Modern aspects of antithrombotic treatment: an introduction.
Intracardiac thrombosis and cardioembolisms may have impressive effects on quality of life, prognosis and therapeutic costs in patients with valve disease or replacement devices. Distinct pathophysiological differences exist regarding intracardiac thrombus formation in low-versus high-pressure areas. Important cardiac confounders for low-pressure areas are left atrial geometry and function, including atrial fibrillation or loss of active atrial contraction. In high-pressure areas, flow velocity and shear stress are raised, and this may result in flow turbulence, for example when blood passes a stenotic area. Other major factors which correlate with intracardiac thrombus formation are implantation of polymer material and the degree of endocardial damage resulting for example, from infective or rheumatic endocarditis. Because of the interaction of platelets and the plasma clotting system, a combination of oral anticoagulation therapy and antiplatelet drugs should prevent more thromboembolic events than might anticoagulation alone. Recent studies in patients with prosthetic heart valves have indicated a positive risk-benefit profile if low-dose antiplatelet drugs are added to moderate intensive oral anticoagulation therapy. Thromboembolic events and bleeding complications due to oral anticoagulation therapy are accepted key parameters to demonstrate the superiority of one replacement device over another. However, there is no consistent system for reporting morbid events. In order to organize low and narrow target INR ranges, point-of-care patient self-testing modalities have been introduced and used effectively in large sample sizes. In the near future, some promising new drugs--including direct thrombin or factor Xa inhibitors with broader therapeutic ranges and thus fewer side effects--will become available. The test for these drugs will be their potential to prevent intracardiac thrombosis and cardioembolism in a patient population which is under significant risk.
Horstkotte
Dieter
D
Department of Cardiology, Heart Center North Rhine-Westphalia, Ruhr University Bochum, Bad Oeynhausen, Germany. akohlstaedt@hdz-nrw.de
Piper
Cornelia
C
D000925:Anticoagulants / Q000627:therapeutic use*; D003328:Coronary Thrombosis / Q000150:complications / Q000188:drug therapy*; D004359:Drug Therapy, Combination; D004617:Embolism / Q000150:complications / Q000188:drug therapy*; D006349:Heart Valve Diseases / Q000150:complications; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D015912:Thrombolytic Therapy; D014859:Warfarin / Q000627:therapeutic use
D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D014859:Warfarin