According to Virchow's triad, factors predisposing to thrombus formation can be divided into endothelial, haemodynamic and haemostatic factors.5 Endothelial factors represent biocompatibility of the prosthesis itself and interaction between the prosthesis and the suture zone. Tissue cicatrisation and endothelialisation characteristically require a few weeks to be complete. Haemodynamic factors include both haemodynamic characteristics of the prosthesis, as well as overall cardiac haemodynamic status. Although the profile of new generation mechanical bileaflet valves is largely superior to that of earlier generation prostheses (and thus associated with a lower occurrence of thromboembolic complications), localised regions of turbulent flow can still develop and lead to stasis and thrombus formation. In addition, the location of the prosthesis plays an important role in thrombogenicity. Obstruction of a tricuspid mechanical prosthesis is 20 times more frequent than left‐sided PVT. Similarly for haemodynamic reasons, mitral PVT is 2–3 times more frequent than thrombosis of an aortic prosthesis. Haemodynamic status can also favour thrombosis, particularly in conditions of low flow or reduced cardiac output. Haemostatic factors involve the adequacy of anticoagulant treatment. In this regard, the early postoperative period represents a particular challenge with the need to balance the risks of over‐anticoagulation and associated haemorrhagic complications with those of under‐anticoagulation and thrombosis.6 Similarly, interruption of oral anticoagulant treatment for anticipated non‐cardiac surgery7 and pregnancy8 represent high risk situations for patients with prosthetic valves.
Although PVT can present acutely with a fresh thrombus, it is most often a subacute or chronic phenomenon. Thrombi are typically formed of different clot layers, with variable degrees of organisation. Interestingly, recent surgical studies have underlined the high prevalence of fibrous pannus formation (present between 45–75% of cases), that is also associated with a risk of thrombosis. Caused by an excessive cicatricial response, pannus formation is usually observed in proximity to the suture site and can be located on both sides of the prosthesis, with variable degrees of obstruction.9 Finally, obstruction may also be caused by a vegetation in the context of prosthetic valve endocarditis.