January 2013 | Derek J. Hausenloy and Derek M. Yellon
The article discusses the significant impact of myocardial ischemic injury and reperfusion injury (IRI) on patients with acute myocardial infarction (MI). While timely and effective myocardial reperfusion using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) is crucial for reducing MI size and improving clinical outcomes, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury (MRI). Despite advancements in PCI technology and antiplatelet and antithrombotic agents, there is still no effective therapy for preventing MRI. The article reviews the pathophysiology of MRI, including the roles of oxidative stress, intracellular calcium overload, pH correction, and inflammation. It also highlights emerging therapeutic strategies, such as ischemic postconditioning, remote ischemic conditioning, therapeutic hyperoxemia, hypothermia, and pharmacologic agents, which show promise in reducing MRI and improving clinical outcomes. The authors emphasize the need for further research and clinical trials to translate these promising strategies into effective treatments for patients with CHD.The article discusses the significant impact of myocardial ischemic injury and reperfusion injury (IRI) on patients with acute myocardial infarction (MI). While timely and effective myocardial reperfusion using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) is crucial for reducing MI size and improving clinical outcomes, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury (MRI). Despite advancements in PCI technology and antiplatelet and antithrombotic agents, there is still no effective therapy for preventing MRI. The article reviews the pathophysiology of MRI, including the roles of oxidative stress, intracellular calcium overload, pH correction, and inflammation. It also highlights emerging therapeutic strategies, such as ischemic postconditioning, remote ischemic conditioning, therapeutic hyperoxemia, hypothermia, and pharmacologic agents, which show promise in reducing MRI and improving clinical outcomes. The authors emphasize the need for further research and clinical trials to translate these promising strategies into effective treatments for patients with CHD.