Glycoprotein IIb/IIIa inhibitors and no-reflow.

The no-reflow phenomenon is the inability to perfuse a portion of the myocardium after re-establishment of patency of a previously occluded epicardial coronary artery (1–3). This phenomenon has been described in experimental animal models in which the coronary artery is occluded with a mechanical occluder or snare (1). In animal models no-reflow has been detected by using the fluorescent dye Thioflavin S that stains endothelium receiving flow, radioactive microspheres, carbon black, echocardiographic contrast, and magnetic resonance imaging (MRI) techniques. The phenomenon also has been observed in humans after reperfusion therapy for acute myocardial infarction (MI) in which the occlusion is thrombus mediated, and it has been measured using myocardial contrast echocardiography, nuclear tracers, and MRI (4–6). Perfusion at the tissue level can be severely compromised even when the epicardial coronary artery appears to be fully patent by coronary angiography.