Coronary pressure-flow relation in left ventricular hypertrophy: Importance of changes in back pressure versus changes in minimum resistance

Perfusion abnormalities in the pressure-overloaded hypertrophied left ventricle could result from an increase in minimum coronary resistance or an increase in effective back pressure due to increased extravascular compressive forces. Since the pressure-flow relation of the maximally vasodilated coronary bed allows dissociation of minimum resistance (inverse slope [1/αPF]) and back pressure (pressure at zero flow [P(f=0)]), the present study was undertaken to examine the coronary pressure-flow relation in left ventricular hypertrophy (LVH). Ascending aortic banding in eight dogs at 6-8 weeks of age (LVH group) increased the left ventricular to body weight ratio to 8.7±0.6 g/kg as compared with 4.8±0.2 g/kg in nine normal dogs (p<0.05). Maximum coronary vasodilation was produced by infusion of adenosine (1 mg/kg per minute i.v.). The slope of the coronary pressure-flow relation (αPF) was 5.8±0.5 10^-2 (ml/min per gram)/mm Hg in the LVH group and 9.3±0.6 10^-2 (ml/min per gram)/mm Hg in the normal group (p<0.05). αPF was significantly correlated with the left ventricular to body weight ratio but not with coronary pressure, suggesting that the degree of hypertrophy and not exposure to high coronary pressure was responsible for the observed decrease in αPF. P(f=0) was 24.1±2.6 mm Hg in the LVH group and 11.7±1.2 mm Hg in the normal group (p<0.05). To determine the contribution of the higher left ventricular late-diastolic pressure in the LVH group (13.9±2.2 mm Hg) compared with that in the normal group (6.1±0.7 mm Hg, p<0.01), we infused blood into seven normal dogs until left ventricular diastolic pressure (16.3±1.2 mm Hg) was similar to that in the LVH group. With the higher left ventricular diastolic pressure, P(f=0) increased (22.6±1.8 mm Hg) to levels not significantly different from those in the LVH dogs, suggesting that increased extravascular compressive forces are primarily due to elevated left ventricular intracavitary pressure. Stepwise regression analysis revealed that both left ventricular late-diastolic pressure and the degree of hypertrophy exerted significant independent effects on P(f=0). These findings demonstrate both an increase in minimum coronary resistance and an increase in effective back pressure in the pressure-overloaded severely hypertrophied left ventricle. The increase in minimum coronary vascular resistance is related to the degree of hypertrophy, whereas the increase in effective back pressure results principally from the elevated left ventricular diastolic pressure.