PLATELET-FUNCTION IN ACUTE MYOCARDIAL-INFARCTION TREATED WITH DIRECT ANGIOPLASTY

Citation
M. Gawaz et al., PLATELET-FUNCTION IN ACUTE MYOCARDIAL-INFARCTION TREATED WITH DIRECT ANGIOPLASTY, Circulation, 93(2), 1996, pp. 229-237
Citations number
60
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
93
Issue
2
Year of publication
1996
Pages
229 - 237
Database
ISI
SICI code
0009-7322(1996)93:2<229:PIAMTW>2.0.ZU;2-T
Abstract
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 percutaneou s transluminal coronary angioplasty (PTCA) has not been evaluated. Met hods and Results In 15 patients with anterior AMI, peripheral venous b lood samples were obtained before and 4, 8, 24, and 48 hours after rec analization of the occluded artery by PTCA. Fifteen patients who had s table coronary heart disease and were undergoing elective balloon angi oplasty served as control subjects. Fibrinogen receptor function and s urface expression of P-selectin on platelets were determined by flow c ytometry. In addition, we evaluated generation of platelet-derived mic roparticles and the effect of systemic plasma from patients with AMI o n normal platelet function and on platelet adhesion to human endotheli al cells in culture. We found fibrinogen receptor activity and P-selec tin expression on circulating platelets 8 hours after direct PTCA are decreased (P<.01). This coincided with a decrease in peripheral platel et count (P<.05) and an increase in generation of microparticles (P<.0 02). Twenty-four to 48 hours after PTCA, fibrinogen receptor activity and P-selectin expression increased again. Systemic plasma obtained be fore and after direct PTCA sensitized normal platelets to hyperaggrega te in vitro (P<.002) and stimulated platelet adhesion to endothelial c ells in culture (P<.01). None of the changes found in AMI were detecta ble in the control group. Conclusions After transient apparent deactiv ation of circulating platelets, probably caused by sequestration of hy peracdtive platelets, the level of platelet activation increases in pa tients with AMI treated by direct PTCA. These findings underscore the need for novel antiplatelet strategies in AMI.