ABSTRACT
INTRODUCTION ST-segment myocardial infarction (STEMI) occurs due to sudden thrombotic occlusion of an epicardial coronary artery. The immediate therapeutic goal is to establish patency of the infarct-related artery. The restoration of epicardial coronary artery patency, however, is not equivalent to restoration of nutritive tissue flow, because of the structural disruption of microvasculature, the socalled “no-reflow” phenomenon. With myocardial contrast echocardiography (MCE), microvascular obstruction has been documented in a far greater proportion of patients than could have been deemed possible based on clinical evidence. Patients with the no-reflow phenomenon after immediate reperfusion therapy have an adverse clinical prognosis (1). Therefore, our attention has shifted from epicardial artery patency to the status of the microvasculature.
