Key result
VKAs or NOACs anchor TAV thrombosis treatment, with low-dose thrombolytics reserved for unstable patients.
Why the study?
Transcatheter aortic valve thrombosis manifests as subclinical leaflet thrombosis or clinical valve thrombosis, but its treatment has been understudied.
What is the optimal management strategy for transcatheter aortic valve thrombosis?
What is the optimal management strategy for transcatheter aortic valve thrombosis?
This review proposes a treatment algorithm for TAV thrombosis, highlighting VKAs or NOACs as first-line therapy and low-dose thrombolytics for refractory or unstable cases.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“No one knows how much subclinical valve thrombosis truly matters. Even in low-risk patients, these cases come and go. The rate is definitely higher than what we probably should be seeing—it's over 20%—[but] some disappear, and some appear. So we just don't know what kind of conditions, whether it's patient, anatomic, device-related, or procedure factors, we can pinpoint to better prevent this from happening.”
“We're seeing that the whole idea of management of HALT really needs a paradigm shift in thinking. Up-front prophylaxis with anticoagulant therapy appears to offer little to no benefit in terms of stroke prevention [but] a real risk of bleeding. The data suggest maybe we were too aggressive with stroke prevention [through] anticoagulation.”
“Although SLT does not always manifest with symptoms or hemodynamic dysfunction, its association with transient neurological events and long-term valve degeneration underscores its clinical relevance. The proposed echocardiographic and MSCT follow-up should be essential; however, its widespread implementation is limited by associated costs and routine availability of these techniques. Additionally, the dilemma between efficacy and safety in anticoagulant selection remains challenging.”
Supports anticoagulation cornerstone in TAV thrombosis; leaves open thrombolytic role without prospective confirmation.
Transcatheter aortic valve (TAV) thrombosis may manifest as subclinical leaflet thrombosis (SLT) and clinical valve thrombosis. SLT is relatively common (10%-20%) after transcatheter aortic valve replacement, but clinical implications are uncertain. Clinical valve thrombosis is rare (1.2%) and associated with bioprosthetic valve failure, neurologic or thromboembolic events, heart failure, and death. Treatment for TAV thrombosis has been understudied. In principle, anticoagulation may prevent TAV thrombosis. Non-vitamin K oral anticoagulants, as compared to antiplatelet therapy, are associated with reduced incidence of SLT, although at the cost of higher bleeding and all-cause mortality risk. We present an overview of existing literature for management of TAV thrombosis and propose a rational treatment algorithm. Vitamin K antagonists or non-vitamin K oral anticoagulants are the cornerstone of antithrombotic treatment. In therapy-resistant or clinically unstable patients, ultraslow, low-dose infusion of thrombolytics seems effective and safe and may be preferred over redo-transcatheter aortic valve replacement or explant surgery.
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Adrichem et al. (2024) conducted a review in Transcatheter aortic valve (TAV) thrombosis. Anticoagulation and thrombolytics was evaluated. Vitamin K antagonists or non-vitamin K oral anticoagulants are the cornerstone of antithrombotic treatment for TAV thrombosis, with low-dose thrombolytics as an option for unstable patients.
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