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18th World Congress on Heart Disease



Jeffrey S. Borer, M.D., New York, USA


Intra cardiac thrombosis and thromboembolism long have been associated with heart valve diseases (VHD). However, except when atrial fibrillation (AF) coincides with VHD, anticoagulation seldom is considered unless a valve has been replaced, particularly with a mechanical prosthesis. The recent availability of new oral anticoagulants (NOACs), more convenient to use than the long-available warfarin regimens, requires reconsideration if this issue. In fact, VHD is thrombogenic even without AF. VHD promotes (1) turbulent flow with shear stresses that cause platelet activation; (2) excess thrombin generation; (3) high platelet CD40L, promoting aggregation; (4) roughened platelet surfaces activating platelets; (5) high P-selectin, fibrinogen, von Willebrand factor and anticardiolipiin antibody titres; (6) endothelial dysfunction; (7) residual rheumatic inflammation after rheumatic fever. Moreover, prosthetic valve material activates platelets, but, at least when the mitral valve is involved, mitral replacement/repair with normalization of hemodynamics reduces platelet activation. In summary, VHD and, especially, prostheses used to replace diseased valves, are thrombogenic and are sources of systemic emboli, even without AF. VHD, especially mitral, are risk factors for AF. Antithrombotic therapy is standard when VHD and AF coincide and when valve prostheses are implanted. It is now time to reconsider such therapy in certain settings of VHD alone; NOACs may improve the therapeutic to adverse relation of antithrombotic therapy associated with warfarin, and now must be further studied in this setting.



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