In a porcine model with coronary anatomy similar to humans, right ventricular ischemic injury progresses in a wavefront fashion from endocardium to epicardium, with irreversible injury occurring within 15-30 minutes.
May inform RV ischemia timing in human-like models; leaves open clinical translation and requires prospective validation.
Past studies of acute canine right ventricular (RV) ischemia have failed to demonstrate early irreversible injury or decreased function. However, the dog frequently has an extensive collateral circulation not found in all humans. The aim of this study was to measure RV global and regional function after right coronary occlusion in 32 closed-chest pigs. RV function was assessed by biplane ventriculography, and myocardial injury was examined by immunohistochemical localization of creatine kinase (CK) and by electron microscopy. Global RV ejection fraction and apical and midventricular regional function declined significantly after 10 min of occlusion. Injury to the myocardium progressed from the endocardium to the epicardium. Significant injury was observed in myocytes of the endocardium, midmyocardium, and epicardium at 10, 30, and 60 min of occlusion, respectively. Regional RV function and the extent of myocardial injury showed a high correlation (r = 0.96, P less than 0.01). The strong CK immunostaining seen in control hearts was diminished in myocytes along the endocardium at 15 min of occlusion. Depletion of immunoreactive CK in myocytes progressed toward the epicardium with longer ischemic times. These findings demonstrate that RV ischemic injury progresses in a wavefront fashion in the pig, which has similar coronary anatomy to humans, and irreversible myocardial injury occurred after 15-30 min of ischemia.
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Spinale et al. (1990) studied this question.
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