Abstract
The laboratory assessment of platelet biology and coagulation has traditionally focused on abnormalities, congenital or acquired, that provide insights for understanding hemostatic defects, unexplained bleeding, and pharmacologic titration of compounds designed to attenuate thrombotic potential. Because atherosclerotic vascular disease is associated with thrombotic events and there exists a clear link between atherosclerosis, inflammation, and thrombosis, the development of markers that have pathobiologic, prognostic, and treatment-related relevance has taken on a role of considerable importance.
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DeBoer, A.C., Turpie, A.G., Butt, R.W., Johnston, R.V., and Genton, E. (1982). Platelet release and thromboxane synthesis in symptomatic coronary artery disease. Circulation 66:327–333.
Gallino, A., Haeberli, A., Baur, H. R., and Straub, P.W. (1985). Fibrin formation and platelet aggregation in patients with severe coronary artery disease: relationship with the degree of myocardial ischemia. Circulation 72:27–30.
Gershlick, A.H. (1990). Are there markers of the blood vessel wall interaction and of thrombus formation that can be used clinically?. Circulation 81(Suppl. I):128–134.
Fitzgerald, G.A., Pederson, A.K., and Patrono, C. (1983). Analysis of prostacyclin and thromboxane biosynthesis in cardiovascular disease. Circulation 67:1174–1177.
Becker, R.C., Tracy, R., Bovill, E.G., Mann, K.G., and Ault, K. (1994). The clinical use of flow cytometry for assessing platelet activation in acute coronary syndromes. TIMI-III Thrombosis and Coagulation Study Group. Coronary Artery Dis. 5:339–345.
Becker, R.C., Bovill, E.G., Corrao, J.M., Ball, S.P., Ault, K., Mann, K., et al. (1994). Platelet activation determined by flow cytometry persists despite antithrombotic therapy in patients with unstable angina and non-Q-wave myocardial infarction. TIMI-III Thrombosis and Coagulation Study Group. Thromb. Thrombol. 1:95–100.
Furman, M.I., Barnard, M.R., Krueger, L.A., and Michelson, A.D. (2000). Circulating monocyte-platelet aggregates are a more sensitive marker of platelet activation than P-selectin positive platelets. Circulation 102:II-776.
Xio, Z. and Theroux, P. (1998). Platelet activation with unfractionated heparin at therapeutic concentrations and comparisons with a low molecular weight heparin and with a direct thrombin inhibitor. Circulation 87:251–256.
Cox, D., Smith, B., Quinn, M., Theroux, P., Crean, P., and Fitzgerald, D.J. (2000). Evidence of platelet activation during treatment with a GPIIb/IIIa antagonist in patients presenting with acute coronary syndromes. J. Am. Coll. Cardiol. 36:1514–1519.
Rho, R., Tracy, R.P., Ball, S.P., Becker, R.C., with technical assistance provided by C. F. Becker (1995). Plasma markers of procoagulant activity among individuals with coronary artery disease. J. Thromb. Thrombol. 2:239–243.
Scharfstein, J.S., Abendschein, D.R., Eisenberg, P.R., George, D., Cannon, C.P., Becker, R.C., et al. (1996). Usefulness of fibrinogenolytic and procoagulant markers during thrombolytic therapy in predicting clinical outcomes in acute myocardial infarction. Am. J. Cardiol. 78:503–510.
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Becker, R.C. Markers of platelet activation and thrombin generation. Cardiovasc Toxicol 1, 141–145 (2001). https://doi.org/10.1385/CT:1:2:141
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DOI: https://doi.org/10.1385/CT:1:2:141