Fractional contributions of the right and left coronary arteries to perfusion of normal and hypertrophied right ventricles of conscious dogs.

Abstract

SUMMARY The extent to which the blood supply of normal and hypertrophied right ventricles originates from the right and left coronary arteries was investigated in conscious dogs. Right ventricular (RV) hypertrophy, induced by gradual, chronic (4-6 months) stenosis of the main pulmonary artery, was characterized by a 72% increase (P < 0.001) in RV weight to body weight ratio and a 106% increase (P < 0.001) in total RV transmural blood flow per gram (radioactive microsphere technique). In normal dogs, left main coronary artery occlusion (CAO) reduced blood flow only slightly to the central core of the RV free wall, but markedly (P < 0.001) to the peripheral zones. Right main CAO reduced blood flow in both RV central and peripheral zones to similar absolute levels in both normal animals and dogs with RV hypertrophy. Keeping in mind that pre-CAO control levels were greater in the presence of hypertrophy, the magnitude of the reduction in blood flow was significantly greater (P < 0.01) with right CAO in dogs with hypertrophy. Endocardial-epicardial perfusion ratios of both RV central and peripheral zones were significantly reduced (P < 0.02) both at rest and during right CAO in dogs with RV hypertrophy as compared to normal dogs with matched heart rates. These data indicate that the left coronary artery usually supplies a substantial fraction (~37%) of total RV free wall perfusion in normal, conscious dogs. Moreover, it is seen that the marked, selective increases in transmural RV blood flow in RV hypertrophy are provided by the right but not the left coronary artery. Circ Res 47:190-200, 1980 NUMEROUS investigations have examined the coronary circulation in normal and hypertrophied left ventricles. Although right ventricular hypertrophy is not encountered in patients as frequently as is left ventricular hypertrophy, it remains an important clinical entity, e.g., in patients with acquired pulmonary hypertension from a variety of etiolo