Late open artery hypothesis and cardiac electrical stability

The concept that late reperfusion resulting in a patent infarct artery causes benefit beyond myocardial salvage (also referred to as the open artery hypothesis) remains somewhat controversial. The seminal animal studies are reviewed in this chapter that lead to two decades of inquiry into the open artery hypothesis. In the rat, Hochman and Choo showed that late reperfusion independent of myocardial infarct size may still improve healing of the infarct, resulting in a thicker infarct wall, less infarct expansion, less LV dilation, and improved cardiac function. Translational evidence for late reperfusion having a benefit on ventricular cavity size during chronic post-infarct healing is reviewed in association with cardiac electrical stability. Consistent with that idea, randomized clinical trials have clearly shown that reperfusion within 6 h reduces mortality and reduces the incidence of induced ventricular tachycardia. Although, the 6-h cutoff for reperfusion in acute MI patients is based primarily on old thrombolytic data. More recent trials with longer time to reperfusion cutoff levels have been performed with percutaneous transluminal coronary angioplasty (PTCA) with or without stents. Notably, the benefits of late reperfusion do not depend on the amount of salvaged myocardium at risk in these clinical studies, and reperfusion as late as 12-h and possibly up to 24-h post-MI exert a beneficial effect on ventricular remodeling. Beyond 24 h, however, the data are less encouraging. The results of more recent clinical trials further diminish the enthusiasm for late reperfusion and do not support the concept that late reperfusion improves cardiac electrical stability. In fact some evidence suggests it may be worse.