Relative Left Ventricular Mass Research Articles

Following infarction, the relationship of left ventricular mass to ejection fraction is determined by infarct location

Following infarction, the relationship of left ventricular mass to ejection fraction is determined by infarct location

Relation of left ventricular hemodynamic load and contractile performance to left ventricular mass in hypertension.

The weak relation of systolic blood pressure to left ventricular mass in hypertensive patients is often interpreted as evidence of nonhemodynamic stimuli to muscle growth. To test the hypothesis that left ventricular chamber size, reflecting hemodynamic volume load and myocardial contractility, influences the development of left ventricular hypertrophy in hypertension, we studied actual and theoretic relations of left ventricular mass to left ventricular diastolic chamber volume, pressure and volume load, and an index of contractility. Data were obtained from independently measured M-mode and two-dimensional echocardiograms in 50 normal subjects and 50 untreated patients with essential hypertension. Two indices of overall left ventricular load were assessed: total load (systolic blood pressure x left ventricular endocardial surface area) and peak meridional force (systolic blood pressure x left ventricular cross sectional area). A theoretically optimal left ventricular mass, allowing each subject to achieve mean normal peak stress, was calculated as a function of systolic blood pressure and M-mode left ventricular end-diastolic diameter. Left ventricular mass measured by M-mode echo correlated better with two-dimensional echocardiogram derived left ventricular end-diastolic volume (r = 0.56, p less than 0.001) than with systolic blood pressure (r = 0.45, p less than 0.001) and best with total load or peak meridional force (r = 0.68 and 0.70, p less than 0.001). In multivariate analysis both end-diastolic volume and blood pressure were independent predictors of systolic mass (p less than 0.001) and explained most of its variability (R = 0.75, p less than 0.001). Theoretically optimal left ventricular mass was more closely related to end-diastolic volume (r = 0.72, p less than 0.001) than to systolic blood pressure (r = 0.46, p less than 0.001); thus, the relatively weak correlation between blood pressure and optimal mass reflected the influence of left ventricular cavity size, rather than a lack of proportionality between load and hypertrophy. Actual and theoretically optimal left ventricular mass were closely related (r = 0.76, p less than 0.001), indicating that left ventricular hypertrophy in most cases paralleled hemodynamic load. Left ventricular mass was positively related to stroke index and inversely to contractility (as estimated by the end-systolic stress/volume index ratio), the main determinants of left ventricular chamber volume. In multivariate analysis, systolic blood pressure, stroke index, and the end-systolic stress/volume index ratio were each independently related to left ventricular mass index (all p less than 0.001, multiple R = 0.81) and accounted for 66% of its overall variability.(ABSTRACT TRUNCATED AT 400 WORDS)

Relationship of left ventricular mass to defibrillation threshold for the implantable defibrillator: A combined clinical and animal study

Defibrillation results when a critical mass of myocardium is depolarized. The relationship between echocardiographic determinations of left ventricular mass, volume, and cavity radius to wall thickness ratio and defibrillation threshold for the implantable defibrillator was examined. Ten patients with two large patch defibrillating lead systems were studied. Defibrillation threshold was determined intraoperatively as the lowest energy terminating ventricular fibrillation. Left ventricular mass, volume, and radius/posterior wall thickness ratio were calculated from two-dimensional echocardiograms. A significant correlation was found between left ventricular mass and defibrillation threshold (r = 0.78, p < 0.01). The correlations between defibrillation threshold and left ventricular volume (r = 0.59) and radius/wall thickness ratio (r = 0.55) were not significant. Subsequently, 11 dogs undergoing defibrillation trials with a transvenous catheter and a chest wall patch were studied. Defibrillation threshoid was defined as the lowest energy-terminating ventricular fibrillation (four separate attempts). Subsequently, the heart was dissected, and the left ventricle (including the septum) was weighed. The correlation between left ventricular weight and defibrillation threshold (r = 0.76) was significant ( p < 0.01). We conclude that noninvasive assessment of left ventricular mass and direct measurement of left ventricular weight are significantly correlated with defibrillation threshold and consistent with the critical mass hypothesis.

Relation of left ventricular mass to geometry of the proximal coronary arteries in the dog

Proximal epicardial coronary artery luminal diameters were measured from silicone casts formed in situ in freshly excised hearts under a constant pressure of 100 mm Hg. Twenty-five coronary arteries from 15 normal dogs and 22 coronary arteries in 13 dogs with either chronic pressure or volume overload hypertrophy were studied. Mean left ventricular (LV) body weight ratios were 4.75 ± 1.01 g/kg in the normal dogs, 8.4 ± 1.7 g/kg in the pressure-overload dogs, and 6.2 ± 0.6 g/kg in the volume-overload dogs. The cross-sectional area of the left circumflex (LC) coronary artery was determined at 11 branch sites. The ratio of the area of the branches to the area of the parent vessel was 1.095 ± 0.105, indicating that the cross-sectional area after a branch point increased. A poor correlation existed between LV mass and coronary artery diameter in both normal and hypertrophy groups for the LC (r = 0.44), the left anterior descending (LAD) (r = 0.63), and the combined LC and LAD (r = 0.52). The mean cross-sectional area of the combined LC and LAD was 0.12 cm 2 in the normal group and 0.15 cm 2 in the hypertrophy group; this increase was not statistically significant (p = 0.13). When the mean cross-sectional area of the combined vessels was adjusted for heart weight, there was a decrease in the cross-sectional area/100 g of myocardium in the hypertrophy group compared with the control group. These data demonstrate that coronary artery luminal diameter in the dog does not increase commensurately with the increase in mass associated with myocardial hypertrophy.

Effect of heart rate on myocardial blood flow in dogs with left ventricular hypertrophy

Because of the previous suggestion that subendocardial perfusion may be inadequate in the hypertrophied heart, this study was carried out to examine the response of transmural myocardial blood flow to pacing induced tachycardia in dogs with chronic left ventricular hypertrophy. Myocardial hypertrophy, produced by banding the ascending aorta of puppies at 5-6 wk of age, resulted in an 87% average increase in relative left ventricular mass compared with the control dogs. Myocardial blood flow was examined during ventricular pacing at heart rates of 100, 200, and 250 beats/min using radionuclide-labeled microspheres. Mean blood flow per unit myocardial mass was similar in the two groups of dogs at a heart rate of 100 beats/min and increased regularly during pacing in both groups of animals. Increasing heart rates did not change the transmural pattern of myocardial blood flow in the normal dogs, but in the animals with left ventricular hypertrophy pacing at 250 beats/min resulted in a significant redistribution of perfusion away from the subendocardium, with the ratio of subendocardial/subepicardial blood flow falling from 1.03 +/- 0.08 at 100 beats/min to 0.83 +/0 0.06 at 250 beats/min (P < 0.01). This redistribution of blood flow away from the subendocardium was especially marked in the regions encompassing the papillary muscles and the intervening left ventricular lateral wall.