Management of Valve Thrombosis in TAVI: Current Evidence-Based Approach

The expansion of transcatheter aortic valve implantation (TAVI) into younger and lower-risk populations has brought bioprosthetic valve thrombosis to the forefront as a clinically relevant phenomenon, both due to its potential impact on thromboembolic events and valve durability. Although clinically overt thrombosis is infrequent, subclinical leaflet thrombosis—identified as hypoattenuated leaflet thickening (HALT) on computed tomography—is a common finding and likely underdiagnosed in routine practice based on echocardiography.

From a pathophysiological standpoint, the three components of Virchow’s triad interact: flow stasis (particularly within the neosinuses, i.e., the spaces between the prosthesis and the sinus of Valsalva where flow is slower), a prothrombotic state, and endothelial injury (related to prosthetic expansion, overexpansion, or commissural misalignment). Additional factors such as male sex, higher body mass index, renal insufficiency, absence of anticoagulation, and prosthesis underexpansion have been associated with an increased risk of subclinical thrombosis.

Reported rates of HALT are approximately 12–18% at 3 months and up to 25–30% at 1 year, while clinically significant thrombosis is uncommon (<3%). Importantly, subclinical thrombosis is a dynamic phenomenon, with the potential for progression, spontaneous resolution, or response to anticoagulant therapy.

Subclinical thrombosis after TAVI: incidence, pathophysiology, and clinical relevance

The clinical impact of subclinical thrombosis remains a matter of debate. While most studies do not show a consistent association with mortality or cerebrovascular events, there is evidence suggesting a relationship with an increased risk of structural valve deterioration and prosthetic failure in the mid-term.

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Diagnosis is primarily based on cardiac computed tomography, considered the gold standard for detecting HALT and reduced leaflet motion (RLM). Echocardiography, particularly transesophageal echocardiography (TEE), plays a complementary role in assessing hemodynamic impact. A key warning sign is an increase in the mean transvalvular gradient ≥10 mmHg compared to baseline, which should prompt suspicion and further evaluation with computed tomography, even in asymptomatic patients. Additional echocardiographic and tomographic “red flags” include reduced leaflet motion, progressive gradient increase, decreased effective orifice area, or direct visualization of HALT with impaired leaflet motion, all of which support consideration of thrombosis and potential anticoagulation.

From a therapeutic perspective, evidence supports an individualized strategy. Oral anticoagulation (with vitamin K antagonists or DOACs) has proven effective in preventing and resolving subclinical thrombosis, albeit at the cost of increased bleeding risk and without demonstrated clinical benefit in patients without a prior indication. Therefore, current guidelines recommend a “less is more” approach, favoring single antiplatelet therapy in most patients.

In cases of confirmed thrombosis with hemodynamic impact, full anticoagulation is indicated. The article suggests that in patients who develop thrombosis while on DOACs, switching to vitamin K antagonists with strict INR monitoring may be considered. After resolution, long-term management should be individualized based on thrombotic and bleeding risk, with no uniform recommendation for indefinite anticoagulation. In cases of inadequate response to treatment, stepwise strategies may be considered, including treatment intensification (e.g., combination with antiplatelet agents in selected cases) or even reintervention.

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Thrombolysis is mentioned as an alternative in selected scenarios, particularly in unstable patients or in those with failure or contraindication to anticoagulation, using low-dose and slow-infusion regimens (e.g., alteplase 25 mg over 25 hours). Evidence is limited, and its use should be highly individualized.

Follow-up is based on clinical and imaging reassessment, typically with echocardiography and, in selected cases, repeat computed tomography to document resolution.

In summary, TAVI-associated thrombosis is common in its subclinical form (up to 30% at 1 year) and rare in its clinical presentation (<3%), with a still uncertain but potentially relevant impact on valve durability. Identification of “red flags,” targeted use of computed tomography, and an individualized antithrombotic strategy represent the current pillars of management.

Original Title: Transcatheter aortic valve thrombosis: mechanisms, diagnosis and clinical management.