Platelet function in acute myocardial infarction treated with direct angioplasty

• Published in: Circulation (New York, N.Y.) Vol. 93; no. 2; pp. 229 - 237
• Main Authors: GAWAZ, M, NEUMANN, F.-J, OTT, I, SCHIESSLER, A, SCHÖMIG, A
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 15.01.1996; American Heart Association, Inc
• Subjects: Adult; Aged; Aged, 80 and over; Angioplasty, Balloon, Coronary; Biological and medical sciences; Blood Platelets - physiology; Cardiology. Vascular system; Cells, Cultured; Coronary heart disease; Endothelium, Vascular - cytology; Female; Heart; Humans; Male; Medical sciences; Middle Aged; Myocardial Infarction - blood; Myocardial Infarction - therapy; Platelet Adhesiveness; Platelet Count; Human; Infarct; Acute; Cuffed tube; Instrumentation therapy; Cardiovascular disease; Exploration; Instrumental dilatation; Coronary heart disease; Percutaneous route; Platelet; Treatment; Platelet function; Myocardium
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.93.2.229

In acute myocardial infarction (AMI), platelets play a key role in thrombotic processes that limit the patency of the recanalized, infarct-related coronary artery and contribute to reperfusion injury. Platelet function in the course of AMI treated by direct percutaneous transluminal coronary angioplasty (PTCA) has not been evaluated. In 15 patients with anterior AMI, peripheral venous blood samples were obtained before and 4, 8, 24, and 48 hours after recanalization of the occluded artery by PTCA. Fifteen patients who had stable coronary heart disease and were undergoing elective balloon angioplasty served as control subjects. Fibrinogen receptor function and surface expression of P-selectin on platelets were determined by flow cytometry. In addition, we evaluated generation of platelet-derived microparticles and the effect of systemic plasma from patients with AMI on normal platelet function and on platelet adhesion to human endothelial cells in culture. We found fibrinogen receptor activity and P-selectin expression on circulating platelets 8 hours after direct PTCA are decreased (P < .01). This coincided with a decrease in peripheral platelet count (P < .05) and an increase in generation of microparticles (P < .002). Twenty-four to 48 hours after PTCA, fibrinogen receptor activity and P-selectin expression increased again. Systemic plasma obtained before and after direct PTCA sensitized normal platelets to hyperaggregate in vitro (P < .001) and stimulated platelet adhesion to endothelial cells in culture (P < .01). None of the changes found in AMI were detectable in the control group. After transient apparent deactivation of circulating platelet, probably caused by sequestration of hyperactive platelets, the level of platelet activation increases in patients with AMI treated by direct PTCA. These findings underscore the need for novel antiplatelet strategies in AMI.