Intramyocardial Hemorrhage in Acute Myocardial Infarction

Timely primary percutaneous coronary intervention to restore myocardial perfusion is pivotal in acute ST elevation myocardial infarction. The major determinants to reduce myocardial injury before intervention are reducing ischemia duration and severity, and the major determinants after intervention are restoring microvascular flow and minimizing reperfusion injury. When necrosis within the myocardium at risk reaches substantial extent, however, restoration of flow may risk to aggravate the injury by causing intramyocardial hemorrhage (IMH). If microvascular perfusion is restored within ≈30 minutes, myocardial injury is usually detected by troponins, whereas late gadolinium enhancement magnetic resonance imaging (MRI)1 may demonstrate little or no enhancement as a sign of necrosis.2,3 Myocardial function is often restored completely. With increasing duration of ischemia, however, myocardial cells will progressively lose control of intracellular homeostasis. This leads to progressive myocyte necrosis as a function of time within the myocardium at risk from endocardium to epicardium called the “wavefront phenomenon” by Reimer et al4 and Reimer and Jennings.5 The rate at which the amount of infarcted myocardium increases as a result of this process is slower in man compared with most animal experiments.2 Also, with increasing ischemia duration the swelling of ischemic tissue on reperfusion impedes microvascular flow. This no-reflow phenomenon, as described in experimental …