Effect of renal hypertension and left ventricular hypertrophy on the coronary circulation in dogs.

Abstract

The purpose of this study was to investigate the effects of pressure-induced left ventricular hypertrophy on the coronary circulation.Hypertrophy was induced by single-kidney renal vascular hypertension in 12 dogs.Ventricular mass in the dogs with hypertrophy was about 50% greater than in 11 controls.A third group of six dogs, with a similar amount of left ventricular hypertrophy but normal blood pressure after repair of the renal artery stenosis, also was studied.Total and regional myocardial blood flow was measured with radioactive microspheres at rest, during pacing at a rate of 200 (in the control and hypertensive dogs), and during maximal vasodilation induced with adenosine (4.7 juM/kg x min).Results were as follows.(1) Regional distribution of coronary flow was normal at rest in dogs with hypertension and left ventricular hypertrophy and in dogs with hypertrophy alone.(2) Pacing caused at 16% decrease in the endocardial-epicardial perfusion ratio only in the hypertrophied ventricles of the hypertensive dogs.(3) During maximal coronary vasodilation, the coronary vascular resistance of the entire left ventricle was no different among the three groups: the controls, the hypertensive dogs with left ventricular hypertrophy, and the normotensive dogs with left ventricular hypertrophy (0.14 ± 0.02 SEM, 0.16 ± 0.02, and 0.14 ± 0.02 mm Hg/ml x min, respectively).The use of the minimal coronary vascular resistance measured during maximal vasodilation as an index of the functional cross-sectional area of the coronary bed suggests that the cross-sectional area does not increase with hypertrophy.This failure of the cross-sectional area of the coronary bed to increase commensurate with the degree of hypertrophy is due to an anatomical or architectural alteration of the relationship between the coronary bed and the cardiac muscle and is not due to a functional alteration caused by hypertension alone.Thus, the hypertrophied ventricle may be at greater risk of ischemic injury.CLINICAL SUSPICION of inadequate myocardial perfusion due to pressure-induced hypertrophy of the left ventricle has existed for many years.'"4 Although several investigators have found that blood flow per unit mass of the myocardium of hypertrophied ventricles is normal, 5 " 8 the decreases in capillary density described in hypertrophied myocardium 9 ''" and preliminary reports suggesting relative endocardial hypoperfusion"' 12 imply that the regional distribution of coronary flow may be abnormal in hypertrophied ventricles and that such ventricles might be at increased risk for ischemic injury.To study possible physiological limitations of the coronary circulation in pressure-induced hypertrophy, we produced single-kidney renal vascular hypertension in mongrel dogs.After left ventricular hypertrophy developed, we assessed regional myocardial perfusion at rest, during pacing, and during maximal vasodilation produced by an iv adenosine infusion.We also studied another group of dogs at rest and during adenosine infusion which had ventricular hypertrophy induced in the same manner but were rendered normotensive by repair of the renal artery stenosis.In this manner we were able to isolate the effects of hypertrophy