title: Some considerations about the hypercoagulable states and their treatments.
abstract: Inherited and acquired tendency to the formation of clots represents an important cause of morbidity and mortality for ischemic events in young people (aged between 40 and 50 years) that is more and more frequently identified. The haemostasis' disorders may happen on the venous or arterial side. Arterial thrombus is a 'white' thrombus, also called temporary thrombus. It consists of aggregate platelets only. On the contrary, venous thrombus is 'red' or permanent thrombus composed of platelets, red cells and fibrin. The first is the result of platelets' adhesion or aggregation. Instead, the permanent thrombus derives from the coagulant factors successively acting on 'white' thrombus. The different pathogenesis justifies both the distinction between 'hypercoagulability' and 'thrombophilia' and the different treatments employed. Antiphospholipid antibody syndrome, polycythemia vera, atrial fibrillation-acquired hyperhomocysteinemia, diabetes mellitus and myeloproliferative disease are the most frequent causes of acquired hypercoagulable state, prevalently responsible for deep venous thrombosis. Among the inherited forms, congenital hyperhomocysteinemia, factor V Leiden mutation, proteins C and S deficiency and antithrombin mutation are included. These may induce both venous and arterial acute events. Hyperhomocysteinemia can be congenital and acquired and is more correctly named as 'thrombophilia' rather than 'hypercoagulability'. That happens because it involves the platelets' aggregation rather than the coagulant cascade. The optimal treatment of thrombophilias consists of oral (warfarin) or injectable (heparins) anticoagulants. Direct thrombin inhibitors, platelet glycoprotein IIb/IIIa antagonists, and tissue factor inhibitors also appear to be some attractive approaches. For acquired forms, treatments of their aetiologies must also be carried out. For acquired hyperhomocysteinemia, both antiplatelets' therapy (aspirin + clopidogrel) and new direct thrombin inhibitors (as dabigatran) could be considered. Finally, as secondary prevention of an arterial acute event (stroke, IMA or peripheral ischemia) due to hyperhomocysteinemia, lifetime dual antiplatelets' therapy should be used.
authors.forename: Federico
authors.initials: F
authors.lastname: Cacciapuoti
mesh_terms: D000925:Anticoagulants / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019851:Thrombophilia / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D014859:Warfarin; D006493:Heparin; D001241:Aspirin