EFFECTS OF CARDIAC CONTRACTION AND CAVITY PRESSURE ON MYOCARDIAL BLOOD-FLOW

Regional impairment of cardiac contraction uncouples force generation from left ventricular pressure (LVP) and may alter the determinants of the phasic pattern and transmural distribution of coronary flow. In anesthetized, open-chest dogs with maximal coronary vasodilation, we studied the effects of abolishing local contraction and changing cavity pressure on phasic myocardial inflow and net transmural flow in a region of left ventricular free wall. With contraction present, the normalized amplitude of distal phasic coronary velocity (NAmp) was not significantly different at normal vs. low LVP (1.00 vs. 0.92 +/- 0.09, respectively, P = NS). With regional contraction abolished by subselective intracoronary lidocaine, however, NAmp varied with LVP (1.62 +/- 0.25 at normal LVP, 0.85 +/- 0.22 at low LVP, P < 0.0001). With contraction present, inner-to-outer flow ratio was not consistently different at normal vs. low LVP (0.47 +/- 0.15 vs. 0.64 +/- 0.28, respectively, P = NS) but was consistently higher at low than at normal LVP with contraction absent (1.01 +/- 0.30 vs. 1.84 +/- 0.38, respectively, P < 0.0001). During uniform global function, contraction is the main determinant of phasic amplitude and transmural distribution of myocardial flow. When regional contraction is abolished, allowing passive deformation of the wall during systole, LVP assumes a powerful role.