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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/10.1111/(ISSN)1751-7141" xmlns="http://purl.org/rss/1.0/"><title>Preventive Cardiology</title><description> Wiley Online Library : Preventive Cardiology</description><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F%28ISSN%291751-7141</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/">© Wiley Periodicals, Inc</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1520-037X</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1751-7141</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-09-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Fall 2010</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">13</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">4</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">149</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">212</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1111/prc.2010.13.issue-4/asset/cover.gif?v=1&amp;s=467bd0dd590a3ca95b5f2e791b82abb7633f09cc"/><items><rdf:Seq><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00078.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00083.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00080.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00081.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00068.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00073.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00074.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00079.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00072.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00086.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00075.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00082.x"/></rdf:Seq></items></channel><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00078.x" xmlns="http://purl.org/rss/1.0/"><title>CLINICAL STUDY: Associations Among Cardiometabolic Risk Factor Clustering, Weight Status, and Cardiovascular Disease in an Appalachian Population</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00078.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">CLINICAL STUDY: Associations Among Cardiometabolic Risk Factor Clustering, Weight Status, and Cardiovascular Disease in an Appalachian Population</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kimberly B. Blake, Anoop Shankar, Suresh Madhavan, Alan Ducatman</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-08-16T12:51:46.232308-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00078.x</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/">10.1111/j.1751-7141.2010.00078.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00078.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</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>Prev Cardiol. <em>****;**:**–**.</em></p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>It has been suggested that within the traditional body mass index (BMI) categories there is a heterogeneous pattern of cardiometabolic risk factor clustering. The objective of this research was to determine the associations among obesity, cardiometabolic abnormalities, and cardiovascular disease (CVD) in a large population-based study of Appalachian adults. The study comprised a cross-sectional survey of Appalachian adults residing in 6 communities in Ohio and West Virginia, who were aged 18 years and older (n=14,783, 50.9% women). The authors categorized BMI into normal weight (&lt;25 kg/m<sup>2</sup>), overweight (25–29.9 kg/m<sup>2</sup>), and obese (≥30 kg/m<sup>2</sup>). Cardiometabolic abnormalities were defined as the presence of hypertension, elevated triglycerides (≥150 mg/dL), decreased high-density lipoprotein cholesterol (&lt;40 mg/dL [men], &lt;50 mg/dL [women]), elevated fasting glucose (≥100 mg/dL)/diabetes, insulin resistance (homeostasis model assessment &gt;5.13), or elevated C-reactive protein (&gt;3 mg/L). They found that 25.6% of normal-weight adults displayed clustering of ≥2 cardiometabolic abnormalities; in contrast, 36.8% of overweight/obese adults displayed no clustering. Compared with normal-weight persons without clustering of cardiometabolic abnormalities (referent), the odds ratio of CVD was 1.06 (95% confidence interval [CI], 0.84–1.34) among overweight/obese individuals without cardiometabolic clustering, 2.21 (95% CI, 1.74–2.81) among normal-weight individuals with cardiometabolic clustering, and 2.45 (95% CI, 2.02–2.97) among overweight/obese individuals with cardiometabolic clustering. These results suggest that within the traditional BMI categories, there may be heterogeneity of CVD risk depending on whether there is underlying clustering of cardiometabolic abnormalities.</p></div>]]></content:encoded><description>Prev Cardiol. ****;**:**–**.It has been suggested that within the traditional body mass index (BMI) categories there is a heterogeneous pattern of cardiometabolic risk factor clustering. The objective of this research was to determine the associations among obesity, cardiometabolic abnormalities, and cardiovascular disease (CVD) in a large population-based study of Appalachian adults. The study comprised a cross-sectional survey of Appalachian adults residing in 6 communities in Ohio and West Virginia, who were aged 18 years and older (n=14,783, 50.9% women). The authors categorized BMI into normal weight (&lt;25 kg/m2), overweight (25–29.9 kg/m2), and obese (≥30 kg/m2). Cardiometabolic abnormalities were defined as the presence of hypertension, elevated triglycerides (≥150 mg/dL), decreased high-density lipoprotein cholesterol (&lt;40 mg/dL [men], &lt;50 mg/dL [women]), elevated fasting glucose (≥100 mg/dL)/diabetes, insulin resistance (homeostasis model assessment &gt;5.13), or elevated C-reactive protein (&gt;3 mg/L). They found that 25.6% of normal-weight adults displayed clustering of ≥2 cardiometabolic abnormalities; in contrast, 36.8% of overweight/obese adults displayed no clustering. Compared with normal-weight persons without clustering of cardiometabolic abnormalities (referent), the odds ratio of CVD was 1.06 (95% confidence interval [CI], 0.84–1.34) among overweight/obese individuals without cardiometabolic clustering, 2.21 (95% CI, 1.74–2.81) among normal-weight individuals with cardiometabolic clustering, and 2.45 (95% CI, 2.02–2.97) among overweight/obese individuals with cardiometabolic clustering. These results suggest that within the traditional BMI categories, there may be heterogeneity of CVD risk depending on whether there is underlying clustering of cardiometabolic abnormalities.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00083.x" xmlns="http://purl.org/rss/1.0/"><title>Should We Focus on Novel Risk Markers and Screening Tests to Better Predict and Prevent Cardiovascular Disease? Or Are We Putting the Cart Before the Horse?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00083.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Should We Focus on Novel Risk Markers and Screening Tests to Better Predict and Prevent Cardiovascular Disease? Or Are We Putting the Cart Before the Horse?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nathan D. Wong</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-09-22T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00083.x</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/">10.1111/j.1751-7141.2010.00083.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00083.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">149</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">151</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=10.1111%2Fj.1751-7141.2010.00080.x" xmlns="http://purl.org/rss/1.0/"><title>Should We Focus on Novel Risk Markers and Screening Tests to Better Predict and Prevent Cardiovascular Disease?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00080.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Should We Focus on Novel Risk Markers and Screening Tests to Better Predict and Prevent Cardiovascular Disease?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jonathan R. Enriquez, James A. De Lemos</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-09-22T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00080.x</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/">10.1111/j.1751-7141.2010.00080.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00080.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">152</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">159</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>Editor’s Note: The following Point/Counterpoint articles were derived from a debate presentation sponsored by the American Society for Preventive Cardiology at the March 2010 meeting of the American Heart Association Council on Epidemiology and Prevention, titled “Should We Focus on Novel Risk Marker and Screening Tests to Better Predict and Prevent Cardiovascular Disease?” Dr. James de Lemos presented the pro side, titled “Novel Risk Markers and Screening Tests Will Improve the Prediction and Prevention of Cardiovascular Disease,” and Dr. Donald Lloyd-Jones advocated the con side, titled “Better Implementation of Existing Knowledge Will Save More Lives Than All of the Novel Biomarkers in the World.” The following articles include points from the debate, rebuttal, and questions raised by the audience. We thank all authors for sharing this debate with the readership.</p></div>]]></content:encoded><description>Editor’s Note: The following Point/Counterpoint articles were derived from a debate presentation sponsored by the American Society for Preventive Cardiology at the March 2010 meeting of the American Heart Association Council on Epidemiology and Prevention, titled “Should We Focus on Novel Risk Marker and Screening Tests to Better Predict and Prevent Cardiovascular Disease?” Dr. James de Lemos presented the pro side, titled “Novel Risk Markers and Screening Tests Will Improve the Prediction and Prevention of Cardiovascular Disease,” and Dr. Donald Lloyd-Jones advocated the con side, titled “Better Implementation of Existing Knowledge Will Save More Lives Than All of the Novel Biomarkers in the World.” The following articles include points from the debate, rebuttal, and questions raised by the audience. We thank all authors for sharing this debate with the readership.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00081.x" xmlns="http://purl.org/rss/1.0/"><title>Biomarkers for Coronary Heart Disease Clinical Risk Prediction: A Critical Appraisal</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00081.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Biomarkers for Coronary Heart Disease Clinical Risk Prediction: A Critical Appraisal</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">John T. Wilkins, Donald M. Lloyd-Jones</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-09-22T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00081.x</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/">10.1111/j.1751-7141.2010.00081.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00081.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">160</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">165</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>Editor’s Note: The following Point/Counterpoint articles were derived from a debate presentation sponsored by the American Society for Preventive Cardiology at the March 2010 meeting of the American Heart Association Council on Epidemiology and Prevention, titled “Should We Focus on Novel Risk Marker and Screening Tests to Better Predict and Prevent Cardiovascular Disease?” Dr. James de Lemos presented the pro side, titled “Novel Risk Markers and Screening Tests Will Improve the Prediction and PRevention of Cardiovascular Disease,” and Dr. Donald Lloyd-Jones advocated the con side, titled “Better Implementation of Existing Knowledge Will Save More Lives Than All of the Novel Biomarkers in the World.” The following articles include points from the debate, rebuttal, and questions raised by the audience. We thank all authors for sharing this debate with the readership.</p></div>]]></content:encoded><description>Editor’s Note: The following Point/Counterpoint articles were derived from a debate presentation sponsored by the American Society for Preventive Cardiology at the March 2010 meeting of the American Heart Association Council on Epidemiology and Prevention, titled “Should We Focus on Novel Risk Marker and Screening Tests to Better Predict and Prevent Cardiovascular Disease?” Dr. James de Lemos presented the pro side, titled “Novel Risk Markers and Screening Tests Will Improve the Prediction and PRevention of Cardiovascular Disease,” and Dr. Donald Lloyd-Jones advocated the con side, titled “Better Implementation of Existing Knowledge Will Save More Lives Than All of the Novel Biomarkers in the World.” The following articles include points from the debate, rebuttal, and questions raised by the audience. We thank all authors for sharing this debate with the readership.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00068.x" xmlns="http://purl.org/rss/1.0/"><title>Risk Factors for Subclinical Carotid Atherosclerosis Among Current Smokers</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00068.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk Factors for Subclinical Carotid Atherosclerosis Among Current Smokers</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Heather M. Johnson, Megan E. Piper, Douglas E. Jorenby, Michael C. Fiore, Timothy B. Baker, James H. Stein</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-03-12T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00068.x</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/">10.1111/j.1751-7141.2010.00068.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00068.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">166</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">171</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>This study characterized the determinants of carotid atherosclerosis in a large contemporary sample of current smokers. Associations between risk factors, carotid intima-media thickness (CIMT), and carotid plaque presence were determined by multivariable regression. Participants included 1504 current smokers (58% female) who were a median (interquartile range) of 44.7 (38–53) years old and smoked 25 (15–40) pack-years; 55% had plaque. Pack-years, age, male sex, nonwhite race, body mass index, systolic blood pressure, small low-density lipoproteins (LDLs), and total high-density lipoproteins were independently associated with CIMT (model R<sup>2</sup>=0.434, P&lt;.001). Pack-years (odds ratio [OR], 1.14 per 10 pack-years; P=.001), age (OR, 1.75 per 10 years; P&lt;.001), body mass index (OR, 0.91 per 5 kg/m<sup>2</sup>; P=.035), and small LDLs (OR, 1.11 per 100 nmol/L; P&lt;.001) were independently associated with carotid plaque presence (model χ<sup>2</sup>=210.7, P&lt;.001). The association between pack-years and carotid plaque was stronger in women (OR, 1.09 per 10 pack-years, P<sub>interaction</sub>=.018).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Prev Cardiol. <em>2010;13:166–171.<sup>©</sup>2010 Wiley Periodicals, Inc.</em></p></div>]]></content:encoded><description>This study characterized the determinants of carotid atherosclerosis in a large contemporary sample of current smokers. Associations between risk factors, carotid intima-media thickness (CIMT), and carotid plaque presence were determined by multivariable regression. Participants included 1504 current smokers (58% female) who were a median (interquartile range) of 44.7 (38–53) years old and smoked 25 (15–40) pack-years; 55% had plaque. Pack-years, age, male sex, nonwhite race, body mass index, systolic blood pressure, small low-density lipoproteins (LDLs), and total high-density lipoproteins were independently associated with CIMT (model R2=0.434, P&lt;.001). Pack-years (odds ratio [OR], 1.14 per 10 pack-years; P=.001), age (OR, 1.75 per 10 years; P&lt;.001), body mass index (OR, 0.91 per 5 kg/m2; P=.035), and small LDLs (OR, 1.11 per 100 nmol/L; P&lt;.001) were independently associated with carotid plaque presence (model χ2=210.7, P&lt;.001). The association between pack-years and carotid plaque was stronger in women (OR, 1.09 per 10 pack-years, Pinteraction=.018).Prev Cardiol. 2010;13:166–171.©2010 Wiley Periodicals, Inc.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00073.x" xmlns="http://purl.org/rss/1.0/"><title>Association of Warfarin Use With CHADS2 Score in 441 Patients With Nonvalvular Atrial Fibrillation and No Contraindications to Warfarin</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00073.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Association of Warfarin Use With CHADS2 Score in 441 Patients With Nonvalvular Atrial Fibrillation and No Contraindications to Warfarin</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Harit V. Desai, Wilbert S. Aronow, Kaushang Gandhi, Suhalia Bakerywala, Judy Laimuanpuii, Mala Sharma, Stephen J. Peterson</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-05-20T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00073.x</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/">10.1111/j.1751-7141.2010.00073.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00073.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">172</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">174</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>The authors investigated the use of warfarin at hospital discharge in 557 consecutive patients, mean age 76 years, with nonvalvular atrial fibrillation (AF) at a university hospital. Of 557 patients with AF, 116 (21%) had contraindications to warfarin. Of patients eligible for warfarin, warfarin was used in 8 of 30 patients (27%) with a CHADS<sub>2</sub> score of 0, in 82 of 132 patients (62%) with a CHADS<sub>2</sub> score of 1, in 121 of 175 patients (70%) with a CHADS<sub>2</sub> score of 2, in 72 of 77 patients (94%) with a CHADS<sub>2</sub> score of 3, and in 27 of 27 patients (100%) with a CHADS<sub>2</sub> score of 4 to 6. Warfarin was used in 123 of 168 patients (73%) older than 75 years, in 74 of 79 patients (94%) aged 65 to 75 years, and in 23 of 32 patients (72%) younger than 65 years. Warfarin was used in 80 of 116 patients (69%) with a glomerular filtration rate &lt;60 mL/min/1.73 m<sup>2</sup> and in 140 of 163 patients (86%) with a glomerular filtration rate ≥60 mL/min/1.73 m<sup>2</sup>. There was no significant difference in use of warfarin between men and women and between whites and nonwhites.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Prev Cardiol. <em>2010;13:172–174.<sup>©</sup>2010 Wiley Periodicals, Inc.</em></p></div>]]></content:encoded><description>The authors investigated the use of warfarin at hospital discharge in 557 consecutive patients, mean age 76 years, with nonvalvular atrial fibrillation (AF) at a university hospital. Of 557 patients with AF, 116 (21%) had contraindications to warfarin. Of patients eligible for warfarin, warfarin was used in 8 of 30 patients (27%) with a CHADS2 score of 0, in 82 of 132 patients (62%) with a CHADS2 score of 1, in 121 of 175 patients (70%) with a CHADS2 score of 2, in 72 of 77 patients (94%) with a CHADS2 score of 3, and in 27 of 27 patients (100%) with a CHADS2 score of 4 to 6. Warfarin was used in 123 of 168 patients (73%) older than 75 years, in 74 of 79 patients (94%) aged 65 to 75 years, and in 23 of 32 patients (72%) younger than 65 years. Warfarin was used in 80 of 116 patients (69%) with a glomerular filtration rate &lt;60 mL/min/1.73 m2 and in 140 of 163 patients (86%) with a glomerular filtration rate ≥60 mL/min/1.73 m2. There was no significant difference in use of warfarin between men and women and between whites and nonwhites.Prev Cardiol. 2010;13:172–174.©2010 Wiley Periodicals, Inc.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00074.x" xmlns="http://purl.org/rss/1.0/"><title>Is Acute High-Dose Secondhand Smoke Exposure Always Harmful to Microvascular Function in Healthy Adults?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00074.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Is Acute High-Dose Secondhand Smoke Exposure Always Harmful to Microvascular Function in Healthy Adults?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Robert L. Bard, Joseph T. Dvonch, Niko Kaciroti, Susan A. Lustig, Robert D. Brook</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-05-20T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00074.x</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/">10.1111/j.1751-7141.2010.00074.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00074.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">175</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">179</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>Prev Cardiol.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Long-term exposure to secondhand smoke (SHS) is associated with impaired vascular function. The authors investigated the vascular and blood pressure (BP) reactions to acute SHS exposure. Twenty-five healthy nonsmoking adults underwent a 1-hour exposure to SHS (mean fine particulate matter &lt;2.5 μm level=315±116 μg/m<sup>3</sup>). Microvascular endothelial-dependent vasodilatation (EDV) (EndoPAT, Itamar Medical, Caesarea, Israel) and aortic hemodynamics/compliance (SphygmoCor, AtCor Medical, West Ryde, Australia) were measured before and after the SHS exposure with BP measured every 15 minutes during and for a 24-hour period before and after the exposure. SHS exposure did not change EDV, aortic hemodynamics, arterial compliance, or 24-hour BP. However, diastolic BP significantly increased during the SHS exposure period by 3.4±5.6 mm Hg. Our brief SHS exposure did not impair microvascular endothelial function or arterial compliance in healthy nonsmoking adults, but brachial diastolic BP increased.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Prev Cardiol. <em>2010;13:175–179.<sup>©</sup>2010 Wiley Periodicals, Inc.</em></p></div>]]></content:encoded><description>Prev Cardiol.Long-term exposure to secondhand smoke (SHS) is associated with impaired vascular function. The authors investigated the vascular and blood pressure (BP) reactions to acute SHS exposure. Twenty-five healthy nonsmoking adults underwent a 1-hour exposure to SHS (mean fine particulate matter &lt;2.5 μm level=315±116 μg/m3). Microvascular endothelial-dependent vasodilatation (EDV) (EndoPAT, Itamar Medical, Caesarea, Israel) and aortic hemodynamics/compliance (SphygmoCor, AtCor Medical, West Ryde, Australia) were measured before and after the SHS exposure with BP measured every 15 minutes during and for a 24-hour period before and after the exposure. SHS exposure did not change EDV, aortic hemodynamics, arterial compliance, or 24-hour BP. However, diastolic BP significantly increased during the SHS exposure period by 3.4±5.6 mm Hg. Our brief SHS exposure did not impair microvascular endothelial function or arterial compliance in healthy nonsmoking adults, but brachial diastolic BP increased.Prev Cardiol. 2010;13:175–179.©2010 Wiley Periodicals, Inc.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00079.x" xmlns="http://purl.org/rss/1.0/"><title>Patient-Related Diet and Exercise Counseling: Do Providers’ Own Lifestyle Habits Matter?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00079.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Patient-Related Diet and Exercise Counseling: Do Providers’ Own Lifestyle Habits Matter?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michael Howe, Adam Leidel, Sangeetha M. Krishnan, Alissa Weber, Melvyn Rubenfire, Elizabeth A. Jackson</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-08-16T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00079.x</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/">10.1111/j.1751-7141.2010.00079.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00079.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">180</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">185</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><em>The goal of this research was to evaluate the personal health behaviors of physicians in training and attending physicians in association with patient-related lifestyle counseling. Physicians at a major teaching hospital were surveyed regarding their personal lifestyle behavior, perceived confidence, and frequency of counseling patients regarding lifestyle behaviors. One hundred eighty-three total responses were received. Trainees were more likely to consume fast food and less likely to consume fruits and vegetables than attendings. Attending physicians were more likely to exercise 4 or more days per week and more than 150 minutes per week. Attending physicians were more likely to counsel their patients regarding a healthy diet (70.7% vs 36.3%,</em> P&lt;<em>.0001) and regular exercise (69.1% vs 38.2%,</em> P<em>&lt;.0001) compared with trainees. Few trainees or attendings were confident in their ability to change patients’ behaviors. Predictors of confidence in counseling for exercise included the provider’s own exercise time of &gt;150 minutes per week, being overweight, and reported adequate training in counseling. Only adequate training in counseling was a predictor of strong self-efficacy for counseling in diet. Many physicians lack confidence in their ability to counsel patients regarding lifestyle. Personal behaviors including regular exercise and better training in counseling techniques may improve patient counseling.</em></p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Prev Cardiol. <em>2010;13:180–185.<sup>©</sup>2010 Wiley Periodicals, Inc.</em></p></div>]]></content:encoded><description>The goal of this research was to evaluate the personal health behaviors of physicians in training and attending physicians in association with patient-related lifestyle counseling. Physicians at a major teaching hospital were surveyed regarding their personal lifestyle behavior, perceived confidence, and frequency of counseling patients regarding lifestyle behaviors. One hundred eighty-three total responses were received. Trainees were more likely to consume fast food and less likely to consume fruits and vegetables than attendings. Attending physicians were more likely to exercise 4 or more days per week and more than 150 minutes per week. Attending physicians were more likely to counsel their patients regarding a healthy diet (70.7% vs 36.3%, P&lt;.0001) and regular exercise (69.1% vs 38.2%, P&lt;.0001) compared with trainees. Few trainees or attendings were confident in their ability to change patients’ behaviors. Predictors of confidence in counseling for exercise included the provider’s own exercise time of &gt;150 minutes per week, being overweight, and reported adequate training in counseling. Only adequate training in counseling was a predictor of strong self-efficacy for counseling in diet. Many physicians lack confidence in their ability to counsel patients regarding lifestyle. Personal behaviors including regular exercise and better training in counseling techniques may improve patient counseling.Prev Cardiol. 2010;13:180–185.©2010 Wiley Periodicals, Inc.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00072.x" xmlns="http://purl.org/rss/1.0/"><title>Subclinical Atherosclerosis: Evolving Role of Carotid Intima-Media Thickness</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00072.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Subclinical Atherosclerosis: Evolving Role of Carotid Intima-Media Thickness</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Farouk Mookadam, Sherif E. Moustafa, Steven J. Lester, Tahlil Warsame</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-04-29T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00072.x</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/">10.1111/j.1751-7141.2010.00072.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00072.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">186</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">197</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>Cardiovascular risk factors have utility in risk prediction but have limitations in predicting individual risk. Identifying an individual’s risk remains a challenge. Emerging technologies such as carotid artery ultrasonography and measures of carotid intima-media thickness (CIMT) may be useful in identifying the susceptible patient who may benefit from more aggressive preventive therapy. This screening test is noninvasive, reproducible, inexpensive, and radiation-free. Recent data have improved our understanding of the application of CIMT as a screening tool for cardiovascular disease. CIMT measurement may place an individual into a higher- or lower-risk category, allowing for appropriate institution of preventive strategies.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Prev Cardiol. <em>2010;13:186–197.<sup>©</sup>2010 Wiley Periodicals, Inc.</em></p></div>]]></content:encoded><description>Cardiovascular risk factors have utility in risk prediction but have limitations in predicting individual risk. Identifying an individual’s risk remains a challenge. Emerging technologies such as carotid artery ultrasonography and measures of carotid intima-media thickness (CIMT) may be useful in identifying the susceptible patient who may benefit from more aggressive preventive therapy. This screening test is noninvasive, reproducible, inexpensive, and radiation-free. Recent data have improved our understanding of the application of CIMT as a screening tool for cardiovascular disease. CIMT measurement may place an individual into a higher- or lower-risk category, allowing for appropriate institution of preventive strategies.Prev Cardiol. 2010;13:186–197.©2010 Wiley Periodicals, Inc.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00086.x" xmlns="http://purl.org/rss/1.0/"><title>Will Increasing Referral to Cardiac Rehabilitation Improve Participation?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00086.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Will Increasing Referral to Cardiac Rehabilitation Improve Participation?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Thomas Boyden, Melvyn Rubenfire, Barry Franklin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-09-22T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00086.x</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/">10.1111/j.1751-7141.2010.00086.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00086.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">198</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">202</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=10.1111%2Fj.1751-7141.2010.00075.x" xmlns="http://purl.org/rss/1.0/"><title>Move More, Sit Less: A First-Line, Public Health Preventive Strategy?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00075.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Move More, Sit Less: A First-Line, Public Health Preventive Strategy?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Barry A. Franklin, Jenna Brinks, Lucy Sternburgh</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-06-10T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00075.x</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/">10.1111/j.1751-7141.2010.00075.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00075.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">203</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">208</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=10.1111%2Fj.1751-7141.2010.00082.x" xmlns="http://purl.org/rss/1.0/"><title>The Thiazolidinedione Controversy in Cardiovascular Risk</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00082.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Thiazolidinedione Controversy in Cardiovascular Risk</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Philip R. Liebson</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2010-09-22T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-7141.2010.00082.x</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/">10.1111/j.1751-7141.2010.00082.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1751-7141.2010.00082.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">209</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">212</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item></rdf:RDF>