Effect of intracoronary adenosine on reflow in patients with acute ST Elevation Myocardial Infarction undergoing Primary PCI

Abstract

ST elevation myocardial infarction is caused by total thrombotic coronary artery occlusion, most of our treatment strategies focused on epicardial coronary arteries yet little interest was given to microvascular occlusion and its consequences. When a coronary artery is occluded, detrimental changes occur in the cardiac capillaries and arterioles. After relief of the occlusion, blood flow to the ischemic tissue may still be impeded, a phenomenon known as no reflow. The no-reflow phenomenon is becoming increasingly recognized because of the spread of primary intervention for acute myocardial infarction and the emergence of contrast myocardial echocardiography. With the clinician focusing on both epicardial coronary arteries and the microvasculature, there is a need for a safe and effective treatment for no reflow. After prolonged cessation of coronary occlusion and restoration of blood flow to the epicardial coronary arteries, there is sufficient structural damage to the microvasculature to prevent restoration of normal blood flow to the cardiac myocytes. This may lead to inadequate healing of the cardiac scar. In addition, it may prevent the development of future collateral flow (1).