P = 0.04).


Conclusions
In the Chilean registry of MI patients, low HDL-C was the main lipid disturbance. Very early statin use after MI appears to be associated with a borderline significant and independent reduction of in-hospital mortality.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.20903" xmlns="http://purl.org/rss/1.0/"><title>Effects of the Aging Process on Left Ventricular Systolic and Diastolic Synchronicity Indexes: Insights From 160 “Completely” Healthy Volunteers</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.20903</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Effects of the Aging Process on Left Ventricular Systolic and Diastolic Synchronicity Indexes: Insights From 160 “Completely” Healthy Volunteers</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hyung-Kwan Kim, Dae-Won Sohn, Sung-A Chang, Keun-Ho Park, Jin-Shik Park, Yong-Jin Kim, Byung-Hee Oh, Young-Bae Park</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2011-02-11T19:23:15.681863-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.20903</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.20903</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.20903</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigations</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="section" id="abs1-1" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Growing attempt to use left ventricular (LV) systolic (LVSIsys) and diastolic (LVSIdia) synchronicity indexes in the process of selecting potential responders to cardiac resynchronization therapy has created a need for normative reference values.</p></div></div><div class="section" id="abs1-2" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>This study sought: (1) to determine normal reference ranges for LVSIsys and LVSIdia, and (2) to assess their relationships to age and conventional parameters reflecting LV systolic and diastolic functions.</p></div></div><div class="section" id="abs1-3" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We recruited 160 healthy volunteers (104 men) free of any systemic or cardiovascular disease. Maximal difference and standard deviation of time to peak systolic and peak early diastolic myocardial velocities for LVSIsys and LVSIdia were measured using 6 and 12 segment models.</p></div></div><div class="section" id="abs1-4" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Normal ranges for LVSIsys and LVSIdia obtained in this study were slightly higher than previously reported. The normal aging process did not significantly change LVSIsys, whereas LVSIdia progressively and consistently increased with age. Significant correlations were observed between LVSIdia and parameters representing LV diastolic function, that is, early mitral inflow velocity and its deceleration time, and early mitral annulus velocity. A physiologic increase in LV mass/Ht<sup>2.7</sup> showed a weak, but significant correlation with LVSIdia (<em>r</em> = 0.15–0.22), but not with LVSIsys. On multivariate analysis, an age-dependent increase in LVSIdia was confirmed.</p></div></div><div class="section" id="abs1-5" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In this study, we propose age-specific reference ranges for LVSIsys and LVSIdia. LVSIsys remains stable throughout age groups, whereas LVSIdia progressively increases with age. We believe that the reference values provided here will be useful for defining abnormal LV synchronous contraction and relaxation. Copyright © 2011 Wiley Periodicals, Inc.</p></div><div class="para"><p>This work was presented in part at the Annual Scientific Session of the American Society of Echocardiography, Seattle, Washington, June 16–20, 2007.</p></div></div>]]></content:encoded><description>BackgroundGrowing attempt to use left ventricular (LV) systolic (LVSIsys) and diastolic (LVSIdia) synchronicity indexes in the process of selecting potential responders to cardiac resynchronization therapy has created a need for normative reference values.HypothesisThis study sought: (1) to determine normal reference ranges for LVSIsys and LVSIdia, and (2) to assess their relationships to age and conventional parameters reflecting LV systolic and diastolic functions.MethodsWe recruited 160 healthy volunteers (104 men) free of any systemic or cardiovascular disease. Maximal difference and standard deviation of time to peak systolic and peak early diastolic myocardial velocities for LVSIsys and LVSIdia were measured using 6 and 12 segment models.ResultsNormal ranges for LVSIsys and LVSIdia obtained in this study were slightly higher than previously reported. The normal aging process did not significantly change LVSIsys, whereas LVSIdia progressively and consistently increased with age. Significant correlations were observed between LVSIdia and parameters representing LV diastolic function, that is, early mitral inflow velocity and its deceleration time, and early mitral annulus velocity. A physiologic increase in LV mass/Ht2.7 showed a weak, but significant correlation with LVSIdia (r = 0.15–0.22), but not with LVSIsys. On multivariate analysis, an age-dependent increase in LVSIdia was confirmed.ConclusionsIn this study, we propose age-specific reference ranges for LVSIsys and LVSIdia. LVSIsys remains stable throughout age groups, whereas LVSIdia progressively increases with age. We believe that the reference values provided here will be useful for defining abnormal LV synchronous contraction and relaxation. Copyright © 2011 Wiley Periodicals, Inc.This work was presented in part at the Annual Scientific Session of the American Society of Echocardiography, Seattle, Washington, June 16–20, 2007.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22107" xmlns="http://purl.org/rss/1.0/"><title>Risk Factors, Therapeutic Approaches, and In-Hospital Outcomes in Mexicans With ST-Elevation Acute Myocardial Infarction: The RENASICA II Multicenter Registry</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22107</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk Factors, Therapeutic Approaches, and In-Hospital Outcomes in Mexicans With ST-Elevation Acute Myocardial Infarction: The RENASICA II Multicenter Registry</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Úrsulo Juárez-Herrera, Carlos Jerjes-Sánchez, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-14T10:54:08.59525-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22107</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22107</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22107</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Quality and Outcomes</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">241</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">248</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22107-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Ischemic heart disease is a growing health problem in Latin America. We aimed to analyze risk factors, acute management, and short-term outcome of Mexicans with ST-elevation myocardial infarction (STEMI).</p></div></div>
<div class="section" id="clc22107-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Modifiable risk factors are associated with the occurrence of STEMI in Mexicans, and potentially preventable acute complications are responsible for most short-term deaths.</p></div></div>
<div class="section" id="clc22107-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Among 8600 patients enrolled in Registro Nacional de los Síndromes Coronarios Agudos II (RENASICA II) with a suspected acute coronary syndrome, we analyzed 4555 patients (56%; age 21–100 y) with confirmed STEMI who presented within 24 hours from symptoms' onset.</p></div></div>
<div class="section" id="clc22107-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Smoking (66%), hypertension (50%), and diabetes (43%) were the main risk factors. Most patients (74%) presented with Killip class I (class IV in 4%). Anterior-located STEMI occurred in 56% of cases, and posterior-inferior in 40% of cases. Significant Q waves were present in 43%, right bundle branch block in 7%, left bundle branch block in 5%, first-degree atrioventricular block in 2%, and high-degree atrioventricular block in 2%. A total of 1685 (37%) patients received fibrinolytic therapy (streptokinase, 82%; alteplase, 17%; tenecteplase, 1%), with 31% of patients receiving therapy in &lt;2 hours, 36% in 2–4 hours, 19% in 4–6 hours, and 15% in &gt;6 hours. Thirty percent of patients received either percutaneous coronary intervention or coronary artery bypass grafting during hospitalization. Major adverse cardiovascular events were recurrent ischemia (12%), reinfarction (4%), cardiogenic shock (4%), and stroke (1%). The main predictors of 30-day mortality (10%) in multivariate analysis were age ≥65 years (odds ratio [OR]: 2.47, 95% confidence interval [CI]: 1.94-3.13), Killip class IV (OR: 10.60, 95% CI: 6.09-18.40), and cardiogenic shock (OR: 18.76, 95% CI: 10.60-33.20).</p></div></div>
<div class="section" id="clc22107-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Largely modifiable risk factors and preventable short-term complications are responsible for most STEMI cases and outcomes in this Mexican population.</p></div></div>
]]></content:encoded><description>


Background
Ischemic heart disease is a growing health problem in Latin America. We aimed to analyze risk factors, acute management, and short-term outcome of Mexicans with ST-elevation myocardial infarction (STEMI).


Hypothesis
Modifiable risk factors are associated with the occurrence of STEMI in Mexicans, and potentially preventable acute complications are responsible for most short-term deaths.


Methods
Among 8600 patients enrolled in Registro Nacional de los Síndromes Coronarios Agudos II (RENASICA II) with a suspected acute coronary syndrome, we analyzed 4555 patients (56%; age 21–100 y) with confirmed STEMI who presented within 24 hours from symptoms' onset.


Results
Smoking (66%), hypertension (50%), and diabetes (43%) were the main risk factors. Most patients (74%) presented with Killip class I (class IV in 4%). Anterior-located STEMI occurred in 56% of cases, and posterior-inferior in 40% of cases. Significant Q waves were present in 43%, right bundle branch block in 7%, left bundle branch block in 5%, first-degree atrioventricular block in 2%, and high-degree atrioventricular block in 2%. A total of 1685 (37%) patients received fibrinolytic therapy (streptokinase, 82%; alteplase, 17%; tenecteplase, 1%), with 31% of patients receiving therapy in &lt;2 hours, 36% in 2–4 hours, 19% in 4–6 hours, and 15% in &gt;6 hours. Thirty percent of patients received either percutaneous coronary intervention or coronary artery bypass grafting during hospitalization. Major adverse cardiovascular events were recurrent ischemia (12%), reinfarction (4%), cardiogenic shock (4%), and stroke (1%). The main predictors of 30-day mortality (10%) in multivariate analysis were age ≥65 years (odds ratio [OR]: 2.47, 95% confidence interval [CI]: 1.94-3.13), Killip class IV (OR: 10.60, 95% CI: 6.09-18.40), and cardiogenic shock (OR: 18.76, 95% CI: 10.60-33.20).


Conclusions
Largely modifiable risk factors and preventable short-term complications are responsible for most STEMI cases and outcomes in this Mexican population.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22104" xmlns="http://purl.org/rss/1.0/"><title>Tricuspid Regurgitation in Patients With Pacemakers and Implantable Cardiac Defibrillators: A Comprehensive Review</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22104</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Tricuspid Regurgitation in Patients With Pacemakers and Implantable Cardiac Defibrillators: A Comprehensive Review</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rasha Al-Bawardy, Amar Krishnaswamy, Mandeep Bhargava, Justin Dunn, Oussama Wazni, E. Murat Tuzcu, William Stewart, Samir R. Kapadia</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-25T08:56:19.67697-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22104</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22104</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22104</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">249</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">254</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Implantable cardiac devices, including defibrillators and pacemakers, may be the cause of tricuspid regurgitation (TR) or may worsen existing TR. This review of the literature suggests that TR usually occurs over time after lead implantation. Diagnosis by clinical exam and 2-dimensional echocardiography may be augmented by 3-dimensional echocardiography and/or computed tomography. The mechanism may be mechanical perforation or laceration of leaflets, scarring and restriction of leaflets, or asynchronized activation of the right ventricle. Pacemaker-related TR might cause severe right-sided heart failure, but data regarding associated mortality are lacking. This comprehensive review summarizes the data regarding incidence, mechanism, and treatment of lead-related TR.</p></div>
]]></content:encoded><description>

Implantable cardiac devices, including defibrillators and pacemakers, may be the cause of tricuspid regurgitation (TR) or may worsen existing TR. This review of the literature suggests that TR usually occurs over time after lead implantation. Diagnosis by clinical exam and 2-dimensional echocardiography may be augmented by 3-dimensional echocardiography and/or computed tomography. The mechanism may be mechanical perforation or laceration of leaflets, scarring and restriction of leaflets, or asynchronized activation of the right ventricle. Pacemaker-related TR might cause severe right-sided heart failure, but data regarding associated mortality are lacking. This comprehensive review summarizes the data regarding incidence, mechanism, and treatment of lead-related TR.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22113" xmlns="http://purl.org/rss/1.0/"><title>Electrical Plasticity and Cardioprotection in Myocardial Ischemia—Role of Selective Sodium Channel Blockers</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22113</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Electrical Plasticity and Cardioprotection in Myocardial Ischemia—Role of Selective Sodium Channel Blockers</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rosalinda Madonna, Cihan Cevik, Maher Nasser</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-25T12:53:14.244113-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22113</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22113</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22113</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">255</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">261</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>The concept of electrical protection of the ischemic myocardium is in constant evolution and has recently been supported by experimental and clinical studies. Historically, antiplatelet agents, angiotensin-converting enzyme inhibitors, β-blockers, and statins have been all proposed as drugs conferring anti-ischemic cardioprotection. This was supported by the evidence consistently indicating that all these drugs were capable of reducing mortality and the risk of repeat myocardial infarction. The electrical plasticity paradigm is, however, a novel concept that depicts the benefits of improved sodium channel blockade with drugs such as ranolazine and cariporide. Although it has been hypothesized that the protective role of ranolazine depends on decreased fatty acid β-oxidation affecting preconditioning, we speculate against such a hypothesis, because inhibition of β-oxidation requires higher concentrations of the drug, above the therapeutic range. Rather, we discuss the key role of calcium overload reduction through inhibition of the late sodium current (I<sub>Na</sub>). Mechanisms driving cardioprotection involve the block of a cascade of complex ionic exchanges that can result in intracellular acidosis, excess cytosolic calcium, myocardial cellular dysfunction, and eventually cell injury and death. In this review we discuss the studies that demonstrate how electrical plasticity through sodium channel blockers can promote cardioprotection against ischemia in coronary heart disease.</p></div>
]]></content:encoded><description>

The concept of electrical protection of the ischemic myocardium is in constant evolution and has recently been supported by experimental and clinical studies. Historically, antiplatelet agents, angiotensin-converting enzyme inhibitors, β-blockers, and statins have been all proposed as drugs conferring anti-ischemic cardioprotection. This was supported by the evidence consistently indicating that all these drugs were capable of reducing mortality and the risk of repeat myocardial infarction. The electrical plasticity paradigm is, however, a novel concept that depicts the benefits of improved sodium channel blockade with drugs such as ranolazine and cariporide. Although it has been hypothesized that the protective role of ranolazine depends on decreased fatty acid β-oxidation affecting preconditioning, we speculate against such a hypothesis, because inhibition of β-oxidation requires higher concentrations of the drug, above the therapeutic range. Rather, we discuss the key role of calcium overload reduction through inhibition of the late sodium current (INa). Mechanisms driving cardioprotection involve the block of a cascade of complex ionic exchanges that can result in intracellular acidosis, excess cytosolic calcium, myocardial cellular dysfunction, and eventually cell injury and death. In this review we discuss the studies that demonstrate how electrical plasticity through sodium channel blockers can promote cardioprotection against ischemia in coronary heart disease.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22102" xmlns="http://purl.org/rss/1.0/"><title>Evaluation of the CHADS2 Risk Score on Short- and Long-Term All-Cause and Cardiovascular Mortality After Syncope</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22102</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Evaluation of the CHADS2 Risk Score on Short- and Long-Term All-Cause and Cardiovascular Mortality After Syncope</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Martin Huth Ruwald, Anne-Christine Ruwald, Christian Jons, Morten Lamberts, Morten Lock Hansen, Michael Vinther, Lars Køber, Christian Torp-Pedersen, Jim Hansen, Gunnar Hilmar Gislason</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-02-28T15:59:48.423799-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22102</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22102</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22102</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">262</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">268</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22102-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Syncope risk stratification is difficult and has not been implemented clinically.</p></div></div>
<div class="section" id="clc22102-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>The CHADS2 score can be applied as a risk stratification tool for predicting mortality after an episode of syncope.</p></div></div>
<div class="section" id="clc22102-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>All patients discharged from emergency departments with a first-time diagnosis of syncope from 2001 to 2009 where identified from nationwide registers in Denmark and matched on sex and age with a control population. Risk of all-cause or cardiovascular death was analyzed by multivariable Cox models.</p></div></div>
<div class="section" id="clc22102-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>A total of 37 705 patients were included. There were a total of 7761 deaths (21%), of which 52% were cardiovascular vs 27 862 (15%) deaths in the control population. The risk of cardiovascular death was significantly increased with increasing CHADS<sub>2</sub> score (CHADS<sub>2</sub> score: 1–2, hazard ratio [HR]: 9.11, 95% confidence interval [CI]: 8.25-10.07; CHADS<sub>2</sub> score: 3–4, HR: 17.32, 95% CI: 15.42-19.47; CHADS<sub>2</sub> score: 5–6, HR: 26.66, 95% CI: 21.40-33.21) relative to CHADS<sub>2</sub> score of 0. A CHADS<sub>2</sub> score of 0 was associated overall with very low event rates (15.1 deaths per 1000 person-years) but was associated with increased relative risk in the syncope population compared to controls. Syncope predicted 1-week, 1-year, and long-term mortality across CHADS<sub>2</sub> scores compared to controls but did not reach significance in CHADS<sub>2</sub> scores of 5 to 6.</p></div></div>
<div class="section" id="clc22102-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Increasing CHADS<sub>2</sub> score significantly predicts mortality in patients discharged with a diagnosis of syncope, and a CHADS<sub>2</sub> score of 0 was associated with a very low absolute mortality. Compared to controls, syncope was associated with increased short- and long-term mortality, particularly in the lower CHADS<sub>2</sub> scores.</p></div></div>
]]></content:encoded><description>


Background
Syncope risk stratification is difficult and has not been implemented clinically.


Hypothesis
The CHADS2 score can be applied as a risk stratification tool for predicting mortality after an episode of syncope.


Methods
All patients discharged from emergency departments with a first-time diagnosis of syncope from 2001 to 2009 where identified from nationwide registers in Denmark and matched on sex and age with a control population. Risk of all-cause or cardiovascular death was analyzed by multivariable Cox models.


Results
A total of 37 705 patients were included. There were a total of 7761 deaths (21%), of which 52% were cardiovascular vs 27 862 (15%) deaths in the control population. The risk of cardiovascular death was significantly increased with increasing CHADS2 score (CHADS2 score: 1–2, hazard ratio [HR]: 9.11, 95% confidence interval [CI]: 8.25-10.07; CHADS2 score: 3–4, HR: 17.32, 95% CI: 15.42-19.47; CHADS2 score: 5–6, HR: 26.66, 95% CI: 21.40-33.21) relative to CHADS2 score of 0. A CHADS2 score of 0 was associated overall with very low event rates (15.1 deaths per 1000 person-years) but was associated with increased relative risk in the syncope population compared to controls. Syncope predicted 1-week, 1-year, and long-term mortality across CHADS2 scores compared to controls but did not reach significance in CHADS2 scores of 5 to 6.


Conclusions
Increasing CHADS2 score significantly predicts mortality in patients discharged with a diagnosis of syncope, and a CHADS2 score of 0 was associated with a very low absolute mortality. Compared to controls, syncope was associated with increased short- and long-term mortality, particularly in the lower CHADS2 scores.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22108" xmlns="http://purl.org/rss/1.0/"><title>Influence of Body Mass Index on Recurrence and Quality of Life in Atrial Fibrillation Patients After Catheter Ablation: A Meta-Analysis and Systematic Review</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22108</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Influence of Body Mass Index on Recurrence and Quality of Life in Atrial Fibrillation Patients After Catheter Ablation: A Meta-Analysis and Systematic Review</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jianhui Zhuang, Yuyan Lu, Kai Tang, Wenhui Peng, Yawei Xu</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-14T11:02:00.776436-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22108</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22108</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22108</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">269</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">275</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22108-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Accumulating evidence has demonstrated that overweight and obesity, expressed as high body mass index (BMI), are associated with the development of atrial fibrillation (AF) and quality of life (QoL) in AF patients. However, the role of high BMI as a risk factor for prognosis and QoL in AF patients undergoing ablation remains controversial.</p></div></div>
<div class="section" id="clc22108-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>We hypothesized that elevated BMI was correlated with AF recurrence and QoL after an ablative procedure.</p></div></div>
<div class="section" id="clc22108-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We performed a comprehensive search of PubMed, EMBASE, and the Cochrane Library. Studies were included if they investigated the association of BMI with AF recurrence and QoL after ablation.</p></div></div>
<div class="section" id="clc22108-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Of the 151 articles identified, 12 studies that enrolled 3286 individuals met the inclusion criteria. Overall, compared with normal-BMI patients, AF recurrence occured more frequently in high-BMI patients after ablation (odds ratio: 1.32, 95% confidence interval: 1.17-1.5, <i>P</i> &lt; 0.001). However, the pooled esimate of odds ratio adjusted for multiple confounders did not reach significance. The summary weighted mean difference of BMI between patients with and without recurrence was 0.43 (95% confidence interval: 0.05-0.81, <i>P</i> = 0.027). In addition, QoL scores were significantly lower in high-BMI than in normal-BMI patients before the ablative procedure, whereas the gap of QoL between normal-BMI and high-BMI groups was decreased at follow-up.</p></div></div>
<div class="section" id="clc22108-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Results of this meta-analysis suggest 2 points, namely that the tight association between overweight/obesity and AF recurrence after ablation may be partly due to other concomitant conditions, and that impaired QoL in high-BMI groups is significantly improved after ablation.</p></div></div>
]]></content:encoded><description>


Background
Accumulating evidence has demonstrated that overweight and obesity, expressed as high body mass index (BMI), are associated with the development of atrial fibrillation (AF) and quality of life (QoL) in AF patients. However, the role of high BMI as a risk factor for prognosis and QoL in AF patients undergoing ablation remains controversial.


Hypothesis
We hypothesized that elevated BMI was correlated with AF recurrence and QoL after an ablative procedure.


Methods
We performed a comprehensive search of PubMed, EMBASE, and the Cochrane Library. Studies were included if they investigated the association of BMI with AF recurrence and QoL after ablation.


Results
Of the 151 articles identified, 12 studies that enrolled 3286 individuals met the inclusion criteria. Overall, compared with normal-BMI patients, AF recurrence occured more frequently in high-BMI patients after ablation (odds ratio: 1.32, 95% confidence interval: 1.17-1.5, P &lt; 0.001). However, the pooled esimate of odds ratio adjusted for multiple confounders did not reach significance. The summary weighted mean difference of BMI between patients with and without recurrence was 0.43 (95% confidence interval: 0.05-0.81, P = 0.027). In addition, QoL scores were significantly lower in high-BMI than in normal-BMI patients before the ablative procedure, whereas the gap of QoL between normal-BMI and high-BMI groups was decreased at follow-up.


Conclusions
Results of this meta-analysis suggest 2 points, namely that the tight association between overweight/obesity and AF recurrence after ablation may be partly due to other concomitant conditions, and that impaired QoL in high-BMI groups is significantly improved after ablation.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22109" xmlns="http://purl.org/rss/1.0/"><title>The Comparison in Reduction of QT Dispersion After Primary Percutaneous Coronary Intervention According to Existence of Thrombectomy in ST-Segment Elevation Myocardial Infarction</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22109</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Comparison in Reduction of QT Dispersion After Primary Percutaneous Coronary Intervention According to Existence of Thrombectomy in ST-Segment Elevation Myocardial Infarction</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gokhan Alici, Muslum Sahin, Birol Ozkan, Goksel Acar, Rezzan Deniz Acar, Mehmet Vefik Yazicioglu, Mustafa Bulut, Ali Metin Esen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-16T17:06:14.824435-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22109</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22109</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22109</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">276</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">279</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22109-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Primary percutaneous coronary intervention (PPCI) is the standard treatment in patients with ST-segment elevation myocardial infarction (STEMI). Thrombectomy devices are used to remove thrombus or to prevent embolization of thrombus and plaque during PPCI. QT dispersion (the difference between maximal and minimal QT interval calculated on a standard 12-lead electrocardiogram) represents the regional nonuniformity of ventricular repolarization. It may reflect early coronary reperfusion in reducing electrophysiological instability by decreasing QT dispersion in the recovery phase after acute STEMI.</p></div></div>
<div class="section" id="clc22109-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Our aim was to show whether an additional effect of thrombectomy on reducing QT dispersion will be seen in patients undergoing PPCI for STEMI.</p></div></div>
<div class="section" id="clc22109-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The study population included 80 consecutive patients who were admitted to the hospital within 12 hours after the onset of acute STEMI and angiographic evidence of intraluminal thrombus in the infarct-related artery. Patients with atrial fibrillation or flutter, intraventricular conduction abnormalities, pre-excitation, cardiogenic shock, cardiomyopathy, ventricular hypertrophy, and severe valvular heart disease were excluded from the study.</p></div></div>
<div class="section" id="clc22109-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>There were no significant differences between groups regarding gender, age, cardiovascular risk factors, and time from symptom onset to treatment, except for smoking, which was much higher in the PPCI plus thrombectomy group. Infarct-related artery distribution (left anterior descending artery [LAD] to non-LAD), and neither the rate of balloon predilatation nor stent implantation were different between groups. Successful coronary patency was achieved in each case. QT interval measurements were similar between groups at admission. However, at 24 hours, QT and QTc dispersions were less in the PPCI plus thrombectomy group (41 ± 9 vs 33 ± 7 ms, <i>P</i> &lt; 0.05 and 45 ± 8 vs 35 ± 7 ms, <i>P</i> = 0.03, respectively), but not in the other QT interval measurements. When patients were divided into 2 groups according to infarct-related artery (LAD and non-LAD groups), QT interval measurement parameters did not show any significant differences.</p></div></div>
<div class="section" id="clc22109-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Thrombectomy additional to PPCI helps more effective reperfusion at the microvascular level and provides additional prognostic information.</p></div></div>
]]></content:encoded><description>


Background
Primary percutaneous coronary intervention (PPCI) is the standard treatment in patients with ST-segment elevation myocardial infarction (STEMI). Thrombectomy devices are used to remove thrombus or to prevent embolization of thrombus and plaque during PPCI. QT dispersion (the difference between maximal and minimal QT interval calculated on a standard 12-lead electrocardiogram) represents the regional nonuniformity of ventricular repolarization. It may reflect early coronary reperfusion in reducing electrophysiological instability by decreasing QT dispersion in the recovery phase after acute STEMI.


Hypothesis
Our aim was to show whether an additional effect of thrombectomy on reducing QT dispersion will be seen in patients undergoing PPCI for STEMI.


Methods
The study population included 80 consecutive patients who were admitted to the hospital within 12 hours after the onset of acute STEMI and angiographic evidence of intraluminal thrombus in the infarct-related artery. Patients with atrial fibrillation or flutter, intraventricular conduction abnormalities, pre-excitation, cardiogenic shock, cardiomyopathy, ventricular hypertrophy, and severe valvular heart disease were excluded from the study.


Results
There were no significant differences between groups regarding gender, age, cardiovascular risk factors, and time from symptom onset to treatment, except for smoking, which was much higher in the PPCI plus thrombectomy group. Infarct-related artery distribution (left anterior descending artery [LAD] to non-LAD), and neither the rate of balloon predilatation nor stent implantation were different between groups. Successful coronary patency was achieved in each case. QT interval measurements were similar between groups at admission. However, at 24 hours, QT and QTc dispersions were less in the PPCI plus thrombectomy group (41 ± 9 vs 33 ± 7 ms, P &lt; 0.05 and 45 ± 8 vs 35 ± 7 ms, P = 0.03, respectively), but not in the other QT interval measurements. When patients were divided into 2 groups according to infarct-related artery (LAD and non-LAD groups), QT interval measurement parameters did not show any significant differences.


Conclusions
Thrombectomy additional to PPCI helps more effective reperfusion at the microvascular level and provides additional prognostic information.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22112" xmlns="http://purl.org/rss/1.0/"><title>Cost-Effectiveness of Dabigatran Compared With Warfarin for Stroke Prevention in Patients With Atrial Fibrillation—A Real Patient Data Analysis in a Hong Kong Teaching Hospital</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22112</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cost-Effectiveness of Dabigatran Compared With Warfarin for Stroke Prevention in Patients With Atrial Fibrillation—A Real Patient Data Analysis in a Hong Kong Teaching Hospital</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Andy M. Chang, Jason C. S. Ho, Bryan P. Yan, Cheuk Man Yu, Yat Yin Lam, Vivian W. Y. Lee</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-14T10:53:21.239085-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22112</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22112</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22112</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">280</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">285</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22112-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>To compare the management cost and cost-effectiveness of dabigatran with warfarin in patients with nonvalvular atrial fibrillation (AF) from the hospital's and patients' perspectives.</p></div></div>
<div class="section" id="clc22112-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Dabigatran is more cost-effective than warfarin for stroke prevention of AF in Hong Kong.</p></div></div>
<div class="section" id="clc22112-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The analysis was performed in conjunction with a drug utilization evaluation of dabigatran study in a teaching hospital in Hong Kong. The study recruited 244 patients who received either dabigatran or warfarin for stroke prevention of AF. A cost-effectiveness analysis was performed and was expressed as an incremental cost-effectiveness ratio (ICER) in averting a cardiac event or a bleeding event. A sensitivity analysis was used on all relevant variables to test the robustness.</p></div></div>
<div class="section" id="clc22112-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>From the hospital's perspective, the dabigatran group had a lower total cost of management than that of the warfarin group (median: US$421 vs US$1306, <i>P</i> &lt; 0.001) (US$1 = HK$7.75) and was dominant over warfarin. From the patients' perspective, the total cost of management in the dabigatran group was higher than that in warfarin group (median: US$1751 vs US$70, <i>P</i> &lt; 0.001), and the ICER in preventing a cardiac or bleeding event of dabigatran vs warfarin was estimated at US$68 333 and US$20 500, respectively. If dabigatran was subsidized by the hospital, a higher cost would be incurred by the hospital (median: US$1679 vs US$1306, ICER (cardiac and bleeding events): US$15 163 and US$4549, respectively).</p></div></div>
<div class="section" id="clc22112-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The study favored dabigatran for stroke prophylaxis in patients with nonvalvular AF in Hong Kong under the current hospital's perspective and provided a reference for further comparisons under patient and subsidization perspectives.</p></div></div>
]]></content:encoded><description>


Background
To compare the management cost and cost-effectiveness of dabigatran with warfarin in patients with nonvalvular atrial fibrillation (AF) from the hospital's and patients' perspectives.


Hypothesis
Dabigatran is more cost-effective than warfarin for stroke prevention of AF in Hong Kong.


Methods
The analysis was performed in conjunction with a drug utilization evaluation of dabigatran study in a teaching hospital in Hong Kong. The study recruited 244 patients who received either dabigatran or warfarin for stroke prevention of AF. A cost-effectiveness analysis was performed and was expressed as an incremental cost-effectiveness ratio (ICER) in averting a cardiac event or a bleeding event. A sensitivity analysis was used on all relevant variables to test the robustness.


Results
From the hospital's perspective, the dabigatran group had a lower total cost of management than that of the warfarin group (median: US$421 vs US$1306, P &lt; 0.001) (US$1 = HK$7.75) and was dominant over warfarin. From the patients' perspective, the total cost of management in the dabigatran group was higher than that in warfarin group (median: US$1751 vs US$70, P &lt; 0.001), and the ICER in preventing a cardiac or bleeding event of dabigatran vs warfarin was estimated at US$68 333 and US$20 500, respectively. If dabigatran was subsidized by the hospital, a higher cost would be incurred by the hospital (median: US$1679 vs US$1306, ICER (cardiac and bleeding events): US$15 163 and US$4549, respectively).


Conclusions
The study favored dabigatran for stroke prophylaxis in patients with nonvalvular AF in Hong Kong under the current hospital's perspective and provided a reference for further comparisons under patient and subsidization perspectives.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22111" xmlns="http://purl.org/rss/1.0/"><title>Quantitation of the Mitral Tetrahedron in Patients With Ischemic Heart Disease Using Real-Time Three-Dimensional Echocardiography to Evaluate the Geometric Determinants of Ischemic Mitral Regurgitation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22111</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Quantitation of the Mitral Tetrahedron in Patients With Ischemic Heart Disease Using Real-Time Three-Dimensional Echocardiography to Evaluate the Geometric Determinants of Ischemic Mitral Regurgitation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chin-Feng Hsuan, Hsi-Yu Yu, Wei-Kung Tseng, Lung-Chun Lin, Kwan-Lih Hsu, Chau-Chung Wu</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-14T10:56:39.230018-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22111</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22111</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22111</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">286</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">292</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22111-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Ischemic mitral regurgitation (IMR) is common in ischemic heart disease and results in poor prognosis. However, the exact mechanism of IMR has not been fully elucidated.</p></div></div>
<div class="section" id="clc22111-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>Quantitation of the  mitral tetrahedron using three-dimentianl (3D) echocardiography is capable of evaluating the geometric determinants and mechanisms of IMR.</p></div></div>
<div class="section" id="clc22111-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Forty patients with a history of ST-elevation myocardial infarction at least 6 months earlier were studied. Parameters of mitral deformation and global left ventricular (LV) function and shape were evaluated by 2-dimensional echocardiography. The effective regurgitant orifice (ERO) of IMR was obtained by the quantitative continuous-wave Doppler technique. Three-dimensional (3D) echocardiography was applied to assess the mitral tetrahedron.</p></div></div>
<div class="section" id="clc22111-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Mitral valvular tenting area (<i>P</i> &lt; 0.001), mitral annular area (<i>P</i> = 0.032), dilation of the LV in diastole, impairment of the LV ejection fraction, and volume of the spherically shaped LV in systole were greater in patients with an ERO ≥20 mm<sup>2</sup> than in those with an ERO &lt;20 mm<sup>2</sup>. In the mitral tetrahedron, only the interpapillary muscle roots distance showed a significant difference (<i>P</i> = 0.004). Multivariate analysis with the logistic regression model showed the systolic mitral tenting area (odds ratio [OR]: 280.49, 95% confidence interval [CI]: 4.59-1.72 × 10<sup>4</sup>, <i>P</i> = 0.007) and interpapillary muscle distance (OR: 1.50, 95% CI: 1.03-2.19, <i>P</i> = 0.036) to be independent factors in predicting significant IMR (ERO ≥20 mm<sup>2</sup>).</p></div></div>
<div class="section" id="clc22111-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>3D echocardiography can be effectively applied in measuring the mitral tetrahedron and evaluating the mechanism of IMR. Mitral valvular tenting and interpapillary muscle distance are 2 independent factors of significant IMR.</p></div></div>
]]></content:encoded><description>


Background
Ischemic mitral regurgitation (IMR) is common in ischemic heart disease and results in poor prognosis. However, the exact mechanism of IMR has not been fully elucidated.


Hypothesis
Quantitation of the  mitral tetrahedron using three-dimentianl (3D) echocardiography is capable of evaluating the geometric determinants and mechanisms of IMR.


Methods
Forty patients with a history of ST-elevation myocardial infarction at least 6 months earlier were studied. Parameters of mitral deformation and global left ventricular (LV) function and shape were evaluated by 2-dimensional echocardiography. The effective regurgitant orifice (ERO) of IMR was obtained by the quantitative continuous-wave Doppler technique. Three-dimensional (3D) echocardiography was applied to assess the mitral tetrahedron.


Results
Mitral valvular tenting area (P &lt; 0.001), mitral annular area (P = 0.032), dilation of the LV in diastole, impairment of the LV ejection fraction, and volume of the spherically shaped LV in systole were greater in patients with an ERO ≥20 mm2 than in those with an ERO &lt;20 mm2. In the mitral tetrahedron, only the interpapillary muscle roots distance showed a significant difference (P = 0.004). Multivariate analysis with the logistic regression model showed the systolic mitral tenting area (odds ratio [OR]: 280.49, 95% confidence interval [CI]: 4.59-1.72 × 104, P = 0.007) and interpapillary muscle distance (OR: 1.50, 95% CI: 1.03-2.19, P = 0.036) to be independent factors in predicting significant IMR (ERO ≥20 mm2).


Conclusions
3D echocardiography can be effectively applied in measuring the mitral tetrahedron and evaluating the mechanism of IMR. Mitral valvular tenting and interpapillary muscle distance are 2 independent factors of significant IMR.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22116" xmlns="http://purl.org/rss/1.0/"><title>Red Blood Cell Distribution Width Is a Predictor of Readmission in Cardiac Patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22116</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Red Blood Cell Distribution Width Is a Predictor of Readmission in Cardiac Patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Georges Ephrem</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-28T09:20:56.742806-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22116</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22116</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22116</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Investigation</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">293</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">299</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="clc22116-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Three-quarters of rehospitalizations ($44 billion yearly estimated cost) may be avoidable. A screening tool for the detection of potential readmission may facilitate more efficient case management.</p></div></div>
<div class="section" id="clc22116-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Hypothesis</h4><div class="para"><p>An elevated red blood cell distribution width (RDW) is an independent predictor of hospital readmission in patients with unstable angina (UA) or non–ST-elevation myocardial infarction (NSTEMI).</p></div></div>
<div class="section" id="clc22116-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The study is a retrospective observational cohort analysis of adults admitted in 2007 with UA or NSTEMI. Data were gathered by review of inpatient medical records. The rate of 30-day nonelective readmission and time to nonelective readmission were recorded until November 1, 2011, and compared by RDW group using the 95th percentile (16.3%) as a cutoff.</p></div></div>
<div class="section" id="clc22116-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The median follow-up time of the 503 subjects (average age, 65 ± 13 years; 56% male) was 3.8 years (interquartile range: 0.3–4.3 years). Those readmitted within 30 days were older, had more comorbidities and higher RDW and creatinine levels, and were more likely to have had an intervention. At 3.8 years of follow-up, subjects with high RDW (&gt;16.3%) were more likely to be readmitted compared to those with normal RDW (≤16.3%) (72.28% vs 59.95%, P = 0.003). In multivariable analyses, high RDW was a statistically significant predictor of readmission in general (hazard ratio: 1.35 (95% confidence interval [CI]:1.02-1.79), P = 0.033) but not of 30-day rehospitalization (odds ratio: 1.34 (95% CI: 0.78-2.31), P = 0.292). Its area under the receiver operating characteristic curve was 0.54 (sensitivity 23% and specificity 85%).</p></div></div>
<div class="section" id="clc22116-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>An elevated RDW is an independent predictor of hospital readmission in patients with UA or NSTEMI.</p></div></div>
]]></content:encoded><description>


Background
Three-quarters of rehospitalizations ($44 billion yearly estimated cost) may be avoidable. A screening tool for the detection of potential readmission may facilitate more efficient case management.


Hypothesis
An elevated red blood cell distribution width (RDW) is an independent predictor of hospital readmission in patients with unstable angina (UA) or non–ST-elevation myocardial infarction (NSTEMI).


Methods
The study is a retrospective observational cohort analysis of adults admitted in 2007 with UA or NSTEMI. Data were gathered by review of inpatient medical records. The rate of 30-day nonelective readmission and time to nonelective readmission were recorded until November 1, 2011, and compared by RDW group using the 95th percentile (16.3%) as a cutoff.


Results
The median follow-up time of the 503 subjects (average age, 65 ± 13 years; 56% male) was 3.8 years (interquartile range: 0.3–4.3 years). Those readmitted within 30 days were older, had more comorbidities and higher RDW and creatinine levels, and were more likely to have had an intervention. At 3.8 years of follow-up, subjects with high RDW (&gt;16.3%) were more likely to be readmitted compared to those with normal RDW (≤16.3%) (72.28% vs 59.95%, P = 0.003). In multivariable analyses, high RDW was a statistically significant predictor of readmission in general (hazard ratio: 1.35 (95% confidence interval [CI]:1.02-1.79), P = 0.033) but not of 30-day rehospitalization (odds ratio: 1.34 (95% CI: 0.78-2.31), P = 0.292). Its area under the receiver operating characteristic curve was 0.54 (sensitivity 23% and specificity 85%).


Conclusions
An elevated RDW is an independent predictor of hospital readmission in patients with UA or NSTEMI.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22078" xmlns="http://purl.org/rss/1.0/"><title>Response to Independent Association Between Obstructive Sleep Apnea and Noncalcified Coronary Plaque Demonstrated by Noninvasive Coronary Computed Tomography Angiography</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22078</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Response to Independent Association Between Obstructive Sleep Apnea and Noncalcified Coronary Plaque Demonstrated by Noninvasive Coronary Computed Tomography Angiography</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Aibek E. Mirrakhimov, Erkin M. Mirrakhimov</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-11-14T08:47:19.428633-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22078</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22078</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22078</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">300</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">300</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22119" xmlns="http://purl.org/rss/1.0/"><title>Obstructive sleep apnea and coronary artery pathology</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22119</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Obstructive sleep apnea and coronary artery pathology</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sunil Sharma</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T08:19:32.110527-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22119</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22119</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22119</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">300</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">301</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22115" xmlns="http://purl.org/rss/1.0/"><title>Response to Impact of Lesion Length on Functional Significance in Intermediate Coronary Lesions</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22115</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Response to Impact of Lesion Length on Functional Significance in Intermediate Coronary Lesions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sevket Balta, Sait Demirkol, Zekeriya Arslan, Murat Unlu, Turgay Celik, Mustafa Cakar</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-27T07:13:49.390052-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22115</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22115</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22115</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">301</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">301</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22091" xmlns="http://purl.org/rss/1.0/"><title>Letter to the Editor</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22091</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Letter to the Editor</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Tomokazu Iguchi, Takao Hasegawa</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T10:46:10.302011-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22091</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22091</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22091</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the Editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">301</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">302</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22136" xmlns="http://purl.org/rss/1.0/"><title>Addendum</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22136</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Addendum</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-13T08:59:37.266379-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22136</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22136</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22136</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Addendum</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">303</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">303</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22079" xmlns="http://purl.org/rss/1.0/"><title>Comparing the New European Cardiovascular Disease Prevention Guideline With Prior American Heart Association Guidelines: An Editorial Review</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22079</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comparing the New European Cardiovascular Disease Prevention Guideline With Prior American Heart Association Guidelines: An Editorial Review</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Van-Khue Ton, Seth S. Martin, Roger S. Blumenthal, Michael J. Blaha</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-04T11:56:07.620825-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1002/clc.22079</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1002/clc.22079</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1002%2Fclc.22079</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E1</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E6</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Atherosclerotic heart disease and stroke remain the leading causes of death and disability worldwide. Cardiovascular disease (CVD) prevention can improve the well-being of a population and possibly cut downstream healthcare spending, and must be the centerpiece of any sustainable health economy model. As lifestyle and CVD risk factors differ among ethnicities, cultures, genders, and age groups, an accurate risk assessment model is the critical first step for guiding appropriate use of testing, lifestyle counseling resources, and preventive medications. Examples of such models include the US Framingham Risk Score and the European SCORE system. The European Society of Cardiology recently published an updated set of guidelines on CVD prevention. This review highlights the similarities and differences between European and US risk assessment models, as well as their respective recommendations on the use of advanced testing for further risk reclassification and the appropriate use of medications. In particular, we focus on head-to-head comparison of the new European guideline with prior American Heart Association statements (2002, 2010, and 2011) covering risk assessment and treatment of asymptomatic adults. Despite minor disagreements on the weight of recommendations in certain areas, such as the use of coronary calcium score and non–high-density lipoprotein cholesterol in risk assessment, CVD prevention experts across the 2 continents agree on 1 thing: prevention works in halting the progression of atherosclerosis and decreasing disease burden over a lifetime.</p></div>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>The authors have no funding, financial relationships, or conflicts of interest to disclose.</p></div>
]]></content:encoded><description>

Atherosclerotic heart disease and stroke remain the leading causes of death and disability worldwide. Cardiovascular disease (CVD) prevention can improve the well-being of a population and possibly cut downstream healthcare spending, and must be the centerpiece of any sustainable health economy model. As lifestyle and CVD risk factors differ among ethnicities, cultures, genders, and age groups, an accurate risk assessment model is the critical first step for guiding appropriate use of testing, lifestyle counseling resources, and preventive medications. Examples of such models include the US Framingham Risk Score and the European SCORE system. The European Society of Cardiology recently published an updated set of guidelines on CVD prevention. This review highlights the similarities and differences between European and US risk assessment models, as well as their respective recommendations on the use of advanced testing for further risk reclassification and the appropriate use of medications. In particular, we focus on head-to-head comparison of the new European guideline with prior American Heart Association statements (2002, 2010, and 2011) covering risk assessment and treatment of asymptomatic adults. Despite minor disagreements on the weight of recommendations in certain areas, such as the use of coronary calcium score and non–high-density lipoprotein cholesterol in risk assessment, CVD prevention experts across the 2 continents agree on 1 thing: prevention works in halting the progression of atherosclerosis and decreasing disease burden over a lifetime.
The authors have no funding, financial relationships, or conflicts of interest to disclose.
</description></item></rdf:RDF>