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

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

Substantial morbidity and mortality continues to be linked to thrombotic occasions has motivated the quick growth of the to be had armamentarium to wrestle pathologic thrombosis. Pathologic thrombosis performs a necessary function 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 remedy in Cardiovascular Disease conscientiously examines person and numerous mixtures of the to be had antithrombotic regimens together with fibrinolytic brokers, antiplatelet remedies (aspirin, thieneopyridines, glycoprotein IIb/IIIa inhibitors), and anticogulant cures (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). a close evaluate, Antithrombotic Drug remedy in Cardiovascular Disease provides the facts demonstrating the efficacy of accessible antithrombotic treatments in particular sickness states akin to atrial traumatic inflammation, cardiomyopathy, valvular middle illness, and heparin-induced thrombocytopenia (HIT).

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Sample text

Studies have shown that factor IX is principally activated not by the contact factors but by the tissue factor/factor VIIa complex, as described later, and physiologic hemostasis is thought to proceed principally through that extrinsic pathway (32). However, recent studies with factor XI and XII knockout mice have indicated that deficiency of these factors may impair formation of occlusive thrombi in arterial injury models and may be attractive targets for new antithrombotic agents (26,28,33). The Extrinsic Pathway The so-called Extrinsic Pathway of coagulation, comprising tissue factor and factor VII, is activated by tissue injury or cellular activation and is likely the primary mechanism for in vivo hemostasis (2,34).

Diagram of the coagulation cascade, depicting the intrinsic and extrinsic pathways of activation. The extrinsic pathway of activation is started with exposure of tissue factor (TF), coupled with factor VIIa that leads to the activation of factor X. The intrinsic pathway is started by the contact activation factors (factor XII, high molecular weight kininogen (HMWK), and prekallikrein (PK)) with eventual activation of factor X by the tenase complex (factors IXa, VIIIa, calcium (Ca++), and phospholipid).

Segers K, Dahlback B, Nicolaes GA (2007) Coagulation factor V and thrombophilia: Background and mechanisms. Thromb Haemost 98:530–542 110. Bertina RM (1999) Molecular risk factors for thrombosis. Thromb Haemost 82:601–609 111. Poort SR, Rosendaal FR, Reitsma PH, Bertina RM (1996) A common genetic variation in the 3’-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood 88:3698–3703 112. Heit JA (2006) Epidemiology of venous thromboembolism.

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