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Prognostic significance of platelet function in the early phase of ST-elevation myocardial infarction treated with primary angioplasty

Zenon Huczek, Krzysztof J. Filipiak, Janusz Kochman, Radoslaw Piatkowski, Marcin Grabowski, Marek Roik, Janusz Kochanowski, Grzegorz Opolski

Med Sci Monit 2008; 14(3): CR144-151

ID: 836580


Background: There are limited data concerning global platelet function response to antiplatelet therapy in ST-segment elevation myocardial infarction (STEMI). The aim was to determine the frequency and clinical significance of inadequate inhibition of two major platelet activation pathways: the thromboxane A2 (TXA2)- and ADP-dependent, in the early phase of STEMI.
Material and Method: Platelet function was measured with a Platelet Function Analyzer-100 in 125 consecutive survivors of STEMI on days 3 (48+/-2 h) and 30 after stenting. Inadequate inhibition of the TXA2-dependent activation pathway was defined as a collagen-epinephrine closure time <193 and of the ADP-dependent as a collagen-adenosine closure time <130 seconds.
Results: The study population was divided into groups I (n=67/53%; both pathways inhibited, complete inhibition), II (n=21/17%; one pathway inhibited, partial inhibition), and III (n=37/30%; neither pathway inhibited, no inhibition). LV remodeling occurred more frequently in groups II and III than in group I (40% and 62% vs. 14%, P=0.038 and <0.0001, respectively). At six months the combined rate of death, nonfatal reinfarction, stroke, and rehospitalization for heart failure was 3% in group I, 23.8% in II, and 54.1% in III (log rank=39.2, P for trend <0.0001). By multivariate regression analysis, no or partial inhibition were independent predictors of LV remodeling and combined clinical outcome.
Conclusions: Inadequate platelet function inhibition in acute phase STEMI despite standard antiplatelet therapy is associated with increased risk of poor LV performance and combined clinical events. This may suggest the need for intensified antiplatelet therapy in the early phase of STEMI.

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