The leftward shift in the LV pressure-volume relationship during ischemia is not solely explained by right ventricular constraint or incomplete ventricular relaxation.
Warrants caution attributing LV compliance shifts solely to RV effects in ischemia; leaves open intrinsic mechanisms in animal models.
The constraint of the right ventricle (RV) on the end-diastolic pressure-volume (PV) relationship of the nonischemic and ischemic left ventricle (LV) was studied. The model used was the isovolumic beating LV, with separately perfused ejecting RV with controlled RV distension. The effect of augmented RV distension on the nonischemic LV PV relationship was examined. A change from mild [right ventricular end-diastolic pressure (RVEDP) = 1.5 mm Hg] to severe (RVEDP = 16 mmHg) RV distension resulted in a significant leftward shift of the LV PV relationship. Ischemia was produced for 90 min by reducing flow in the cannulated left main coronary artery and the effect of two levels of stable RV distension on the PV relationship of the ischemic LV was examined. Mild RV distension and moderate (RVEDP = 6 mmHg) RV distension were used. In both groups, there was a progressive leftward shift in the LV PV relationship that was significant by 60 min of ischemia. No change was seen in nonischemic controls. Ventricular relaxation, as described by the time constant of isovolumic relaxation, T, was impaired throughout ischemia but was not sufficiently prolonged to explain the above changes. Thus, the time course of change in the LV PV relationship during ischemia differs from that previously reported after pacing-induced ischemia in humans. Neither the external constraint of the RV nor incomplete relaxation explains this difference.
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Lorell et al. (1981) studied this question.
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