Progressive right ventricular failure is not explained by myocardial ischemia in a pig model of right ventricular pressure overload.

Abstract

BACKGROUND: Current concepts of acute pulmonary embolism suggest that right ventricular (RV) dilatation and failure are the consequence of pressure overload-induced RV hypoperfusion and ischemia. METHODS: Sixteen human-sized hybrid pigs were instrumented for the measurement of RV and aortic pressure, aortic and right coronary artery blood flow (RCA BF), RV oxygen consumption (RV MVO(2)) and RV free wall segment length. The pulmonary artery was constricted (PAC) to increase RV peak pressure acutely 2.5-fold (from 27+/-2 to 64+/-3 mmHg, n=9), and the constriction was maintained for 6h. RESULTS: At 10 min after PAC, a RV work index (RVWI, RV pressure-segment length loops) was increased 2.3-fold, indicating an initial RV adaptation to increased afterload. At 1h, 3h and 6h after PAC, however, RVWI decreased progressively towards control levels, while RCA BF and RV MVO(2) continued to increase. The arterial-coronary venous pH difference did not increase throughout the protocol. Arterial troponin T concentration increased from 0.08+/-0.03 to 0.80+/-0.20ng/ml at 6h after PAC. None of the parameters changed in control animals (n=7). CONCLUSION: We conclude that in our model RV failure during PAC develops in spite of increased coronary blood flow and MVO(2). Thus, mechanisms different from ischemia may contribute to progressive RV failure after pulmonary embolism.