Mitral valve thrombosis after TMVR: where do we stand?

January 16, 2020

  • The risk of THV thrombosis seems to be relevant after TMVR.
  • Routine anticoagulant therapy and serial clinical and imaging follow-up is suggested to mitigate this risk.
  • Future dedicated studies are needed to better investigate THV thrombosis and refine antithrombotic strategies after TMVR.

Numerous devices for transcatheter mitral valve replacement (TMVR) are being developed for patients with severe symptomatic mitral regurgitation (MR) who are unsuitable for open heart surgery. Early studies have provided promising results, but as with any bioprosthetic valves delivered surgically or percutaneously, there is a potential for thrombosis.

In a recent review article, dr. Matteo Pagnesi and colleagues (San Raffaele Scientific Institute, Milan, Italy) review the current evidence regarding the thrombotic risk after TMVR as well as the antithrombotic strategies to mitigate it. Randomized trials are still needed to determine the best antithrombotic strategies for patients undergoing TMVR, but this review makes clinicians aware that valve thrombosis is a major issue in this setting, more so than in aortic interventions.

Thrombotic Risk after TMVR

According to available early evidence, the thrombotic risk seems to be relevant after transcatheter mitral valve replacement (TMVR), with multiple mechanisms implicated in transcatheter heart valve (THV) thrombosis involving procedure-, device-, and patient-related factors. A detailed pre-procedural screening is important to identify patients with particularly high thrombotic risk features and evaluate the patient’s individual bleeding risk. An anticoagulation-based antithrombotic strategy should be considered to prevent THV thrombosis and thromboembolic (TE) events after TMVR, tailoring the intensity and duration of the prescribed antithrombotic regimen to the individual bleeding and thrombotic risk profile. Serial clinical and imaging follow-up is suggested to promptly detect and treat thrombotic THV dysfunction. AF, atrial fibrillation; LV ¼ left ventricular; MV, mitral valve; ViMAC, valve-in-mitral annular calcification; ViR , valve-in-ring; ViV , valve-in-valve.

Limited Evidence Available

Due to the lack of evidence regarding antithrombotic strategies after TMVR, Pagnesi et al begin their review by looking at the literature on surgical bioprosthetic aortic or mitral valve replacement. In the aortic space, there are data suggesting that embolic events are reduced with a combination of warfarin and aspirin, with some evidence that extending anticoagulation for up to 6 months improves survival and reduces stroke and other thromboembolic events at the cost of more bleeding. There are no “robust” studies on surgical bioprosthetic MV replacement, but the authors say that thrombotic risk appears to be higher here when compared with aortic operations.

European and US guidelines recommend consideration of oral anticoagulation using a VKA for 3 to 6 months after surgical bioprosthetic MV replacement. However, there are no recommendations for antithrombotic therapy after TMVR, a procedure still in the early stages of development. A review of studies on TMVR for native disease, degenerated bioprostheses (valve-in-valve), failed annuloplasty (valve-in-ring), and severe mitral annular calcification (valve-in-MAC) showed rates of valve thrombosis ranging from about 6% to 14.4% over various lengths of follow-up. Most patients received a VKA plus aspirin at discharge, and there are hints in the data to suggest that this strategy cuts the risk of thrombosis relative to not being on oral anticoagulation.

It seems reasonable to prescribe oral anticoagulation with VKA in the first months after any TMVR procedure in patients who do not have an indication for long-term anticoagulation to mitigate the risk of transcatheter heart valve thrombosis. The duration of anticoagulant therapy and the eventual association of antiplatelet therapy could be tailored through a careful evaluation of the patient’s individual bleeding risk, even though this strategy is empirical and not based on dedicated studies.

Late Valve Thrombosis

Pagnesi et al also raise the issue of late valve thrombosis occurring after the initial postprocedural period covered by oral anticoagulation therapy. Considering the wide time frame of device thrombosis after TMVR, serial echocardiographic surveillance and clinical follow-up is fundamental to promptly detect and treat thrombotic transcatheter heart valve dysfunction.

In cases of clinical suspicion (new-onset heart failure symptoms with acute or subacute presentation, new thromboembolic events) and suggestive transthoracic echocardiographic features of transcatheter heart valve thrombosis (direct visualization of thrombus in rare cases, 50% mean gradient increase, thickened cusps, restricted leaflet mobility), prompt evaluation with transesophageal echocardiography or [CT] scan is indicated, with specific treatment according to clinical presentation and patients’ profile in cases of confirmed transcatheter heart valve thrombosis (initiation or intensification of anticoagulation, thrombolysis, surgery, or transcatheter valve-in-valve).

Some patients will have such a high bleeding risk that anticoagulation may not be advisable, the authors note, and close follow-up will be important in this scenario, too.

In patients deemed to be at very high (prohibitive) bleeding risk, with an expected risk of anticoagulant-related bleeding events potentially higher and more concerning than the transcatheter heart valve-related thromboembolic risk, the adoption of an antiplatelet-only strategy without anticoagulation seems to be inevitable. In these cases, strict clinical and imaging follow-up is recommended to exclude the occurrence of thrombosis.


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