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

被引:18
作者
Saupe, KW
Lim, CC
Ingwall, JS
Apstein, CS
Eberli, FR
机构
[1] Boston Univ, Sch Med, Cardiac Muscle Res Lab, Whitaker Cardiovasc Inst, Boston, MA 02118 USA
[2] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, NMR Lab Physiol Chem, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Boston, MA USA
[4] Univ Hosp Bern, Swiss Cardiovasc Ctr, CH-3010 Bern, Switzerland
关键词
hypertrophy; left ventricular; hypertension; essential; stenosis aortic; ischemia; metabolism;
D O I
10.1161/01.HYP.35.5.1167
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Comparisons of myocardium remodeled by the 2 most common causes of left ventricular hypertrophy (LVH), hypertension and aortic constriction, are limited. 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 or 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 ischemia, 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 P-i resonance in the P-31 nuclear magnetic resonance spectrum, whose position indicates myocardial pH, split into 2 peaks during low-flow ischemia, which indicates distinct regions of pH 6.9 (moderate acidosis) and pH 6.2 (severe acidosis), Concentrations of ATP, PCr, P-i, and H+ of the moderately acidotic 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 degree of LV stiffening. We conclude that in Dahl rats, LVH secondary to hypertension protects against ischemia-induced diastolic dysfunction by minimizing the size of the region of severe acidosis.
引用
收藏
页码:1167 / 1172
页数:6
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