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- W222030266 abstract "Background: Thrombin and platelets are directly involved in arterial thrombosis, typically occurring at sites of atherosclerotic plaque rupture among patients with acute coronary syndromes. Understanding the dynamic nature of pathologic thrombosis has important clinical implications. Methods: Fibrinopeptide A (FPA), thrombin-antithrombin complexes (TAT), and prothrombin activation fragment 1.2 (F1.2), plasma markers of fibrin formation (thrombin activ- ity) and thrombin generation, and platelet activation, deter- mined by the recognition of a surface-expressed platelet a-granule protein, P-seleetin, using flow eytometry, were measured in 36 consecutive patients with unstable angina and non-Q-wave myocardial infarction participating in the Thrombolysis In Myocardial Ischemia (TIMI) III B trial. Results: Thrombin generation (TAT 12.1 -+ 17.8 ng/ml vs. 3.4 -+ 1.0 ng/ml; F1.2 0.19 - 0.14 nmol/l vs. 0.12 - 0.8 nmol/l), fibrin formation (FPA 15.8 - 23.5 ng/ml vs. 7.5 -+ 2.3 ng/ ml), and platelet activation) 10.6 - 2.4% vs. 2.5 -+ 2.0%) were increased significantly in patients compared with healthy, age-matched controls (p < 0.01). Fibrin formation, repre- sented by plasma FPA levels, did not correlate with the per- centage of activated platelets (r = -.10, p = 0.69). Thrombin generation and platelet activation also did not correlate. A statistically insignificant trend between TAT and platelet ac- tivation was observed (r = .42, p = 0.07); however, even with TAT levels in excess of 20 ng/ml (nearly sixfold greater than normal healthy controls) platelet activation was increased by only 1.7-fold. Conclusions: Thrombin generation, fibrin formation, and platelet activation are increased modestly among patients with unstable angina and non-Q-wave myo- cardial infarction. Despite the involvement of platelets and coagulation proteins in arterial thrombotic processes, their relative contributions may vary, providing a pathophysio- logic basis for the dynamic expression of disease and response to treatment observed commonly in clinical practice. Rupture or fissuring of intimal plaques is known to occur frequently in the evolution of human atheroscle- rotic coronary artery disease. Plaque ruptures vary considerably in size and depth. While most are micro- scopic, others are extensive; both occur at the plaques periphery, where the fibrous cap is thinnest and most heavily infiltrated by foam cells (lipid-laden macro-" @default.
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- W222030266 title "Dynamic Nature of Thrombin Generation, Formation, and Platelet Activation in Unstable Angina and Non-Q-Wave Myocardial Infarction Fibrin" @default.
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