It is frequently stated that hypertrophied ventricles tolerate
ischemia less well than nonhypertrophied ventricles. The authors' earlier studies in a rat
supravalvular aortic stenosis model and canine valvular
aortic stenosis model, both with concentric
left ventricular hypertrophy, disclosed accelerated rates of
ischemic contracture and diminished basal myocardial high energy
phosphate stores. These studies have been extended to ten patients with severe
left ventricular hypertrophy caused by valvular
aortic stenosis and normal coronary arteries.
ATP (endocardial and epicardial) from transmural left ventricular biopsies taken at operation before aorta cross-clamping, and frozen immediately in liquid
nitrogen, were compared with similar biopsies from patients with nonhypertrophied myocardium supplied by normal coronary arteries. The subendocardial high energy
phosphate levels in the nonhypertrophied myocardium was greater than high energy
phosphate levels in the subepicardium of nonhypertrophied ventricles (
ATP-micromoles/gram-
protein, epi = 36.8 +/- 3.3, endo = 37.7 +/- 3.3) (p = NS). However, in the hypertrophied myocardium the subendocardium consistently showed significantly depressed high-energy
phosphate levels when compared with subepicardial levels (
ATP-hypertrophied myocardium, epi = 31.5 +/- 1.6, endo = 25.9 +/- 1.7) (p less than 0.05). This uniform depression of
ATP stores, greatest in the subendocardium, in
left ventricular hypertrophy suggests a common
biologic mechanism for the enhanced sensitivity to
ischemia. Of importance for patients may be the prior observation in rats that repletion of
ATP( stores before
ischemia eliminates the accelerated rate to
ischemic contracture. Diminished subendocardial
ATP stores appear to be an intrinsic property of severely hypertrophied myocardium and probably contribute to its enhanced sensitivity to
ischemia.