Role of adenosine as an adjunct therapy in the prevention and treatment of no-reflow phenomenon in acute myocardial infarction with ST segment elevation: review of the current data

Copyright © Polskie Towarzystwo Kardiologiczne INTRODUCTION Numerous clinical studies have indicated the beneficial effects of timely, optimal (without residual stenosis) and sustained patency of an occluded epicardial artery on infarct size reduction, left ventricular (LV) function and clinical outcomes. While these observations validate the experimental findings of time-dependent myocardial salvage, patients with large regions of ischaemia continue to exhibit significant morbidity and mortality. So it is clear that additional strategies are needed to improve outcomes. Emerging evidence suggests that maximising myocardial salvage not only involves restoring the full patency of large epicardial coronary arteries, but also maintains blood flow in microcirculation of the reperfused bed [1]. Experimental models convincingly document the concept of progressive microcirculatory failure (the ‘no-reflow phenomenon’) and no-reflow appears to be an important component of the potential deleterious effect of reperfusion — myocardial reperfusion injury. In animal models, abnormalities of tissue perfusion are associated with an increase of the infarct size, and agents that preserve microvascular flow result in a significant reduction of irreversible myocyte necrosis. Diagnostic techniques to measure tissue perfusion have validated this concept in humans and it is now clear that abnormal tissue perfusion occurs frequently in patients with acute coronary syndromes (ACS) undergoing reperfusion therapy [1–6].