title: Comparison of hearts with 2 types of pressure-overload left ventricular hypertrophy.
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 ((31)P 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 (31)P 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.
authors.affiliation: Cardiac Muscle Research Laboratory, Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118, USA. ksaupe@aol.com
authors.forename: K W
authors.initials: KW
authors.lastname: Saupe
authors.forename: C C
authors.initials: CC
authors.lastname: Lim
authors.forename: J S
authors.initials: JS
authors.lastname: Ingwall
authors.forename: C S
authors.initials: CS
authors.lastname: Apstein
authors.forename: F R
authors.initials: FR
authors.lastname: Eberli
mesh_terms: D000818:Animals; D001024:Aortic Valve Stenosis / Q000473:pathology / Q000503:physiopathology*; D001794:Blood Pressure; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology*; D009200:Myocardial Contraction; D051381:Rats