Coronary blood flow in experimental canine left ventricular hypertrophy.

Abstract

With maximal coronary vasodilation due to adenosine or carbochrome, mean coronary vascular resistance was 84% higher in LVH than in normal hearts; with isoproterenol, resistance was 54% higher in LVH. These changes were similar in right and left ventricles. Minimal coronary resistance at end diastole also was higher in LVH-64% and 94% for the two sets of vasodilators, respectively. There were no significant differences in capillary or large vessel proportional volumes in LVH and control dogs, but arterial capacity could not be estimated. The raised minimal coronary resistance suggests the possibility that, with stress, coronary flow, especially to subendocardial muscle, might be inappropriate and perhaps cause ischemic damage. However, the changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself.LEFT ventricular hypertrophy (LVH) may impair cardiac function but the mechanisms for this change are not clear. Hypertrophy alters excitation-contraction coupling, energy utilization, and contractile proteins, 1 but it is not known whether these changes are primary or secondary to other mechanisms. One of those other mechanisms, myocardial ischemia, could occur in two ways: Roberts and Wearn 2 showed that in rabbits with left ventricular Original manuscript received February 28, 1977; accepted for publication March 7, 1978. hypertrophy the capillary-fiber ratio remained at its normal value of 1:1 so that the mean diffusion distance must have increased; these findings have been confirmed in man. 3 ' 4 Then Linzbach 3 and Woods 5 reported that, although the main coronary arteries increased in diameter in people with LVH, this increase in diameter did not match the increased heart weight. They therefore inferred that in hypertrophy there might be a reduced coronary vascular reserve that might impair cardiac function. However, no one has shown that the increased diffusion distance for oxygen does impair cardiac function nor that coronary vascular reserve is reduced in hypertrophy.We wished to test another hypothesis that involves myocardial blood flow, one which also fits in with the known vulnerability of the subendocardial muscle to is-

Effects of exerimental right ventricular hypertrophy on myocardial blood flow in conscious dogs.

“…Indeed, Dowell (24) has reported that left ventricular hypertrophy induced by aortic stenosis is associated with a decrease in the vascular denisty of the left ventricular myocardium. Further support for this hypothesis comes from a recent study by O'Keefe et al (5), which reports that moderate left ventricular hypertrophy induced by aortic stenosis is associated with a thickening of the vascular wall of coronary vessels that supply the hypertrophied ventricle. Whereas a reduction in vascular density could act to limit compensatory vasodilation with the development of left ventricular hypertrophy, the increases in right ventricular blood flow observed in this study appear not to be the result of an increase in vascular density of the hypertrophied right ventricle because the capillary:muscle fiber number ratio was unchanged after 4-5 mo of pressure overload.…”

Mean transit time for the assessment of myocardial perfusion by videodensitometry.

“…Inverse appearance time (l/Tapp), Dmax, DmaxlTapp, inverse time of maximal intensity (1I/T), and 1fTmn were calculated and the relations of these parameters to measured flow were investigated. Tm0 proved to be the most reliable parameter for this purpose (r=0.97+0.02; mean± SD), followed by Tmax [26][27][28][29][30][31][32][33][34][35][36] kg) were anesthetized with sodium pentobarbital 25 mg/kg i.v., a left thoracotomy was performed, and epicardial pacing electrodes were sutured on the left atrium. The proximal part of the left circumflex artery (LCx) was gently dissected free, over a distance of 1.0-1.5 cm proximal of the origin of the first large obtuse marginal branch.…”

Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries.

“…A variety of possible causes have been suggested: a reduction in coronary reserve, an occlusive disease of small coronary arteries not visualized by coronary arteriography, an inadequate growth of the coronary microvasculature, or an augmentation of the extravascular component of coronary resistance. [5][6][7][8][9][10][11][12][13] To further evaluate hypertensive patients with angina but with normal coronary arteriograms, the following studies were performed in addition to left ventricular and coronary angiography: (1) coronary blood flow (CBF) was measured at rest and during dipyridamoleinduced coronary vasodilation and (2) biopsy specimens were taken from left ventricular myocardium for microscopic evaluation of intramyocardial vessels and of the myocardial cells.…”