LOAD DEPENDENCE OF LEFT-VENTRICULAR DIASTOLIC PRESSURE-VOLUME RELATIONS DURING SHORT-TERM CORONARY-ARTERY OCCLUSION

We evaluated the effect of altered loading conditions on left ventricular (LV) diastolic pressure-volume relations during acute coronary artery occlusion that was produced by inflation of an intracoronary balloon. Open-chest anesthetized dogs (n = 18) were instrumented so the LV pressure (micromanometer =) and LV volume (conductance) could be measured without disturbing the pericardium. The effects of brief periods of occlusion (1-2 minutes) were assessed under steady-state conditions before and after dextran infusion with the pericardium present and absent and during vena caval occlusion. Under steady-state conditions before dextran infusion with the pericardium removed, at an LV end-diastolic pressure (EDP) of 8.4 +/- 1.4 mm Hg, occlusion resulted in a rightward shift in the diastolic portion of the LV pressure-volume loop (DELTA-LVEDP, 2.7 +/- 2.3 mm Hg; DELTA-LVEDV, 6.3 +/- 4.7 ml, both p < 0.05 versus control). After dextran infusion (LVEDP, 20.9 +/- 6.0 mm Hg), occlusion resulted in a rightward and upward shift in the diastolic portion of the LV pressure-volume loop (DELTA-LVEDP, 5.8 +/- 4.4 mm Hg; DELTA-LVEDV, 4.2 +/- 3.0 ml, both p < 0.05 versus control). At low cardiac volumes before dextran infusion, the intact pericardium did not affect the response to occlusion. By contrast, after dextran infusion in the presence of an intact pericardium, LVEDP significantly increased (DELTA, 6.4 +/- 3.6 mm Hg, p < 0.05) but LVDEV did not (DELTA, 0.7 +/- 1.5 ml, p = NS). There was a parallel upward shift in the diastolic portion of the LV pressure-volume loop that was eliminated by removal of the pericardium. Thus, the change in LV diastolic pressure and volume during occlusion varied and depended on the baseline cardiac volume and presence of the pericardium. Before dextran infusion with the pericardium present and absent, coronary artery occlusion did not alter the LV diastolic chamber stiffness parameter, which was calculated from the diastolic interval of an averaged steady-state beat (.040 +/- 0.019 versus 0.036 +/- 0.015 mm Hg/ml, p = NS). After dextran infusion with the pericardium present and absent, coronary artery occlusion increased the LV diastolic chamber stiffness parameter (0.057 +/- 0.034 and 0.074 +/- 0.034 mm Hg/ml, both p < 0.05 versus controls, respectively). Vena caval occlusion eliminated the shifts in the diastolic portion of the LV pressure-volume loop with the pericardium present and absent. In addition, the LV end-diastolic pressure-volume relation obtained by vena caval occlusion during occlusion with the pericardium present and absent was similar to that of the nonischemic LV. Thus, these data indicate that right ventricular and pericardial influences are responsible, in large part, for the shifts observed in the LV diastolic pressure-volume relations during acute coronary artery occlusion. In conclusion, the shift in position of the diastolic portion of the LV pressure-volume loop during coronary artery occlusion varies and is modulated by both the volume status of the LV and the pericardium. Despite these varying responses, the LV diastolic pressure-volume relations before and during acute coronary artery occlusion are similar when examined throughout the same LV pressure-volume range.