By Edward F. Plow PHD, Peter Kelly MD (auth.), Arman T. Askari, A. Michael Lincoff (eds.)

ISBN-10: 1603272348

ISBN-13: 9781603272346

Substantial morbidity and mortality is still linked to thrombotic occasions has influenced the speedy enlargement of the to be had armamentarium to wrestle pathologic thrombosis. Pathologic thrombosis performs a vital position within the pathogenesis of acute coronary syndromes (ACS), ischemic problems of percutaneous coronary intervention (PCI), venous thromboembolic sickness, and embolic issues of arrhythmias and numerous cardiomyopathies. Written through specialists within the box, Antithrombotic Drug treatment in Cardiovascular Disease conscientiously examines person and diverse mixtures of the to be had antithrombotic regimens together with fibrinolytic brokers, antiplatelet treatments (aspirin, thieneopyridines, glycoprotein IIb/IIIa inhibitors), and anticogulant remedies (unfractionated heparin, low-molecular-weight heparins, direct thrombin inhibitors, and artificial issue X inhibitors), non-ST-segment elevation (NSTE) ACS and ST-segment elevation myocardial infarction (STEMI). an in depth review, Antithrombotic Drug remedy in Cardiovascular Disease provides the facts demonstrating the efficacy of obtainable antithrombotic cures in particular affliction states resembling atrial traumatic inflammation, cardiomyopathy, valvular center sickness, and heparin-induced thrombocytopenia (HIT).

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Extra resources for Antithrombotic Drug Therapy in Cardiovascular Disease

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This provides a binding site for coagulation complexes, such as the tenase and prothrombinase complexes. Because microparticles arise from the cell membrane, their protein antigen composition is characteristic of their cell of origin and can be used to identify their source. Circulating microparticles may contribute to the support of coagulation and development of thrombosis or may have anticoagulant properties, depending on their number and cell of origin or the producing stimuli. The microparticle’s anionic phospholipid surface has been shown to support thrombin generation through assembly of procoagulant complexes, and may be associated with clinical procoagulant states and other diseases (83,84,146).

Del Conde I, Shrimpton CN, Thiagarajan P, Lopez JA (2005) Tissue-factor-bearing microvesicles arise from lipid rafts and fuse with activated platelets to initiate coagulation. Blood 106:1604–1611 87. Steppich B, Mattisek C, Sobczyk D, Kastrati A, Schomig A, Ott I (2005) Tissue factor pathway inhibitor on circulating microparticles in acute myocardial infarction. Thromb Haemost 93:35–39 88. Hugel B, Zobairi F, Freyssinet JM (2004) Measuring circulating cell-derived microparticles. J Thromb Haemost 2:1846–1847 89.

HIT is a syndrome associated with thrombocytopenia and thrombosis developing approximately 5–14 days following heparin therapy (18). The inciting antigen in HIT is thought to be heparin/platelet factor 4 (116), with complexes of antibodies/heparin/platelet factor 4 binding to the FcgIIa receptor on platelets and endothelial cells, triggering platelet and endothelial activation with release of prothrombotic microparticles (117). In the APS, the antigen is variable, but is typically a protein associated with phospholipid membranes or cardiolipin; common antigens include b2-glycoprotein I and prothrombin (118), resulting in laboratory detection of anticardiolipin antibodies, anti-b2 glycoprotein I antibodies and/or the lupus anticoagulant.

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Antithrombotic Drug Therapy in Cardiovascular Disease by Edward F. Plow PHD, Peter Kelly MD (auth.), Arman T. Askari, A. Michael Lincoff (eds.)


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