Myocardial Ischemia–Reperfusion Injury: Unraveling Pathophysiology, Clinical Manifestations, and Emerging Prevention Strategies

Abstract

Myocardial ischemia–reperfusion injury (MIRI) remains a challenge in the context of reperfusion procedures for myocardial infarction (MI). While early revascularization stands as the gold standard for mitigating myocardial injury, recent insights have illuminated the paradoxical role of reperfusion, giving rise to the phenomenon known as ischemia–reperfusion injury. This comprehensive review delves into the intricate pathophysiological pathways involved in MIRI, placing a particular focus on the pivotal role of endothelium. Beyond elucidating the molecular intricacies, we explore the diverse clinical manifestations associated with MIRI, underscoring its potential to contribute substantially to the final infarct size, up to 50%. We further navigate through current preventive approaches and highlight promising emerging strategies designed to counteract the devastating effects of the phenomenon. By synthesizing current knowledge and offering a perspective on evolving preventive interventions, this review serves as a valuable resource for clinicians and researchers engaged in the dynamic field of MIRI.

Advances in Nanoparticles in the Prevention and Treatment of Myocardial Infarction

“…Thrombolytic therapy or direct percutaneous coronary intervention in time after the occurrence of MI, followed by the use of lipid-lowering drugs and anti-coagulants, are the most effective treatment interventions for patients with MI, which can significantly reduce myocardial infarction size and mortality [ 2 , 3 ]. Percutaneous coronary intervention can restore the blood flow of the infarcted coronary artery, but it is prone to ischemia-reperfusion (I/R) injury, including further tissue damage and myocardial cell apoptosis, which will eventually lead to the development of heart failure and other poor prognosis [ 4 , 5 ]. In addition, the body will undergo some pathological changes after MI, such as reactive oxygen species (ROS) production, mitochondrial dysfunction, calcium overload, and other mechanisms that induce cell death and inflammatory response [ 6 ].…”