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(Circulation. 1996;93:229-237.)
© 1996 American Heart Association, Inc.
Articles |
Platelet Function in Acute Myocardial Infarction Treated With Direct Angioplasty
Presented in part at the 67th Scientific Sessions of the American Heart Association, Dallas, Tex, November 1994.
From the 1. Medizinische Klinik der Technischen Universität München, Germany.
Correspondence to Dr Meinrad Gawaz, 1. Medizinische Klinik der Technischen Universität München, Klinikum rechts der Isar, Ismaninger Straße 22, 81675 München, Germany.
Background 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.
Methods and Results 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.
Conclusions After transient apparent deactivation of circulating platelets, 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.
Key Words: platelets • revascularization • myocardial infarction • thrombosis • angioplasty
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