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Thrombin-induced platelet-fibrin clot strength: Relation to high on-clopidogrel platelet reactivity, genotype, and post-percutaneous coronary intervention outcomes

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
Topic:

Theme Issue
GTH – State of the Art

DOI: https://doi.org/10.1160/TH13-08-0643
Issue: 2014: 111/4 (Apr) pp. 565–779
Pages: 713-724

Thrombin-induced platelet-fibrin clot strength: Relation to high on-clopidogrel platelet reactivity, genotype, and post-percutaneous coronary intervention outcomes

Online Supplementary Material

Y.-H. Jeong (1, 2), K. P. Bliden (1), A. R. Shuldiner (3), U. S. Tantry (1), P. A. Gurbel (1)

(1) Sinai Center for Thrombosis Research, Baltimore, Maryland, USA; (2) Department of Internal Medicine, Gyeongsang National University Hospital and Gyeongsang National University, Jinju, Korea; (3) Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA

Keywords

clopidogrel, Platelet, percutaneous coronary intervention, cytochrome P450, clot strength

Summary

The relationship between thrombin-induced platelet-fibrin clot strength (MATHROMBIN), genotype and high on-treatment platelet reactivity (HPR) is unknown. The aim of this study is to assess the influence of MATHROMBIN measured by thrombelastography on HPR and long-term major adverse cardiovascular events (MACE) in percutaneous coronary intervention (PCI)-treated patients during aspirin and clopidogrel therapy. MATHROMBIN, platelet aggregation, genotype, and two-year MACE were assessed in 197 PCI-treated patients. HPR was defined as 5 µM ADP-induced PR ≥ 46% measured by conventional aggregometry. Both high MATHROMBIN(≥ 68 mm) and CYP2C19*2 allele carriage were independently associated with ADP-induced platelet aggregation (β coefficient: 8.3% and 12.0%, respectively). The combination of CYP2C19*2 allele carriage and high MATHROMBIN increased the predictive value for the risk of HPR (odds ratio: 13.89; 95% confidence interval: 3.41 to 55.56; p < 0.001). MACE occurred in 25 patients (12.7%). HPR and high MATHROMBIN were both associated with MACE (hazard ratio: 3.09 and 2.24, respectively), and patients with both HPR and high MATHROMBIN showed an increased risk for MACE (adjusted hazard ratio: 5.56; 95% confidence interval: 1.85 to 16.67; p = 0.002). In conclusion, this is the first study to demonstrate that high platelet-fibrin clot strength is an independent determinant of HPR in PCI-treated patients. Combining the measurements of platelet aggregation and platelet-fibrin clot strength may enhance post-PCI risk stratification and deserves further study.

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