Skip main navigation

Assessment of Left Ventricular Mass by Cardiovascular Magnetic Resonance

Originally published 2002;39:750–755


    Left ventricular hypertrophy is associated with significant excess mortality and morbidity. The study and treatment of this condition, in particular the prognostic implications of changes in left ventricular mass, require an accurate, safe, and reproducible method of measurement. Cardiovascular magnetic resonance is a suitable tool for this purpose, and this review assesses the technique in comparison with others and examines the clinical and research implications of the improved reproducibility.

    The importance of left ventricular hypertrophy (LVH) in medicine is not widely appreciated. The Framingham Study, among others, showed that increased left ventricular (LV) mass is associated with a significant excess of cardiovascular mortality and morbidity.1 This is independent of the presence of coronary artery disease2 or hypertension,1 with a tripling of the mortality rate in subjects with1–3 and without2 either of these. The risks of coronary, peripheral, or cerebrovascular disease are also raised, even among normotensive subjects with LVH.1,4,5

    The accurate measurement of LV mass has in the past been difficult, partly because of the oblique angle at which the heart lies within the chest, its continuous movement, and the lack of a technique for imaging the whole left ventricle. Initial measurements with ECG data were surrogate markers for LV mass, with values affected by positioning of the leads, orientation of the heart, and obesity.6–8 Nevertheless, criteria were developed for identifying LVH with ECG9,10 that correlated to an extent with true LVH but were insensitive and nonspecific (specificity, 6% to 56%).11–13 Imaging techniques have now supplanted the ECG, and we review these with particular reference to cardiovascular magnetic resonance (CMR).


    Echocardiography (echo) was a distinct advance for LV mass measurement over the ECG, with direct visualization of the myocardium and real-time imaging, and many important studies examining the prognostic effects of LVH have used this method.1,2,14 However, obtaining good quality images is dependent on a skilled operator, patient position and anatomy, obesity, and angle of the transducer beam,15,16 and images of sufficient quality for LV mass measurement may not be obtained in up to one third of cases.16–18 The assumed geometric shape for both M-mode and 2D echo may lead to error, particularly as variations in ventricular geometry affect calculated LV mass.19 The landmark trials, such as Framingham,1 overcame the deficiencies in accuracy and reproducibility of echo with large numbers of subjects.

    M-mode is the commonest echocardiographic method for measuring LV mass, the images being easier to obtain and the calculations straightforward. Although validated against postmortem mainly normal hearts,20,21 it suffers most from the assumption of geometric shape, and this variability is reflected in the poor accuracy of the technique, with standard errors of the estimate (SEE) of 29 to 97 g (95% confidence interval [CI], 57 to 190 g).20–23 Interstudy reproducibility is also poor, with SDs of the difference between successive measurements of 22 to 40 g (95% CI, 45 to 78 g).21,24–27 The importance of operator skill is underlined by the large interobserver variability of a similar degree (SEE, 28 to 41 g; 95% CI, 55 to 80 g).21,24,25

    2D echo has advantages over M-mode echo, as measurement is made of the ventricular length and minor axis in 2 planes. It still, however, assumes a prolate ellipsoid shape of the left ventricle and, to an extent, uniform wall thickness and is thus prone to similar inaccuracies as M-mode echo. The accuracy (SEE, 31 to 39 g)22,23 and reproducibility28–30 are moderately improved over those of M-mode, although the increased difficulty in obtaining suitable quality images for evaluation may limit the ability to determine LV mass.

    3D echo removes the assumption of shape and wall thickness. It has been shown to be more accurate than 2D or M-mode echo22,31 and is comparable to CMR,32,33 with reasonable reproducibility (95% CI, ±45 g),34 particularly with the newer transesophageal 3D echo (95% CI, ±12.8 g).35 The technique requires skill and time; however, and a number of subjects may not have suitable acoustic windows. There are currently relatively few units worldwide practicing the technique on a regular basis, and the transesophageal route may not be acceptable to some subjects.

    Electron-Beam Computed Tomography

    The fast imaging time of electron beam computed tomography (EBCT), when coupled with blood-pool contrast agents, has facilitated 3D cardiac imaging precise enough to measure LV mass. The technique is similar to 3D echo and CMR in that multiple contiguous image planes are summed to measure myocardial volume, employing Simpson’s rule. When multiplied by the density of myocardial tissue (1.05 g/cm3), the LV mass is obtained. The ability to acquire many slices in a single breath-hold is also an advantage. There is good reported accuracy36,37 (SEE, 16 g in humans) and reproducibility,38 although human validation studies are limited. The disadvantages are the exposure to ionizing radiation and need for an intravenous contrast agent to delineate the cardiac blood pool. In addition, the image slices are not true short axes but an approximation, because of the limitations of available image planes, which decrease accuracy because of partial volume effects.

    Cardiovascular Magnetic Resonance

    3D techniques such as EBCT and 3D echo are clearly better than 1D or 2D methods with assumptions about ventricular shape. CMR shares this advantage without the ionizing radiation or need for contrast agents with EBCT and without the problems of acoustic windows for echo. The free choice of imaging planes and good tissue visualization mean that virtually all images are of sufficient quality for LV mass determination.

    CMR Technique

    For the most accurate measurements, the image stack should be parallel to the true LV short axis, minimizing partial volume errors (Figure). The short axis is identified by first piloting the vertical long axis (VLA) plane from transaxial images, passing through the center of the mitral valve and apex of the LV. A horizontal long axis (HLA) plane is then obtained perpendicular to the VLA, again passing through the center of the mitral valve and apex. From the HLA, a stack of short-axis images is obtained, covering the length of the LV. ECG-gated cine CMR is acquired to measure LV mass at a single time point within the cardiac cycle (the standard is end-diastole). In addition, acquiring each image slice within a single breath-hold removes respiratory artifact. Usually 10 slices will cover the ventricle, and with a 10-second breath-hold per slice, this can be achieved in <10 minutes. With the newest scanners, cine stack can be obtained in a single breath-hold, reducing the time taken for a scan to ≈8 seconds.39 The image stack can also provide volume information by summing the endocardial area on each slice to derive left (and right) ventricular volumes. The cine nature of the images allows end-diastolic and end-systolic volume to be measured and thus also stroke volume, as well as regional ventricular function.

    Diagrammatic representation of the LV with typical CMR short axis images obtained.

    Accuracy and Reproducibility

    The accuracy of CMR measurements of LV mass has been validated using postmortem hearts, imaged ex vivo for humans26,40 or in vivo for animal studies41–46 (Table 1). These show good agreement between the CMR-obtained and true LV masses, with SD of the difference of ≈8 g (95% CI, ≈15 g) in human studies and 10 g (95% CI, ≈19 g) in canine studies. The gold-standard validation of comparing in vivo images with subsequent postmortem weights has not been performed in humans, and this important comparison remains to be done.

    Table 1. Accuracy of CMR-Determined LV Mass in Human and Animal Studies

    StudyNo.SDD95% CIMean DifferenceMean % DifferenceNotes
    Values are compared to postmortem derived LV mass. Mean values are weighted for sample size. SDD indicates standard deviation of the difference between the 2 measurements; CI, confidence interval (1.96 × SDD); and MI, myocardial infarction.
    *SE of the estimate from regression equation.
    Bottini et al2668.9 g±17.5 g0.7 g4.0%Human
    Katz et al40107.4 g±14.5 g10.2 g5.3%Human
    Human studies (mean values)168.0 g±15.7 g
    McDonald et al41101.8 g±3.5 g4.4 g5.2%Canine
    Shapiro et al42106.7 g*±13.1 gCanine normal
    88.7 g*±17.1 gCanine post-MI
    Caputo et al431313.7 g*±26.9 g10.0%Canine normal + LVH
    Keller et al44103.5 g±6.9 g6.8 g13.3%Canine
    Maddahi et al4584.9 g*±9.6 gCanine; in vivo
    93.4 g*±6.7 gCanine; dead (in-situ)
    Florentine et al461113.1 g*±25.7 gCanine + feline
    Canine studies (mean values)797.0 g±13.7 g

    The reproducibility of LV mass measurements is of importance for assessing changes over time, both for individuals and research studies. This encompasses interstudy (ie, test-retest reliability) and inter- and intraobserver variability in values. Again these are very good for CMR (Table 2),26,27,40,47–53 with interstudy variability having a mean weighted SD of the difference of 7.8 g (95% CI, 15.3 g).26,27,47,48 Mean weighted intra- and interobserver variabilities are 4.8 and 9.0 g, respectively.47,53 By comparison, the mean weighted interstudy SD of the difference for M-mode, 2D, and 3D echo is 27.7,21,24–28 19.2,28,30 and 19.2 g,34,35 respectively.

    Table 2. Reproducibility of CMR-Derived LV Mass Measurements from Human Studies

    Values are standard deviations of the difference between successive scans (g) or % variability. Mean values are for studies with absolute values, weighted by sample size. DCM indicates dilated cardiomyopathy; MI, myocardial infarction.
    Bellenger et al47156.4 g (2.8%)3.0 g (1.6%)5.1 g (2.4%)Normal subjects
    156.4 g (3.0%)5.9 g (2.7%)7.7 g (3.1%)Heart failure
    Bottini et al2648.2 gNormal subjects
    Germain et al272011.2 g (6.7%)Normal subjects
    Grothues et al48204.2 g (2.3%)Normal subjects
    209.6 g (3.8%)Heart failure
    208.4 g (2.8%)LVH
    Semelka et al49115.2%4.4%Normal subjects
    Semelka et al50114.7–6.1%3.4%DCM
    Bogaert et al51124.4%4.1%4.2%Normal subjects
    Matheijssen et al5283.6%3.6%MI
    Yamaoka et al53105.8 g17.8gNormal, LVH, and DCM
    Katz et al40106.1%7.2%
    Mean weighted values7.8 g (n=114)4.8 g (n=40)9.0 g (n=40)

    Clinical Implications

    The greater accuracy and reproducibility of 3D techniques, such as CMR, has important implications for clinical practice and research. The improved reproducibility means that in group studies, much smaller sample sizes can be used to detect the same change in LV mass. Alternatively, using the same sample size, smaller degrees of change can be identified. A comparison between CMR and echo of the sample sizes needed to detect a statistically significant change in mean LV mass of 10 g are shown in Table 3. The numbers needed with CMR are ≈8% of those with M-mode and 17% of those with 2D echo, with considerable savings in cost and study duration. CMR has already been used in clinical trials to identify very small differences in LV mass between groups: 9 to 11 g/m2 with 15 to 20 subjects per group54,55 and 7 g with groups of 30 to 40 subjects each.56

    Table 3. Comparison of Sample Sizes Needed to Detect a Statistically Significant Change in Mean LV Mass of 10 g

    Power (1-β Error)CMR2D EchoM-Mode Echo
    These assume a 2-tailed unpaired t test with 0.05 level of significance (α-error) and refer to the sample size in each group (2 parallel treatment groups would need twice this number in total). We used the mean weighted values of interstudy standard deviation of the difference for M-mode echo (27.7 g),21,24–28 2D echo (19.2 g),28,30 and CMR (7.8 g).26,27,47,48

    For individual patients, the 95% CI for serial studies using M-mode echo of ±45 to 78 g21,24–27 means that serial LV mass measurements cannot detect a change of less than this amount with any certainty. Given that most therapeutic interventions are likely to effect a change that is smaller than this, M-mode echo would not be an ideal method for serial changes. 2D echo has improved reproducibility, which results in better confidence intervals (±39 g),30 and these are ±13 to 45 g for 3D echo, depending on the route used (transesophageal versus transthoracic).34,35 CMR has 95% CIs of ±12 to 22 g,26,27,47,48 and this or another 3D technique should be used for individual changes in LV mass.

    Limitations of CMR

    Patient factors can sometimes limit the usefulness of the technique. Because of the enclosed nature of the CMR scanner, some people find this too claustrophobic. In practice, the incidence of this is ≈3% to 5%, though light intravenous anxiolysis with diazepam to can reduce this to 1%.57 Advances in equipment technology, with shorter and more open magnets together with reduced time in the scanner from faster imaging, will also improve conditions for these patients. The same restrictions as for any MR scanner apply for patients with cranial aneurysm clips, ocular metallic shards, and pacemakers. The need for breath-holding to remove respiratory motion artifact can present problems for some patients with severe cardiac or respiratory disease; for these patients, “navigator” sequences can be used in which free breathing is allowed and the diaphragm is continuously monitored, with imaging adjusted for the diaphragm position.58 This has the disadvantage of slightly increased imaging time, but image quality is well maintained.

    Currently, the availability of CMR scanners capable of cardiac work and the skilled personnel needed to obtain and interpret the images limits the widespread clinical use of this technique, although many pharmacological studies with CMR have already been performed. This is likely to change in the near future, with nearly all new MR scanners having the required hardware and the cardiac software. Although the initial cost of the scanner is high, for research purposes the savings from the reduced number of subjects may offset this substantially. A single study takes ≈15 minutes for postprocessing with standard techniques. Although this is longer than for echo, the new generation of machines coupled with automated image processing will greatly reduce these times and will allow a fast-throughput service.


    LVH is a potent risk factor for cardiovascular disease and is associated with significant increases in morbidity and mortality, but traditionally little has been done to specifically address this issue. This is because until recently, no reliable and reproducible technique existed to quantify LV mass. We now know that the measurement of LV mass is best accomplished with 3D techniques, and CMR has become the gold standard. 3D echo and EBCT achieve an accuracy and reproducibility close to those of CMR and are acceptable alternatives, but problems preclude their regular use. Now that good data exist in particular for the effectiveness of ACE inhibitors in reducing LV mass,59–61 and the prognostic benefits of LV mass reduction are becoming defined,62–64 coupled with a reproducible and accurate measurement technique in CMR, it is likely that more clinical and research attention will be paid to this condition. The fidelity of the CMR technique may also lead to new understanding of the precise mechanisms behind LVH,65 and why its effects on mortality are so profound, even in the absence of coronary artery disease and hypertension, although recent work implicates plaque disruption as an important issue.66

    The British Heart Foundation provided funding for Dr Myerson (FS 97030). This work was also supported by the Coronary Artery Disease Research Association (CORDA) and the Wellcome Trust.


    Correspondence to Prof Dudley Pennell, Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney St, par London SW3 6NP, United Kingdom. E-mail


    • 1 Levy D, Garrison R, Savage D, Kannel W, Castelli W. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990; 322: 1561–1566.CrossrefMedlineGoogle Scholar
    • 2 Ghali J, Liao Y, Simmons B, Castaner A, Cao G, Cooper R. The prognostic role of left ventricular hypertrophy in patients with or without coronary artery disease. Ann Intern Med. 1992; 117: 831–836.CrossrefMedlineGoogle Scholar
    • 3 Kaplinsky E. Significance of left ventricular hypertrophy in cardiovascular morbidity and mortality. Cardiovasc Drugs Ther. 1994; 8: 549–556.CrossrefMedlineGoogle Scholar
    • 4 Roman M, Pickering T, Schwartz J, Pini R, Devereux R. Association of carotid atherosclerosis and left ventricular hypertrophy. J Am Coll Cardiol. 1995; 25: 83–90.CrossrefMedlineGoogle Scholar
    • 5 Kannel W, Cobb J. Left ventricular hypertrophy and mortality: results from the Framingham Study. Cardiology. 1992; 81: 291–298.CrossrefMedlineGoogle Scholar
    • 6 Riekkinen H, Rautaharju P. Body position, electrode level, and respiration effects on the Frank lead electrocardiogram. Circulation. 1976; 53: 40–45.CrossrefMedlineGoogle Scholar
    • 7 Hoekema R, Uijen G, van Erning L, van Oosterom A. Interindividual variability of multilead electrocardiographic recordings: influence of heart position. J Electrocardiol. 1999; 32: 137–148.CrossrefMedlineGoogle Scholar
    • 8 Sugita S, Takada K, Hayano J. Influence of body composition on electrocardiographic identification of left ventricular hypertrophy in adolescents. Cardiology. 1999; 91: 127–133.CrossrefMedlineGoogle Scholar
    • 9 Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949; 37: 161–186.CrossrefMedlineGoogle Scholar
    • 10 Romhilt D, Estes EJ. A point-score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J. 1968; 75: 752–758.CrossrefMedlineGoogle Scholar
    • 11 Romhilt D, Bove K, Norris R, Conyers E, Conradi S, Rowlands D, Scott R. A critical appraisal of the electrocardiographic criteria for the diagnosis of left ventricular hypertrophy. Circulation. 1969; 40: 185–195.CrossrefMedlineGoogle Scholar
    • 12 Reichek N, Devereux R. Left ventricular hypertrophy: relationship of anatomic, echocardiographic and electrocardiographic findings. Circulation. 1981; 63: 1391–1398.CrossrefMedlineGoogle Scholar
    • 13 Woythaler J, Singer S, Kwan O, Meltzer R, Reubner B, Bommer W, DeMaria A. Accuracy of echocardiography versus electrocardiography in detecting left ventricular hypertrophy: comparison with postmortem mass measurements. J Am Coll Cardiol. 1983; 2: 305–311.CrossrefMedlineGoogle Scholar
    • 14 Massie BM, Tubau JF, Szlachcic J, O’Kelly BF. Hypertensive heart disease: the critical role of left ventricular hypertrophy. J Cardiovasc Pharm. 1989; 13: S18–S24.MedlineGoogle Scholar
    • 15 Wallerson D, Devereux R. Reproducibility of echocardiographic left ventricular measurements. Hypertension. 1987; 9 (suppl II): II-6–II-18.Google Scholar
    • 16 Wong M, Shah P, Taylor R. Reproducibility of left ventricular internal dimensions with M mode echocardiography: effects of heart size, body position and transducer angulation. Am J Cardiol. 1981; 47: 1068–1074.CrossrefMedlineGoogle Scholar
    • 17 Valdez R, Motta J, London E, Martin R, Haskell W, Farquhar J, Popp R, Horlick L. Evaluation of the echocardiogram as an epidemiologic tool in an asymptomatic population. Circulation. 1979; 60: 921–929.CrossrefMedlineGoogle Scholar
    • 18 Gardin J, Arnold A, Gottdiener J, Wong N, Fried L, Klopfenstein H, O’Leary D, Tracy R, Kronmal R. Left ventricular mass in the elderly: The Cardiovascular Health Study. Hypertension. 1997; 29: 1095–1103.CrossrefMedlineGoogle Scholar
    • 19 Devereux R, Casale P, Wallerson D, Kligfield P, Hammond I, Liebson P, Campo E, Alonso D, Laragh J. Cost-effectiveness of echocardiography and electrocardiography for detection of left ventricular hypertrophy in patients with systemic hypertension. Hypertension. 1987; 9 (suppl II): II-69–II-76.LinkGoogle Scholar
    • 20 Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method. Circulation. 1977; 55: 613–619.CrossrefMedlineGoogle Scholar
    • 21 Devereux R, Alonso D, Lutas E, Gottlieb G, Campo E, Sachs I, Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986; 57: 450–458.CrossrefMedlineGoogle Scholar
    • 22 Gopal A, Schnellbaecher M, Shen Z, Akinboboye O, Sapin P, King D. Freehand three-dimensional echocardiography for measurement of left ventricular mass: in vivo anatomic validation using explanted human hearts. J Am Coll Cardiol. 1997; 30: 802–810.CrossrefMedlineGoogle Scholar
    • 23 Reichek N, Helak J, Plappert T, Sutton M, Weber K. Anatomic validation of left ventricular mass estimates from clinical two-dimensional echocardiography: initial results. Circulation. 1983; 67: 348–352.CrossrefMedlineGoogle Scholar
    • 24 Gottdiener J, Livengood S, Meyer P, Chase G. Should echocardiography be performed to assess effects of antihypertensive therapy?: test-retest reliability of echocardiography for measurement of left ventricular mass and function. J Am Coll Cardiol. 1995; 25: 424–430.CrossrefMedlineGoogle Scholar
    • 25 Gosse P, Roudaut R, Dallocchio M. Is echocardiography an adequate method to evaluate left ventricular hypertrophy regression? Eur Heart J. 1990; 11: 107–112.CrossrefMedlineGoogle Scholar
    • 26 Bottini P, Carr A, Prisant L, Flickinger F, Allison J, Gottdiener J. Magnetic resonance imaging compared to echocardiography to assess left ventricular mass in the hypertensive patient. Am J Hypertens. 1995; 8: 221–228.CrossrefMedlineGoogle Scholar
    • 27 Germain P, Roul G, Kastler B, Mossard J, Bareiss P, Sacrez A. Inter-study variability in left ventricular mass measurement: comparison between M-mode echocardiography and MRI. Eur Heart J. 1992; 13: 1011–1019.CrossrefMedlineGoogle Scholar
    • 28 Collins H, Kronenberg M, Byrd B. Reproducibility of left ventricular mass measurements by two-dimensional and M-mode echocardiography. J Am Coll Cardiol. 1989; 14: 672–676.CrossrefMedlineGoogle Scholar
    • 29 Himelman R, Cassidy M, Landzberg J, Schiller N. Reproducibility of quantitative two-dimensional echocardiography. Am Heart J. 1988; 115: 425–431.CrossrefMedlineGoogle Scholar
    • 30 Palmieri V, Dahlof B, DeQuattro V, Sharpe N, Bella J, de Simone G, Paranicas M, Fishman D, Devereux R. Reliability of echocardiographic assessment of left ventricular structure and function: the PRESERVE Study. J Am Coll Cardiol. 1999; 34: 1625–1632.CrossrefMedlineGoogle Scholar
    • 31 Gopal A, Keller A, Shen Z, Sapin P, Schroeder K, King DJ, King D. Three-dimensional echocardiography: in vitro and in vivo validation of left ventricular mass and comparison with conventional echocardiographic methods. J Am Coll Cardiol. 1994; 24: 504–513.CrossrefMedlineGoogle Scholar
    • 32 Nosir Y, Lequin M, Kasprzak J, van Domburg R, Vletter W, Yao J, Stoker J, Ten Cate F, Roelandt J. Measurements and day-to-day variabilities of left ventricular volumes and ejection fraction by three-dimensional echocardiography and comparison with magnetic resonance imaging. Am J Cardiol. 1998; 82: 209–214.CrossrefMedlineGoogle Scholar
    • 33 Altmann K, Shen Z, Boxt L, King D, Gersony W, Allan L, Apfel H. Comparison of three-dimensional echocardiographic assessment of volume, mass and function in children with functionally single left ventricles with two-dimensional echocardiography and magnetic resonance imaging. Am J Cardiol. 1997; 80: 1060–1066.CrossrefMedlineGoogle Scholar
    • 34 Gopal A, Schnellbaecher M, Shen Z, Sciacca R, Keller A, Sapin P, King D. Serial assessment of left ventricular mass regression by 3D echocardiography requires three-fold fewer subjects compared to conventional 1D and 2D echocardiography. J Am Coll Cardiol. 1996; 81: 150A. Abstract.Google Scholar
    • 35 Kuhl H, Bucker A, Franke A, Maul S, Nolte-Ernsting C, Reineke T, Hoffmann R, Gunther R, Hanrath P. Transesophageal 3-dimensional echocardiography: in vivo determination of left ventricular mass in comparison with magnetic resonance imaging. J Am Soc Echocardiogr. 2000; 13: 205–215.CrossrefMedlineGoogle Scholar
    • 36 Feiring A, Rumberger J, Reiter S, Skorton D, Collins S, Lipton M, Higgins C, Ell S, Marcus M. Determination of left ventricular mass in dogs with rapid-acquisition cardiac computed tomographic scanning. Circulation. 1985; 72: 1355–1364.CrossrefMedlineGoogle Scholar
    • 37 Mousseaux E, Beygui F, Fornes P, Chatellier G, Hagege A, Desnos M, Lecomte D, Gaux J. Determination of left ventricular mass with electron beam computed tomography in deformed, hypertrophic human hearts. Eur Heart J. 1994; 15: 832–841.CrossrefMedlineGoogle Scholar
    • 38 Schmermund A, Rensing B, SHeedy P, Rumberger J. Reproducibility of right and left ventricular volume measurements by electron-beam CT in patients with congestive heart failure. Int J Card Imaging. 1998; 14: 201–209.CrossrefMedlineGoogle Scholar
    • 39 Motooka M, Matsuda T, Kida M, Inoue H, Hayashi K, Takahashi T, Sasayama S. Single breath-hold left ventricular volume measurement by 0.3-sec turbo fast low-angle shot MR imaging. Am J Roentgenol. 1999; 172: 1645–1649.CrossrefMedlineGoogle Scholar
    • 40 Katz J, Milliken M, Stray-Gundersen J, Buja L, Parkey R, Mitchell J, Peshock R. Estimation of human myocardial mass with MR imaging. Radiology. 1988; 169: 495–498.CrossrefMedlineGoogle Scholar
    • 41 McDonald K, Parrish T, Wennberg P, Stillman A, Francis G, Cohn J, Hunter D, Rapid, accurate and simultaneous noninvasive assessment of right and left ventricular mass with nuclear magnetic resonance imaging using the snapshot gradient method. J Am Coll Cardiol. 1992; 19: 1601–1607.CrossrefMedlineGoogle Scholar
    • 42 Shapiro E, Rogers W, Beyar R, Soulen R, Zerhouni E, Lima J, Weiss J. Determination of left ventricular mass by magnetic resonance imaging in hearts deformed by acute infarction. Circulation. 1989; 79: 706–711.CrossrefMedlineGoogle Scholar
    • 43 Caputo G, Tscholakoff D, Sechtem U, Higgins C. Measurement of canine left ventricular mass by using MR imaging. Am J Roentgenol. 1987; 148: 33–38.CrossrefMedlineGoogle Scholar
    • 44 Keller A, Peshock R, Malloy C, Buja L, Nunnally R, Parkey R, Willerson J. In vivo measurement of myocardial mass using nuclear magnetic resonance imaging. J Am Coll Cardiol. 1986; 8: 113–117.CrossrefMedlineGoogle Scholar
    • 45 Maddahi J, Crues J, Berman D, Mericle J, Becerra A, Garcia E, Henderson R, Bradley W. Noninvasive quantification of left ventricular myocardial mass by gated proton nuclear magnetic resonance imaging. J Am Coll Cardiol. 1987; 10: 682–692.CrossrefMedlineGoogle Scholar
    • 46 Florentine M, Grosskreutz C, Chang W, Hartnett J, Dunn V, Ehrhardt J, Fleagle S, Collins S, Marcus M, Skorton D. Measurement of left ventricular mass in vivo using gated nuclear magnetic resonance imaging. J Am Coll Cardiol. 1986; 8: 107–112.CrossrefMedlineGoogle Scholar
    • 47 Bellenger NG, Davies LC, Francis JM, Coats ACS, Pennell DJ. Reduction in sample size for studies of remodeling in heart failure by the use of cardiovascular magnetic resonance. J Cardiovasc Magn Reson. 2000; 2: 271–278.CrossrefMedlineGoogle Scholar
    • 48 Grothues F, Smith GS, Bellenger NG, Collins P, Klein H, Pennell DJ. Comparison of interstudy reproducibility of cardiovascular magnetic resonance and 2D-echocardiography in normals, patients with congestive heart failure and in patients with left ventricular hypertrophy. Am J Cardiol. In press.Google Scholar
    • 49 Semelka R, Tomei E, Wagner S, Mayo J, Kondo C, Suzuki J, Caputo G, Higgins C. Normal left ventricular dimensions and function: interstudy reproducibility of measurements with cine MR imaging. Radiology. 1990; 174: 763–768.CrossrefMedlineGoogle Scholar
    • 50 Semelka R, Tomei E, Wagner S, Mayo J, Caputo G, O’Sullivan M, Parmley W, Chatterjee K, Wolfe C, Higgins C. Interstudy reproducibility of dimensional and functional measurements between cine magnetic resonance studies in the morphologically abnormal left ventricle. Am Heart J. 1990; 119: 1367–1373.CrossrefMedlineGoogle Scholar
    • 51 Bogaert J, Bosmans H, Rademakers F, Bellon E, Herregods M, Verschakelen J, Van de Werf F, Marchal G. Left ventricular quantification with breath-hold MR imaging: comparison with echocardiography. MAGMA. 1995; 3: 5–12.CrossrefMedlineGoogle Scholar
    • 52 Matheijssen N, Baur L, Reiber J, van der Velde E, van Dijkman P, van der Geest R, de Roos A, van der Wall E. Assessment of left ventricular volume and mass by cine magnetic resonance imaging in patients with anterior myocardial infarction intra-observer and inter-observer variability on contour detection. Int J Card Imaging. 1996; 12: 11–19.CrossrefMedlineGoogle Scholar
    • 53 Yamaoka O, Yabe T, Okada M, Endoh S, Nakamura Y, Mitsunami K, Kinoshita M, Mori M, Murata K, Morita R. Evaluation of left ventricular mass: comparison of ultrafast computed tomography, magnetic resonance imaging, and contrast left ventriculography. Am Heart J. 1993; 126: 1372–1379.CrossrefMedlineGoogle Scholar
    • 54 Gaudio C, Tanzilli G, Ferri F, Villatico Campbell S, Bertocchi F, Motolese M, Campa P. Benazepril causes in hypertension a greater reduction in left ventricular mass than does nitrendipine: a randomized study using magnetic resonance imaging. J Cardiovasc Pharmacol. 1998; 32: 760–768.CrossrefMedlineGoogle Scholar
    • 55 Johnson D, Foster R, Barilla F, Blackwell G, Roney M, Stanley AJ, Kirk K, Orr R, van der Geest R, Reiber J, Dell’Italia L. Angiotensin-converting enzyme inhibitor therapy affects left ventricular mass in patients with ejection fraction >40% after acute myocardial infarction. J Am Coll Cardiol. 1997; 29: 49–54.CrossrefMedlineGoogle Scholar
    • 56 Myerson SG, Montgomery H, Whittingham M, Jubb M, World M, Humphries S, Pennell DJ. Left ventricular hypertrophy with exercise and the angiotensin converting enzyme gene I/D polymorphism: a randomized controlled trial with losartan. Circulation. 2001; 103: 226–230.CrossrefMedlineGoogle Scholar
    • 57 Francis JM, Pennell DJ. The treatment of claustrophobia during cardiovascular magnetic resonance: use and effectiveness of mild sedation. J Cardiovasc Magn Reson. 2000; 2: 139–141.CrossrefMedlineGoogle Scholar
    • 58 Bellenger N, Gatehouse P, Rajappan K, Keegan J, Firmin D, Pennell D. Left ventricular quantification in heart failure by cardiovascular MR using prospective respiratory navigator gating: comparison with breath-hold acquisition. J Magn Reson Imaging. 2000; 11: 411–417.CrossrefMedlineGoogle Scholar
    • 59 Roman M, Alderman M, Pickering T, Pini R, Keating J, Sealey J, Devereux R. Differential effects of angiotensin converting enzyme inhibition and diuretic therapy on reductions in ambulatory blood pressure, left ventricular mass, and vascular hypertrophy. Am J Hypertens. 1998; 11: 387–396.CrossrefMedlineGoogle Scholar
    • 60 Dahlof B, Pennert K, Hansson L. Reversal of left ventricular hypertrophy in hypertensive patients: a metaanalysis of 109 treatment studies. Am J Hypertens. 1992; 5: 95–110.CrossrefMedlineGoogle Scholar
    • 61 Lievre M, Gueret P, Gayet C, Roudaut R, Haugh MC, Delair S, Boissel JP. Ramipril-induced regression of left ventricular hypertrophy in treated hypertensive individuals. Hypertension. 1995; 25: 92–97.CrossrefMedlineGoogle Scholar
    • 62 Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Gattobigio R, Zampi I, Reboldi G, Porcellati C. Prognostic significance of changes in left ventricular mass in essential hypertension. Circulation. 1998; 97: 48–54.CrossrefMedlineGoogle Scholar
    • 63 Levy D, Salomon M, D’Agostino R, Belanger A, Kannel W. Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy. Circulation. 1994; 90: 1786–1793.CrossrefMedlineGoogle Scholar
    • 64 Mathew J, Sleight P, Lonn E, Johnstone D, Pogue J, Yi Q, Bosch J, Sussex B, Probstfield J, Yusuf S for the Heart Outcomes Prevention Evaluation (HOPE) Investigators: reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin-converting enzyme inhibitor Ramipril. Circulation. 2001; 104: 1615–1621.CrossrefMedlineGoogle Scholar
    • 65 Brull D, Dhamrait S, Woods D, Myerson S, Pennell DJ, World M, Humphries S, Regitz-Zagrosek V, Montgomery H. The bradykinin B2 receptor and the human left ventricular growth response. Lancet. 2001; 358: 1155–1156.CrossrefMedlineGoogle Scholar
    • 66 Heidland UE, Strauer BE. Left ventricular muscle mass and elevated heart rate are associated with coronary plaque disruption. Circulation. 2001; 104: 1477–1482.CrossrefMedlineGoogle Scholar


    eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.

    Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.