Abstract

The aim of reperfusion therapy for acute myocardial infarction (AMI) is to rapidly restore coronary blood flow and myocardial perfusion with the objective of salvaging myocardium. The treatment of AMI for many years has focused on achieving patency of the conduit epicardial artery at the site of plaque rupture and occlusive thrombus. Major advances in interventional techniques and adjunctive pharmacological treatment have made it possible to achieve normal (TIMI grade 3) epicardial flow in approximately 95% of patients.1 This success has also highlighted the limitations of current treatment with regards to the goal of restoring myocardial perfusion. A significant proportion of patients, perhaps as many as 40%, do not regain microvascular and myocardial perfusion despite the restoration of TIMI grade 3 flow.1,2 The major source of these data has been acquired from patients treated with primary percutaneous coronary intervention (PCI), but likely also applies to those receiving thrombolytic therapy. Failure to restore myocardial perfusion is associated with larger myocardial infarcts, increased risk of ventricular arrhythmias, cardiac failure, cardiac rupture, cardiogenic shock, major adverse cardiac events following PCI, and death. In its most extreme form, failure of microvascular perfusion is manifested in the cardiac catheterisation laboratory as the “no reflow” phenomenon; however, “slow reflow” and even more subtle degrees of impaired microvascular flow are more frequent. Longer duration from onset of symptoms and anterior myocardial infarction are risk factors for myocardial malperfusion. In addition, we have observed that diabetes mellitus is an independent predictor of diminished myocardial perfusion.3 This article provides a brief overview of the pathophysiology, diagnosis, and management of myocardial malperfusion in patients with AMI.