Role of ischemia-reperfusion injury in coronary MVO

The abrupt restoration of blood flow during the treatment of acute myocardial infarction is associated with coronary microvascular obstruction (MVO) and further myocardial damage, referred to as “ischemia-reperfusion injury.” This chapter reviews and discusses the pathophysiology of MVO during ischemia-reperfusion injury. Proposed mechanisms include oxygen free radicals induced vascular damage, exaggerated capillary vasoconstriction and impaired vasodilatation, external capillary compression by endothelial cell and cardiomyocyte swelling, microembolization from the atherosclerotic plaque, plugging of activated neutrophils interacting with the endothelium and microthrombi formation. Emerging data also suggests that in severe cases of microvascular injury, blood extravasation and local hemorrhage can exacerbate microvascular and myocardial damage. Many of these mechanisms may be synergistic in causing MVO and malperfusion, and it is plausible that depending on the clinical scenarios some mechanisms may predominate over others.