Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

A major complication associated with prosthetic heart valves is valve thrombosis and embolization. Depending on the valve design these complications should be almost eliminated by anticoagulants or aspirin. However, valve thrombosis and embolism may occur despite apparently adequate anticoagulation. The question is whether these thrombi arise as a result of local factors such as the foreign surface and disturbance of flow at the valve site, or as a result of alteration of the hemostatic balance within the blood favoring thrombus formation. Such a disturbance, known as hypercoagulability, is the result of increased platelet activation or coagulation, or diminished fibrinolytic activity. In this article the underlying mechanism of the coagulation and fibrinolytic mechanisms is discussed, with particular emphasis on the pathways, by which activation of the coagulation system or an increase in the inhibition of fibrinolysis might occur. The laboratory tests which might be useful in detecting platelet activation, activation of coagulation or fibrinolytic activity are discussed. The potential significance of raised blood viscosity associated with a rise in fibrinogen is emphasized, in particular the fact that elevated fibrinogen is a risk marker of many types of occlusive vascular disease. Whether raised fibrinogen is causal in the pathogenesis of thrombosis at the valve site, or merely is a consequence of the prosthesis, is not known. There is some information on the fact that patients with intracardiac, and left atrial thrombi in atrial fibrillation, have activation of coagulation as shown by elevated levels of markers and also raised von Willebrand factor levels. However, it is emphasized that large scale prospective studies, in which the risk markers are measured, and then the patients with prosthetic valves followed to determine whether or not they experience clinical embolic events has not been carried out. It is unlikely that a single hemostatic test, or indeed, a number of tests, will be able to predict with accuracy the individual who is at particular risk of embolism. Nevertheless, it is important that we seek to gain further information of the mechanisms of prosthetic valve thrombus formation, and then apply this knowledge in controlled clinical trials. Only this way will better anticoagulant and antithrombotic control of these devastating embolic events be achieved.


Journal article


J Heart Valve Dis

Publication Date





7 - 17


Blood Coagulation, Blood Coagulation Disorders, Blood Coagulation Tests, Blood Platelets, Embolism, Fibrinolysis, Heart Valve Prosthesis, Humans, Risk Factors, Thrombosis