“Rusty Hearts”

Rapidly restoring blood flow in the epicardial coronary artery after an acute obstruction is critical for limiting myocardial tissue damage and salvaging the area at risk. Minimizing the acute injury to the myocardium after an ischemic event (ie, infarct size) has been strongly correlated with improved outcome.1 In fact, large myocardial infarctions (MIs) have been associated with pronounced adverse left ventricular (LV) remodeling and major adverse cardiovascular events (MACE), including sudden death and hospitalization for chronic heart failure.2 Understandably, this has lead to the affirmation that time is muscle, and efforts are routinely made to quickly restore blood flow to ischemic myocardium.See Article by Bulluck et al However, for >40 years, we have known that not all MIs are the same. Pioneering work by Kloner et al3 in large animal models demonstrated that microvascular obstruction (MO), also assessed as no-reflow phenomenon, could complicate some acute MIs. A more severe case of MO has been observed to lead to intramyocardial hemorrhage, a case where the microvasculature ruptures, likely during reperfusion, and red blood cells are extravasated. Notably, MO leads to compromised blood flow to the microvasculature even after the blood flow is re-established to the culprit epicardial coronary artery. These studies and numerous others that followed showed that reperfusion can impart additional acute damage to the myocardium, often referred to as ischemia–reperfusion injury,4 and is a strong predictor of adverse outcome in patients. Thus, the importance of reducing ischemia–reperfusion injury is well recognized and has been the subject of intense investigation for the past few decades.Advances in imaging, particularly cardiac magnetic resonance imaging (CMR), have been central to shedding light on the tissue characteristics of acute MI and enabling the assessment of time-dependent changes in the heart. In particular, late-gadolinium enhancement has been important in …