Subclinical leaflet thrombosis was firstly described in a case report in 2013, 7 days after TAVR while doing routine MDCT imaging ( 17). Based on retrospective observational registries, the incidence of clinical valve thrombosis in TAVR patients is estimated to be 0.6 to 2.8% ( 15, 16). More recently, this phenomenon of clinical valve thrombosis has also been described following TAVR. The patient presented with dyspnea NYHA class 3b and echocardiography revealed a mean transvalvular gradient of 37 mmHg (C,D) The thrombotic mass at the prosthetic leaflets was confirmed by intracardiac echocardiography from the ascending aorta.įollowing surgical aortic valve replacement (SAVR) with a bioprosthesis, the incidence of clinical valve thrombosis has been reported to range between 0.3 and 6.0% ( 11– 14). (A,B) Transesophageal echocardiography (TEE) showing thrombosis and turbulent color flow over a bioprosthetic aortic valve in a patient who underwent transcatheter aortic valve replacement 6 years earlier. The clinical appearance of this phenomenon may be either symptoms of heart failure, or left sided thrombo-embolic event.Ĭlinical valve thrombosis. Prosthetic valve dysfunction may be provoked by reduced leaflet motion or impaired leaflet coaptation caused by thrombus, but it is important that this gets differentiated from other causes such as valve degeneration, fibrotic pannus ingrowth or endocarditis ( Figure 1). Thereby, it is important to make the difference between two different entities: clinical valve thrombosis and subclinical leaflet thrombosis.Ĭlinical valve thrombosis is defined as clinical apparent prosthetic valve dysfunction with the typical finding of a mobile mass/thrombus on the prosthetic heart valve as visualized by echocardiography or multi-detector computed tomography (MDCT). However, despite the less thrombogenic profile of bioprosthetic heart valves, recent studies also report the occurrence of valve/leaflet thrombosis in different types of transcatheter and surgical aortic bioprosthesis ( 2– 10). This is not the case for patients who receive a surgical or transcatheter bioprosthetic heart valve, for which long-term treatment with antiplatelet therapy (APT) seems to be sufficient. Following implantation of mechanical valve prostheses, patients have to take life-long oral anticoagulant (OAC) therapy. This review article summarizes the currently available data within the field of transcatheter aortic valve/leaflet thrombosis and discusses the need for a patient tailored antithrombotic approach.Īlthough prosthetic valve thrombosis is a well-known risk for mechanical heart valves, this risk is much less recognized in bioprosthetic heart valves. Oral anticoagulant therapy protects against and resolves both clinical valve thrombosis and subclinical leaflet thrombosis however, large-scale randomized clinical trials studying different antithrombotic strategies after TAVR are still under way. Whereas, clinical valve thrombosis requires treatment, the clinical impact and need for intervention in subclinical leaflet thrombosis is still uncertain. Even in case of HAM, the transvalvular pressure gradient remains within normal range and does not provoke heart failure symptoms. This phenomenon may also affect leaflet motion and is then classified as Hypo-Attenuation affecting Motion (HAM). Subclinical leaflet thrombosis is most often an incidental finding, characterized by a thin layer of thrombus covering the aortic side of one or more leaflets it is also referred to as Hypo-Attenuating Leaflet Thickening (HALT) as described on multi-detector computed tomography (MDCT) imaging. In clinical valve thrombosis, obstructive thrombus formation leads to an increased transvalvular gradient, often provoking heart failure symptoms. Antithrombotic therapy after TAVR aims to prevent transcatheter heart valve (THV) thrombosis, in which two different entities have to be recognized: clinical valve thrombosis and subclinical leaflet thrombosis. Transcatheter aortic valve replacement (TAVR) has become an established therapeutic option for patients with symptomatic, severe aortic valve stenosis at increased surgical risk.
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