Antithrombotic Therapy after Structural Heart Disease Intervention.

BACKGROUND: Structural heart disease interventions, including transcatheter aortic valve implantation (TAVI), transcatheter edge-to-edge repair (TEER), patent foramen ovale (PFO) closure, and left atrial appendage closure (LAAC), have transformed the management of valvular and congenital heart disease. However, antithrombotic therapy following these procedures remains a major challenge, as clinicians must balance the prevention of thromboembolic events with the risk of bleeding. Evidence from randomized trials and registries has provided guidance, yet optimal strategies are still evolving.

METHODS: This review synthesizes current evidence regarding antithrombotic therapy in structural heart disease. We examined published randomized controlled trials, observational studies, and guideline recommendations from mainly 2015 to 2025. The focus was on post-procedural antithrombotic regimens, including single antiplatelet therapy (SAPT), dual antiplatelet therapy (DAPT), and oral anticoagulation, as well as their impact on clinical outcomes such as stroke, systemic embolism, device-related thrombosis, and major bleeding.

RESULTS: In TAVI, early studies favored DAPT to reduce thromboembolic complications, but subsequent trials demonstrated increased bleeding without significant benefit compared to SAPT. Current guidelines increasingly recommend SAPT in patients without concomitant indications for anticoagulation. In TEER, antithrombotic therapy is less standardized; anticoagulation is generally continued in patients with atrial fibrillation, while antiplatelet therapy is used in sinus rhythm. For PFO closure, short-term DAPT (3-6 months) followed by SAPT is widely adopted to prevent device-related thrombosis, with long-term therapy tailored to stroke risk. In LAAC, anticoagulation combined with antiplatelet therapy is typically prescribed for 45 days to 3 months until device endothelialization occurs, after which SAPT is sufficient. Across all interventions, bleeding risk remains a critical determinant of therapy duration and intensity, particularly in older and comorbid populations.

CONCLUSION: Antithrombotic therapy in structural heart disease requires individualized decision-making that integrates procedural type, patient comorbidities, and bleeding risk. Recent evidence supports a trend toward simplified regimens, with SAPT increasingly favored over DAPT in TAVI and tailored strategies in TEER, PFO closure, and LAAC. Despite advances, significant heterogeneity persists, underscoring the need for further randomized trials to refine optimal regimens. Clinicians must remain vigilant in balancing thromboembolic protection with bleeding avoidance, as antithrombotic therapy continues to play a pivotal role in the success of structural heart interventions.