Determinants and prediction of transmural myocardial perfusion.

Abstract

The vulnerability of subendocardial muscle to ischemic damage is due primarily to the risk of underperfusion. Recent studies of coronary autoregulation showed that as myocardial O2 needs increase beyond the ability of coronary blood flow to supply O2, maximal vasodilatation occurs earliest in subendocardial vessels; any further imbalance then causes subendocardial ischemia, since no further compensatory vasodilatation is possible. In animal experiments, relative subendocarial perfusion (the ratio of flow per gram in subendocardial to subepicardial muscle) can be predicted from the DPTI:SPTI ratio of 2 pressure-time areas, where DPTI = the area between coronary and left ventricular pressures in diastole and SPTI = the area beneath the left ventricular systolic pressure. Early studies demonstrated subendocardial underperfusion when DPTI:SPTI was < 0.7, but more recent studies show that this ratio is about 0.4. Applying the results of animal studies to man must be done cautiously. Peak ventricular systolic pressure is better than SPTI in predicting myocardial O2 needs, but neither measure allows for changes in wall tension or contractility. Increased coronary vascular resistance at maximal vasodilatation results in subendocardial underperfusion at DPTI:SPTI ratios above 0.4; these resistances increase with myocardial edema, hypertrophy, coronary vessel disease or increased blood viscosity. DPTI probably overestimates the actual mean pressure drop across the coronary vascular bed, because in diastole intramyocardial tissue pressures may be 20-30 mm Hg.