Because the myocardium is perfused primarily during diastole, changes in diastolic properties of the left ventricle (LV) should influence the intramyocardial circulation.Methods and Results.
We examined the influence of LV diastolic properties on the magnitude and localization of intramyocardial coronary capacitance by analyzing the coronary pressure-venous flow relation in isolated, isovolumic dog heart preparations. After sudden occlusion of the left coronary artery during a long diastole, we measured precapacitance and postcapacitance resistances (RPRE and RPOST) and calculated intramyocardial coronary capacitance (CIM) from RPOST and the time constant of the coronary venous flow decay. Using this method, we characterized the effects of coronary vasodilation, LV diastolic volume, and LV diastolic chamber stiffness on the coronary circulation. The magnitude of CIM increased from 0.09±0.01 to 0.24±0.20 mL · mm Hg−1 · 100 g−1 (P<.01) after adenosine-induced vasodilation, whereas both RPOST and RPRE decreased significantly. The ratio of RPOST to RPRE+RPOST decreased from 0.35±0.02 to 0.23±0.02 (P<.01), suggesting redistribution of CIM to the distal portion of the coronary vascular tree. An increase in LV volume and wall stress was imposed to increase LV diastolic pressure from 2±0.1 to 25±1 mm Hg: this increased RPOST significantly but not RPRE and decreased the magnitude of CIM. The resistance ratio did not change significantly. Increased LV diastolic chamber stiffness induced by hypoxic perfusion (isovolumic LV diastolic pressure increased from 11±1 to 28±1 mm Hg) raised RPOST and decreased the magnitude of CIM from 0.32±0.12 to 0.17±0.04 mL · mm Hg−1 · 100 g−1 (P<.05). The resistance ratio increased significantly from 0.21±0.05 to 0.33±0.05 with increased LV diastolic chamber stiffness. Adjustment of LV diastolic volume to lower diastolic pressure to 10±1 mm Hg did not alter these changes significantly, suggesting that an intrinsic increase in myocardial stiffness played a major role in these changes.Conclusions.
Extravascular compression by raised LV diastolic volume and/or increased LV diastolic chamber stiffness acted mainly on coronary vessels that determine intramyocardial capacitance and postcapacitance resistance. (Circulation.1993;88:2929–2940.)