Left ventricular contractility predicts how the end-diastolic pressure-volume relation shifts during pacing-induced ischemia in dogs.

Abstract

Two types of ischemia, pacing-induced and coronary occlusion-induced, have different effects on left ventricular diastolic properties. During pacing-induced ischemia, the diastolic pressure-volume relation is said to shift upward, whereas during coronary occlusion, it is said to shift rightward or downward. However, recent studies have shown that the relation can shift in any direction during both types of ischemia. The purpose of this study was to identify determinants of the shift of the end-diastolic pressure-volume relation (EDPVR) during pacing-induced ischemia. We retrospectively analyzed 46 pacing-induced ischemia experiments performed in 15 open-pericardium anesthetized dogs. Pacing ischemia was induced by constricting left anterior descending and left circumflex coronary arteries and pacing the left atrium at 150 to 180 beats per minute for 3 minutes. Left ventricular volume was measured with a conductance catheter. Hemodynamics were recorded during baseline, coronary stenosis, rapid pacing, and pacing-induced ischemia (immediately after rapid pacing). For each condition, hemodynamics were recorded in steady state and then during a brief inferior vena caval occlusion (except for during rapid pacing) to obtain left ventricular end-diastolic and end-systolic pressure-volume relations. The shift of the EDPVR from coronary stenosis to pacing-induced ischemia was assessed by an upward shift index (end-diastolic pressure during pacing-induced ischemia minus the pressure during coronary stenosis at the largest end-diastolic volume common to both conditions, SI-S) and a rightward shift index (the largest end-diastolic volume during pacing-induced ischemia minus the largest volume during coronary stenosis, delta EDVI-S). The index of left ventricular contractility, the end-systolic elastance (Ees), or the slope of the dP/dtmax-end-diastolic volume relation (dE/dtmax) during pacing-induced ischemia was the strongest determinant of the magnitude of SI-S and delta EDVI-S and thus of the shift of the EDPVR. As Ees or dE/dtmax decreased, SI-S decreased and delta EDVI-S increased. Our results suggest that left ventricular contractility is the best determinant of the shift of the EDPVR during pacing-induced ischemia. The more left ventricular contractility decreases, the more the EDPVR shifts downward and rightward.