Primary reperfusion therapies, including primary percutaneous coronary intervention (PCI) and thrombolysis, are the standard of care for the treatment of acute coronary syndromes. Prompt restoration of blood flow to ischemic myocardium limits infarct size and reduces mortality. Paradoxically, however, the return of blood flow can also result in additional cardiac damage and complications, referred to as reperfusion injury [1-3]. Such damage is more likely when reperfusion therapy is delayed.
Effective therapies to reduce or prevent reperfusion injury have proven elusive. Despite an improved understanding of the pathophysiology of this process and encouraging preclinical trials of multiple agents, most of the clinical trials to prevent reperfusion injury have been disappointing [4,5]. Despite these problems, adjunctive therapies to limit reperfusion injury remain an active area of investigation.
This card will discuss the pathophysiology and manifestations of reperfusion injury, as well as potential therapeutic strategies. More general discussions of the clinical use of primary PCI and thrombolytic therapy in acute myocardial infarction are presented separately. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome" and "Fibrinolytic therapy in acute ST elevation myocardial infarction: Initiation of therapy".)
Reperfusion injury refers to myocardial, vascular, or electrophysiological dysfunction that is induced by the restoration of blood flow to previously ischemic tissue. Manifestations include:
- Reperfusion arrhythmias
- Endothelial cell damage leading to microvascular dysfunction
- Myocardial stunning
- Myocyte death and infarction