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Effect of Renal Hypertension and Left Ventricular Hypertrophy on the Coronary Circulation in Dogs
Journal article   Open access   Peer reviewed

Effect of Renal Hypertension and Left Ventricular Hypertrophy on the Coronary Circulation in Dogs

THOMAS MUELLER, MELVIN MARCUS, RICHARD KERBER, JOHN YOUNG, ROBERT BARNES and FRANCOIS ABBOUD
Circulation research, Vol.42(4), pp.543-549
04/1978
DOI: 10.1161/01.RES.42.4.543
PMID: 147145
url
https://doi.org/10.1161/01.RES.42.4.543View
Published (Version of record) Open Access

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 μM/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 groupsthe 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.

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