Why the study?
Left atrial appendage occlusion prevents thromboembolic events in atrial fibrillation patients with bleeding risk, but device-related thrombosis remains a clinical challenge.
A high-fidelity computational model successfully replicated clinical device-related thrombosis post-LAAO, providing mechanistic proof-of-concept that optimized device positioning or low-dose apixaban can prevent localized fibrin accumulation.
BACKGROUND: Left atrial appendage occlusion prevents thromboembolic events in atrial fibrillation patients with bleeding risk, but device-related thrombosis (DRT) remains a challenge. CASE SUMMARY: -VASc score = 3) and prior intracranial hemorrhage underwent successful left atrial appendage occlusion with a 22-mm Amplatzer Amulet. After stepping down from apixaban to aspirin, DRT developed. Thrombi resolved with apixaban but recurred on its discontinuation. A multiscale model integrating hemodynamics, thrombus formation events, and apixaban revealed fibrin buildup beneath the pulmonary ridge, matching clinical thrombus. Optimized placement alone prevented fibrin formation in the virtual model. DISCUSSION: Pulmonary ridge coverage and low-dose direct oral anticoagulants have emerged as effective strategies to reduce DRT. This case links both mechanisms, showing recurrence due to incomplete ridge coverage and antithrombotic decision. TAKE-HOME MESSAGES: Our high-fidelity model offers mechanistic insight about antithrombotic therapy, which cannot be assessed with flow-based simulations alone. The results presented provide proof-of-concept evidence of the model's capabilities.
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Segarra-Queralt et al. (2025) studied this question.
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