Myocardial ischemia – reperfusion injury

Abstract

Aim. To summarize and broaden the idea about mechanisms of acute coronary insufficiency development and pathophysiological features of myocardial reperfusion injury. Today, in the event of acute coronary syndrome, according to the latest recommendations for myocardial revascularization, percutaneous coronary intervention should be performed to determine the anatomy of coronary artery lesions and further percutaneous therapy. But in some patients, after blood flow restoration, reperfusion injury occurs, which is primarily related to the duration of ischemia, infarct size, and the myocardial resistance to ischemia. Treatment of myocardial infarction, like any treatment method, has evolved. In the 60s of the previous century, it included morphine, oxygen, warfarin and bed rest for 4–6 weeks. Then, during the 70s, it consisted of morphine, oxygen, lidocaine, warfarin, bed rest for 2–3 weeks and possibly coronary angiography for the further bypass surgery. The late 1970s saw the rapid progress in thrombolysis, first intravenous and then intracoronary. And starting in the early 1980s, since G. Hartzler performed the first balloon angioplasty for acute coronary artery occlusion, the stage of mechanical myocardial reperfusion has come. At the same time, knowledge about the pathophysiology of acute coronary ischemia was deepened. The World Health Organization developed ECG criteria for acute myocardial infarction using population-based studies in the 1950s–1970s, and additional four normative European regulations since then were issued defining concepts, key points of diagnosis and possible complications of myocardial infarction. Conclusions. The development of myocardial ischemic-reperfusion injury is a staged process that has a complex pathogenesis, its own clinical manifestations, and an association with more negative long-term outcomes of myocardial infarction treatment. Its main components are myocardial swelling involving cardiomyocytes, endotheliocytes, and the interstitial space; downregulation of cytoskeleton and disruption of sarcolemma integrity; increased vascular wall permeability; spasm of arterioles; intravascular accumulation of platelets and leukocytes, and the resultant the most severe form of myocardial damage is intramyocardial hemorrhage. Clinically, this is manifested by the no-reflow phenomenon following percutaneous coronary intervention.