No-reflow: the next challenge in treatment of ST-elevation acute myocardial infarction.

Coronary revascularization is not synonymous with myocardial reperfusion. DeWood et al. almost three decades ago showed that 90% of patients with transmural myocardial infarction had total coronary occlusion at angiography associated with acute thrombosis. This and other studies have paved the way for the use of fibrinolytics in the treatment of transmural or ST-segment elevation myocardial infarction (STEMI). Despite the clear benefits observed with fibrinolysis, a significant proportion of patients failed to achieve adequate reperfusion as witnessed by persistence of total coronary occlusion, slow epicardial flow at angiography, or failure of regression of other signs of ischaemia such as ST-segment elevation. The advances of percutaneous coronary intervention (PCI) led to the use of balloon angioplasty as a treatment modality for STEMI. Angioplasty was associated with improved epicardial flow, greater reperfusion rates, and improved survival. When readily available, angioplasty (with or without use of coronary stenting) has indeed become the standard of care for STEMI. As experience accumulated with primary angioplasty, it also became evident that there was a group of patients who seemed not to benefit fully from prompt restoration of antegrade flow as they failed to show resolution of indirect signs of ischaemia such as electrocardiographic changes, and improvements in perfusion abnormalities. 3 These patients also presented peculiar angiographic phenomena characterized by evidence of ‘slow flow’ in the affected vessel and lack of contrast uptake (‘blush’) by the subtended myocardium. This condition is referred to as no-reflow. –3 The clinical consequences of the no-reflow phenomenon have been rapidly recognized, and highlighted the potential dissociation between coronary revascularization and myocardial reperfusion in STEMI. –3 Pathophysiology of no-reflow