HR, heart rate; APC, atrial premature complex; VPC, ventricular premature complex; VT, ventricular tachycardia; 2DE, two-dimensional echocardiography; SAX, short-axis; LAX, long-axis; 2DST, two-dimensional speckle tracking; PWTDI, pulsed-wave tissue Doppler imaging; AFI, automated function imaging (a 2DST application); PAD, pulmonary artery diameter at end-diastole; AoD, aortic diameter at end-diastole; LADmax, end-systolic left atrial diameter; LAAmax, end-systolic left atrial area; LASAXAmax, end-systolic left atrial area in short-axis view; Active LA FAC, active left atrial fractional area change; IVS, interventricular septal thickness at end-diastole (d) and peak systole (s); LVID, left ventricular internal diameter at end-diastole (d) and peak systole (s); LVPW, left ventricular peripheral wall at end-diastole (d) and peak systole (s); RWTd, relative wall thickness at end-diastole; MWTd, mean wall thickness at end-diastole; LVIV, left ventricular internal volume at end-diastole (d) and peak systole (s); IMP, index of myocardial performance (Tei index); FS, fractional shortening; EF, ejection fraction; S1 peak radial wall motion velocity during isovolumic contraction; Sm, peak radial wall motion velocity during ejection; PEP/ET, pre-ejection period over ejection time ratio; εR, averaged peak radial strain; εL, averaged peak longitudinal strain; εL(AFI), global peak longitudinal strain by automated function imaging; SRR-sys, averaged radial peak systolic strain rate; SRL-sys, averaged longitudinal peak systolic strain rate; E1, peak radial wall motion velocity during isovolumic relaxation; Em, peak radial wall motion velocity during early diastole; Am, peak radial wall motion velocity during late diastole; IVRT, isovolumic relaxation time; E, early-diastolic transmitral blood flow velocity; A, late-diastolic transmitral blood flow velocity.
Laboratory, Electrocardiographic, and Echocardiographic Detection of Myocardial Damage and Dysfunction in an Arabian Mare with Nutritional Masseter Myodegeneration
Article first published online: 30 AUG 2011
Copyright © 2011 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 25, Issue 5, pages 1171–1180, September/October 2011
How to Cite
Schefer, K.D., Hagen, R., Ringer, S.K. and Schwarzwald, C.C. (2011), Laboratory, Electrocardiographic, and Echocardiographic Detection of Myocardial Damage and Dysfunction in an Arabian Mare with Nutritional Masseter Myodegeneration. Journal of Veterinary Internal Medicine, 25: 1171–1180. doi: 10.1111/j.1939-1676.2011.00787.x
- Issue published online: 20 SEP 2011
- Article first published online: 30 AUG 2011
- Manuscript Accepted: 14 JUL 2011
- Manuscript Revised: 30 MAY 2011
- Manuscript Received: 15 FEB 2011
two-dimensional speckle tracking
late-diastolic transmitral blood flow velocity
peak radial wall motion velocity during late diastole
automated function imaging
aortic diameter at end-diastole
atrial premature complex
cardiac troponin I
early diastolic transmitral blood flow velocity
peak radial wall motion velocity during isovolumic relaxation
peak radial wall motion velocity during early diastole
E over A ratio
Em over Am ratio
averaged peak longitudinal strain
global peak longitudinal strain by automated function imaging
averaged peak radial strain
fractional area change
index of myocardial performance (Tei index)
isovolumic relaxation time
interventricular septal thickness at end-diastole
interventricular septal thickness at peak systole
left atrial or left atrium
end-systolic left atrial area
end-systolic left atrial area in short-axis view
end-systolic left atrial diameter
left ventricular or left ventricle
left ventricular internal diameter at end-diastole
left ventricular internal diameter at peak systole
left ventricular internal volume at end-diastole
left ventricular internal volume at peak systole
left ventricular peripheral wall thickness at end-diastole
left ventricular peripheral wall thickness at peak systole
mean wall thickness at end-diastole
pulmonary artery diameter at end-diastole
- PW TDI
pulsed-wave tissue Doppler imaging
relative wall thickness at end-diastole
peak radial wall motion velocity during isovolumic contraction
peak radial wall motion velocity during ejection
averaged radial peak systolic strain rate
averaged longitudinal peak systolic strain rate
tissue Doppler imaging
ventricular premature complex
A 22-year-old, 395 kg Arabian mare used as a pleasure horse was presented to the Equine Department of the Vetsuisse Faculty, University of Zurich, with a 2-day history of dysphagia, salivation, and bilateral swelling of the masseter muscles. Previous treatment with flunixin meglumine had not resulted in improvement. None of the other horses on the premises showed similar clinical signs.
On admission, the mare was slightly lethargic. Her rectal temperature (37.7°C) and respiratory rate (16 breaths/min) were within normal limits, but moderate tachycardia (60 beats/min) was present. On auscultation, neither cardiac murmurs nor arrhythmias were detected and lung sounds were normal. Both masseter muscles were severely swollen and painful, and the mare was hypersalivating. She had a good appetite, but masticatory efforts were ineffective. The motility and tone of the tongue appeared normal, but she was unable to move food to the back of the mouth to be swallowed. The mouth could be manually opened only the width of one finger. Her gait was normal and no other skeletal muscles were swollen, stiff, hardened, or painful. No other abnormalities were detected.
Laboratory findings on the day of admission (day 1) are summarized in Table 1. Hematology results were within the normal reference ranges. Abnormal serum biochemistry results included marked increases in the activities of liver and muscle enzymes. Serum selenium concentration was below the lower limit of the reference range, whereas serum vitamin E concentration was normal. The mare's urine was dark brown and urine dipstick analysis1 showed severe pigmenturia.
|Complete blood count|
|Leukocyte count (×103/μL)||7.2||4.7–8.2|
|Chemistry: metabolites, proteins|
|Bilirubin (total) (μmol/L)||40.2||17.4–35.2|
|Total protein (biuret) (g/L)||55||57–70|
|Chemistry: enzymes (U/L)|
|Gamma glutamyl transferase||9||6–31|
|Cardiac Troponin I (ng/mL)||11.6||2.15||0.6||0.21||0.1||0.09||0.08||0.07||<0.06|
|Vitamin E (mg/L)||2.16||>1|
|Urine specific gravity||1.029||1.009||1.008||1.012||1.030||1.025–1.050|
Upper airway endoscopy (including the guttural pouches), palpation, and endoscopic examination of the oral cavity, radiographic examination of the head and temporomandibular joints as well as a neurologic examination all were normal. Ultrasonographic examination2 of the masseter muscles identified bilateral thickening of the masseter muscles, ranging from 3.5 to 4 cm, with increased muscle echogenicity and patchy blurring of the fasciae within the muscle layers. These findings were compatible with inflammatory infiltration and edema of both masseter muscles as seen in myositis (Fig 1).[1, 2]
Based on history, clinical examination, and laboratory findings, a presumptive diagnosis of nutritional masseter myodegeneration was made. Involvement of other muscle groups was not obvious but could not be conclusively eliminated. Muscle biopsies were not obtained.
Treatment was started with phenylbutazone18 (3.3 mg/kg) IV twice daily and dexamethasone17 (0.04 mg/kg) IV once daily for 8 and 4 days, respectively; a single IM injection of vitamin E and selenium16 (total dose of 16 mg sodium selenite and 400 mg alpha-tocopherol), followed by alpha-tocopherol15 (10 IU/kg/d) PO for 18 days and methocarbamol14 (50 mg/kg) PO for 10 days. Lidocaine13 (1.3 mg/kg bolus IV, followed by 0.03 mg/kg/min IV constant rate infusion) was administered for analgesia for 3 days. Lactated Ringer's solution12 alternated with an isotonic maintenance solution11 was administered at a rate of 90 mL/kg/d. Despite treatment, the mare still appeared painful and lethargic. Additional analgesia therefore was provided starting on day 3 using medetomidine10 (0.25–1.00 μg/kg/h titrated to effect) and metamizole9 (15 mg/kg/h) administered as IV constant rate infusions, decreasing these dosages over the next 12 hours and 2 days, respectively.
Tachycardia persisted despite analgesia and overall improvement in clinical signs. A 24-h Holter ECG8 therefore was performed and revealed sinus tachycardia with sporadic supraventricular and uniform ventricular dysrhythmias (Table 2). Cardiac troponin I (cTnI)7 concentration was markedly increased (11.6 ng/mL; reference range, <0.06 ng/mL), consistent with extensive myocardial damage. Routine transthoracic echocardiography was then performed using conventional two-dimensional (2DE), M-mode, and flow Doppler echocardiography as well as pulsed-wave tissue Doppler imaging (PWTDI) and 2D speckle tracking (2DST) using standard right parasternal long-axis (LAX) and short-axis (SAX) views.6,5 Medetomidine and lidocaine administration had been discontinued 12 and 18 hours, respectively, before echocardiography. Methocarbamol, which was judged to be unlikely to influence cardiovascular function, and all other treatments were continued (see Table 2). Assessment included great vessel diameter and left atrial (LA) size and function by 2DE; left ventricular (LV) size and systolic function by M-Mode (linear measurements) and 2DE (volumetric estimates); and LV systolic and diastolic function by transmitral Doppler flow profiles, PWTDI-based radial wall motion velocity analyses, and 2DST-based strain and strain rate analyses.4[5-9]
|Variables||Method||Day||Reference Values (mean ± SD)|
|Heart rate and rhythm during 24h Holter ECG||Sinus tachycardia (48–68/min), 56 APCs, 52 VPCs, and 6 short runs of VT (89–112/min)||N/A||Normal sinus rhythm (35–49/min), 15 2nd degree AV blocks, 6 APCs and 1 VPC|
|Heart rate and rhythm during echocardiography||Sinus tachycardia (mean HR 57/min), 1 VPC||Normal sinus rhythm (mean HR 41/min)||Normal sinus rhythm (mean HR 42/min)|
|PAD (cm)||2DE LAX||6.1||6.7||5.5||6.6 ± 0.6a|
|AoD (cm)||2DE LAX||6.9||7.2||6.7||7.8 ± 0.7a|
|LA size and function|
|LADmax (cm)||2DE LAX||12.2||11.9||11.2||12.3 ± 1.1b|
|LAAmax (cm2)||2DE LAX||89.7||83.6||78.8||91.3 ± 11.8b|
|LASAXAmax (cm2)||2DE SAX||109.1||111.8||100.6||91.3 ± 11.8b|
|Active LA FAC (%)||2DE LAX||25||29||26||19.1 ± 6.1b|
|IVSd (cm)||M-Mode SAX||3.1||2.6||3.0||3.2 ± 0.2a|
|IVSs (cm)||M-Mode SAX||3.8||4.2||3.8||4.9 ± 0.2a|
|LVIDd (cm)||M-Mode SAX||10.1||11.4||10.0||11.7 ± 1.0a|
|LVIDs (cm)||M-Mode SAX||7.8||7.3||6.9||7.0 ± 1.1a|
|LVPWd (cm)||M-Mode SAX||2.7||2.4||2.5||2.6 ± 0.5a|
|LVPWs (cm)||M-Mode SAX||3.3||3.6||3.6||4.5 ± 0.5a|
|RWTd||M-Mode SAX||0.58||0.44||0.55||0.44 ± 0.05a|
|MWTd (cm)||M-Mode SAX||2.9||2.5||2.7||2.46 ± 0.14a|
|LVIVd (mL)||2DE LAX||843||894||869||1288 ± 229a|
|LVIVs (mL)||2DE LAX||324||383||307||337 ± 87a|
|LV systolic and diastolic function|
|IMP||PW TDI SAX||0.76||0.66||0.49||0.26 ± 0.01a|
|LV systolic function|
|FS (%)||M-Mode SAX||22||36||31||40.7 ± 4.3a|
|EF (%)||2DE LAX||61||57||65||74.0 ± 3.5a|
|S1 (cm/s)||PWTDI SAX||3||5||6||4.9 ± 2.4a|
|Sm (cm/s)||PWTDI SAX||10||11||11||12.0 ± 2.0a|
|PEP/ET||PWTDI SAX||0.45||0.32||0.29||0.24 ± 0.04a|
|εR (%)||2DST SAX||58.7||67.6||77.6||80.4 ± 11.4a|
|εL (%)||2DST LAX||−19.8||−19.4||−22.7||−24.8 ± 2.2a|
|εL(AFI) (%)||AFI LAX||−17.1||−17.4||−23.0||−22.5 ± 1.9a|
|SRR-sys (s−1)||2DST SAX||2.0||1.9||2.0||1.6 ± 0.1a|
|SRL-sys (s−1)||2DST LAX||−1.1||−0.9||−1.2||−1.1 ± 0.1a|
|LV diastolic function|
|E1 (cm/s)||PWTDI SAX||7||6||6||7 ± 1.8a|
|Em (cm/s)||PWTDI SAX||12||15||25||33.7 ± 5.8a|
|Am (cm/s)||PWTDI SAX||14||17||15||12.5 ± 3.6a|
|Em/Am||PWTDI SAX||0.8||0.9||1.7||2.9 ± 0.9a|
|IVRT (ms)||PWTDI SAX||138||126||78||49 ± 16a|
|E (m/s)||Flow Doppler||0.31||0.51||0.56||0.59 ± 0.18b|
|A (m/s)||Flow Doppler||0.49||0.50||0.40||0.37 ± 0.08b|
|E/A||Flow Doppler||0.64||1.03||1.41||1.62 ± 0.42b|
Results of the echocardiographic examinations are summarized in Table 2 and presented in Figures 2-4. Measurements were compared to preliminary normal values obtained on small populations of horses of different breeds. Cardiac structures, valvular competence, and chamber dimensions were normal. Decreased LV systolic function was evident based on prolongation of the ratio of pre-ejection period over ejection time (PEP/ET) by TDI and low fractional shortening (FS), ejection fraction (EF), peak radial wall motion velocity during isovolumic contraction (S1) by TDI, and longitudinal and radial strain (εL, εR) by 2DST.[6, 8, 9] The values for radial and longitudinal strain rate (SRR-sys, SRL-sys) were comparable to those of healthy horses, suggesting preserved intrinsic contractility of the LV myocardium. Peak radial wall motion velocity during early diastole (Em), the ratio of early-diastolic-to-late-diastolic radial wall motion velocity (Em/Am), and the ratio of early-diastolic-to-late-diastolic transmitral blood flow velocity (E/A) all were decreased, whereas the isovolumic relaxation time (IVRT) was prolonged. These findings were consistent with diastolic dysfunction and impaired LV relaxation. Finally, the marked increase of the TDI-based index of myocardial performance (IMP) further corroborated the diagnosis of decreased systolic and diastolic function of the LV.
The mare's general demeanor was good over the following days, and she was bright, alert, and responsive. She showed good appetite but still had severe difficulties in opening the mouth and in mastication. Therefore she was fed via a nasogastric tube for 7 days. The masseter muscle swelling continued to worsen during the first 4 days of hospitalization and then decreased markedly until bilateral muscle atrophy was present. Heart rate returned to normal by day 5. Starting on day 8, phenylbutazone3 was administered PO (instead of IV) at a dosage of 2.5 mg/kg once daily for another 7 days.
Hematologic, biochemical, and urine analyses were repeated at intervals of 2–3 days (Table 1) and indicated marked improvement of muscle enzyme activities (CK, AST, LDH) over the duration of hospitalization. There was also a progressive decrease in cTnI to concentrations that were close to normal on the day of discharge (day 17). Myoglobinuria resolved by day 7. Fluid therapy was therefore slowly decreased and then discontinued on day 7 and 8.
Ultrasonographic examination of the masseter muscles was repeated 4 days after the initial examination. Muscle layers measured between 2.5 and 3 cm, indicating a marked decrease in total muscle thickness compared to day 1 (Fig 1). The overall echotexture of the muscles appeared more homogeneous and less echogenic. The connective tissue septae were more clearly defined and more prominent, suggesting decreased inflammation and possibly early fibrosis.
Echocardiography was repeated on day 7 and 12 (Table 2). On day 7, LV systolic function appeared normal using radial indices (FS, εR), whereas EF and εL still were decreased. Similarly, indices of LV diastolic function (Em, Em/Am, E/A, IVRT) still indicated impaired LV relaxation. On day 12, EF, εR and εL had further improved and were comparable to values of healthy horses. LV relaxation had improved and neither Em/Am reversion nor E/A reversion was present anymore. However, a slight prolongation of IVRT and a decreased Em and Em/Am ratio still indicated mild diastolic dysfunction (Figs 2-4).
The ability to chew and swallow returned slowly, and the mare was discharged on day 17 with the recommendation of stall rest and turn out on pasture for 1 month. Addition to the diet of a mineral and vitamin supplement containing selenium and vitamin E was further recommended. According to telephone follow-up with the owner 1 month after discharge, the mare was able to open her mouth to almost the full extent, the masseter muscles had recovered, and the mare had gained weight. Unfortunately, 6 months after discharge, after the owners had resumed normal exercise, the mare had an accident unrelated to the myopathy and had to be euthanized because of a hopeless prognosis. The horse was not available for necropsy.
Nutritional myodegeneration predominantly occurs in foals <1 year of age[10, 11] and less commonly in adult horses.[12-16] In adults, the muscles of mastication often are affected together with locomotor and cardiac muscles. In acute cases, the masseter muscles are swollen and dysphagia may be the first clinical sign of muscular degeneration. In chronic cases, masticatory function is impaired by muscular atrophy and fibrosis.
Ultrasonography is a valuable modality to assess muscle morphology. The masseter muscles can be easily examined and muscle thickness measured. In this case, marked thickening, increased echogenicity and blurring of the connective tissue septae of the masseter muscles could be documented on day 1. Edematous muscle generally is considered to appear hypoechogenic, but depending on the degree of concurrent inflammation, it also may appear hyperechoic. Changes in echogenicity have been reported for a variety of myopathies in horses and humans.[2, 18] In particular, muscular hyperechogenicity has been described in equine postanesthetic and fibrotic myopathy.[1, 17] Increased echogenicity of muscle has further been described in fatty infiltration of diseased muscle,[2, 18] which is said to have greater impact on muscular echo intensity than muscle fibrosis.[2, 18] A decrease in muscle thickness, decreased overall echogenicity, and a more distinctive appearance of the connective tissue septae were documented bilaterally 4 days after the initial examination. The decrease in muscle thickness most probably reflected decreased muscle inflammation and edema and possibly ensuing atrophy. Decreased echo intensity after initial hyperechogenicity has been reported in horses that recovered from postanesthetic myopathy. Whether hyperechogenicity of the connective tissue septae in this case was attributable to fibrosis, fatty infiltration, differences in scanning technique (eg, imaging depth, transducer placement), or a combination of these factors remains undetermined because of lack of concurrent histopathologic examination.
Vitamin E and selenium are essential antioxidants that protect cell membranes from peroxidation by free radicals. In several reports, horses affected by myopathy, including some with masseter involvement, were deficient in selenium,[12, 14-16] whereas the role of vitamin E is unclear.[12, 15, 16, 19] In the present case, serum selenium concentration was decreased (probably because of nutritional deficiencies, because soil selenium content in Switzerland is low and no mineral supplements had been provided to the mare before presentation) whereas serum vitamin E concentration was normal. Other factors such as stress and increased physical activity may be important for development of clinical signs in the face of antioxidant deficiency.
Degenerative lesions of the myocardium are seen commonly in various species with selenium and vitamin E deficiency.[19-21] However, only a few reports implicate vitamin E and selenium as potential causes of myodegenerative lesions in the heart of adult horses.[12, 13, 15, 19] Myocardial disease probably is under-recognized in clinical practice, because clinical findings are extremely variable and diagnosis is not straightforward. Presumptive diagnosis requires clinical suspicion based on the history and findings on physical examination, echocardiography, ECG, and clinical laboratory test results.
In the present case, myocardial damage was suspected because of relentless tachyarrhythmia in the presence of clinical signs of masseter myopathy, increased muscle enzyme activities, and decreased serum selenium concentration. Measurement of plasma concentration of cTnI, which is considered a highly sensitive and specific biomarker for the diagnosis of acute cardiac cellular injury, allowed confirmation of myocardial damage.
Finally, echocardiography served to detect marked systolic and diastolic LV dysfunction associated with myocardial disease. Detailed description of the echocardiographic methods used to assess LV mechanical function is available elsewhere.[5-9, 23, 24] The use of 2DE and M-mode echocardiography is well established for assessment of chamber size and global systolic LV function in horses.[25, 26] However, regional myocardial dysfunction and diastolic LV dysfunction, which commonly accompany LV systolic dysfunction and may be seen in horses with myocardial disease, are rarely considered because they are more difficult to detect and quantify. Doppler echocardiographic interrogation of transmitral blood flow and LV wall motion analyses using TDI and 2DST provide additional indices for assessment of regional and global systolic and diastolic ventricular function that go beyond the conventional echocardiographic approach.[6-8, 23, 24, 27-30] In this case, for example, LV systolic function on day 7 appeared normal based on FS and εR (both of which only consider radial wall motion), whereas EF based on 2DE-based three-dimensional estimates of LV volume and εL determined by 2DST (both of which also consider longitudinal function of the LV) still indicated impaired systolic function. Similarly, TDI indices of LV diastolic function still suggested impaired LV relaxation. These findings indicate that 2DST and TDI might be more sensitive in the detection of abnormal LV mechanics than conventional methods. In particular, they might be able to detect differences in alterations of radial versus longitudinal myocardial function and differences in deterioration and recovery of systolic versus diastolic ventricular function, respectively. Therefore, these newer methods might be useful diagnostically in selected cases in which myocardial dysfunction is suspected but cannot be documented using conventional echocardiographic methods. However, their true clinical value in horses is largely unknown to date, and interpretation of findings generally is based on concepts extrapolated from studies conducted in other species, including humans.
This case report describes the diagnostic approach for detection of myocardial damage in a horse with nutritional masseter myopathy and provides proof of concept for the clinical use of novel echocardiographic indices for the assessment of systolic and diastolic LV function in horses with myocardial disease. In conjunction with conventional echocardiographic methods, we were able to objectively describe impaired systolic and diastolic LV function (and recovery thereof) in a horse with nutritional myodegeneration using Doppler interrogation of transmitral blood flow and LV wall motion analysis using TDI and 2DST. Additional studies will be necessary to definitively establish the clinical use of these echocardiographic methods in horses with myocardial disease.
Combur-Test, F. Hoffmann-La Roche AG, Basel, Switzerland
GE Logiq e, GE Medical Systems, Glattbrugg, Switzerland
Butadion, Streuli AG, Uznach, Switzerland
Dexadreson, Veterinaria AG, Pfäffikon, Switzerland
Tocoselenit, Dr. E. Graeub AG, Bern, Switzerland
Evit 800, Vita Health Care AG, Laupen, Switzerland
Methocarbamol 40%, Streuli AG
Lidocain HCl 2%, Kantonsapotheke Zürich, Zürich, Switzerland
Ringer-Lactat-Lösung, Fresenius Kabi (Schweiz) AG, Stans, Switzerland
Equi-Biserol, Laboratorium Dr. G. Bichsel AG, Interlaken, Switzerland
Dorbene, Dr. E. Graeub AG
Vetalgin, Veterinaria AG
Televet-100, Roesch&Associates Information Engineering GmbH, Frankfurt, Germany
i-STAT 1 Analyzer, Abbott Point of Care Inc., Birmingham, UK
GE Vivid 7 Dimension (BTO6), GE Medical Systems
M4S Phased Array Transducer, GE Medical Systems
EchoPAC Software Version 6.1.2, GE Medical Systems
Butasan, Vetoquinol AG, Ittigen, Switzerland
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