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