INTRODUCTION After ST-segment elevation myocardial infarction (STEMI), the immediate therapeutic goal is to establish patency of the infarct-related artery. Nevertheless, the successful restoration of epicardial coronary artery patency by thrombolysis, primary angioplasty, or bypass, does not necessarily translate into improved myocardial reperfusion (1-3). Patient’s prognosis after STEMI relates directly to the extent of myocardial injury produced during coronary occlusion (4-9). Postinfarction electrocardiography, echocardiography, and contrast ventriculography are often used to indirectly assess the degree of myocardial damage (10-11), whereas radionuclide studies with 99mTc sestamibi and gadoliniumenhanced magnetic resonance imaging (cMR) can measure infarct size directly (7,12,13). In addition to the extent of infarcted myocardium, the magnitude of structural obstruction or disruption of the microvasculature, called “no-reflow” or “low-reflow” phenomenon, sustained before or during primary percutaneous coronary intervention (PCI) has been related to worse clinical outcome (7), despite successful epicardial revascularization. Therefore, attention has shifted away from merely achieving epicardial artery patency toward the obtainment of an adequate myocardial and microvascular reperfusion.