Comparison of hearts with 2 types of pressure-overload left ventricular hypertrophy

Comparisons of myocardium remodeled by the 2 most common causes of left ven tricular hypertrophy (LVH), hypertension and aortic constriction, are limit ed. We hypothesized that important differences may exist in the myocardium of hearts with these 2 origins of "pressure overload" LVH. Accordingly, we studied isolated hearts from 3 groups of Dahl salt-sensitive rats, controls , and hearts with matched amounts of LVH secondary to either hypertension o r aortic constriction. Isovolumic LV function and myocardial energetics (P- 31 nuclear magnetic resonance spectroscopy) were measured as coronary flow was lowered to 16% of baseline for 48 minutes. During this low-flow ischemi a, isovolumic end-diastolic pressure, a measure of LV stiffness, increased to 52+/-4 mm Hg in controls and 51+/-6 mm Hg in aortic banded hearts but to only 35+/-5 mm Hg in hearts with hypertensive LVH. In all hearts, the Pi r esonance in the 31P nuclear magnetic resonance spectrum, whose position ind icates myocardial pH, split into 2 peaks during low-flow ischemia, which in dicates distinct regions of pH 6.9 (moderate acidosis) and pH 6.2 (severe a cidosis), Concentrations of ATP, PCr, P-i, and H+ of the moderately acidoti c region were not different among groups. However, the size of the severely acidotic region was smallest in the hypertensive LVH hearts, and in all 3 groups, the size of this region correlated (r(2)=0.65 to 0.80) with the deg ree of LV stiffening. We conclude that in Dahl rats, LVH secondary to hyper tension protects against ischemia-induced diastolic dysfunction by minimizi ng the size of the region of severe acidosis.