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(Hypertension. 2000;35:1167.)
© 2000 American Heart Association, Inc.

Scientific Contributions

Comparison of Hearts With 2 Types of Pressure-Overload Left Ventricular Hypertrophy

Kurt W. Saupe; Chee Chew Lim; Joanne S. Ingwall; Carl S. Apstein; Franz R. Eberli

From the Cardiac Muscle Research Laboratory (K.W.S., C.C.L., C.S.A.), Whitaker Cardiovascular Institute, Boston University School of Medicine, Mass; NMR Laboratory for Physiological Chemistry (J.S.I.), Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass; and the Swiss Cardiovascular Center (F.R.E.), Bern University Hospital, Bern, Switzerland.

Correspondence to Dr Kurt Saupe, Cardiac Muscle Research Laboratory, 650 Albany St, X720, Boston, MA 02118. E-mail ksaupe{at}aol.com

Abstract—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 (³¹P 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 ³¹P 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 (r²=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.

Key Words: hypertrophy, left ventricular • hypertension, essential • stenosis aortic • ischemia • metabolism

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