Risk area, infarct size, and the exposure of the wavefront phenomenon of myocardial necrosis in humans

Abstract

In the 1970s, Reimer and Jennings1 performed a multitude of studies in dogs after acute coronary occlusion in which they examined the relation between duration of ischaemia, area at risk, collateral blood flow, and final infarct size. The results of their experiments were summarized by the concept of ‘wavefront phenomenon of myocardial death’. In summary, this concept states that infarct size increases in a transmural wavefront extending from the endocardium to the epicardium with increasing duration of coronary occlusions and with increasing severity of ischaemia. Coronary occlusions lasting <6 h result in subendocardial infarcts, in which infarct size is smaller than the ischaemic area at risk, because some epicardial rim of viable tissue is spared. When coronary occlusion exceeds 6 h, infarcts become transmural with an infarct size encompassing the entire area at risk. The concept of Reimer and Jennings is fundamental to current revascularization therapy of acute ST-elevation myocardial infarcts (STEMI). Indeed, modern treatment strategies of STEMI aim at opening the infarct-related artery as quickly as possible, in order to reduce the duration of ischaemia and to save viable myocardium in the risk area. The importance of saving such viable myocardium was underscored by the recent OAT trial,2 which demonstrated no benefit of opening the infarct-related artery by PTCA in patients having suffered an STEMI more than 3 days ago, likely because in such subacute STEMI the window of action for saving residual viable myocardium had expired. Experimental studies indicate that additional myocardial injury may occur at the time of reperfusion or shortly thereafter.3 This suggests that the relation between risk area and final infarct size for a given duration of occlusion could be still modified at the time of reperfusion by administration of ‘cardioprotective’ drugs. Such ‘cardioprotective’ effects have indeed been suggested in experimental studies … Corresponding author: Tel: +32 2 7642803; fax: +32 2 7642811. E-mail address : bernhard.gerber{at}clin.ucl.ac.be