# Thrombotic Versus Bleeding Risk After Transcatheter Aortic Valve Implantation

## TL;DR

This paper reviews the risks of blood clots and bleeding after a heart valve procedure and suggests the safest and most effective treatment strategies.

## Contribution

The paper provides a comprehensive review of antithrombotic therapy strategies and emerging biomarker-based approaches for personalized risk assessment after TAVI.

## Key findings

- Thrombotic events are mostly early and procedural, while new-onset atrial fibrillation increases late risk.
- Single antiplatelet therapy is best for patients without OAC need, and OAC alone for those with AF.
- Biomarkers and machine learning may help personalize risk assessment in the future.

## Abstract

Background: Transcatheter aortic valve implantation (TAVI) is increasingly used across all risk groups, meaning more patients are living long-term with transcatheter bioprosthetic valves. These patients are often multimorbid and vulnerable to both thrombotic and bleeding complications. Optimal antithrombotic therapy remains uncertain due to differences in trial design, patient demographics, and procedural practices. Methods: We undertook a narrative review that included randomised controlled trials, observational studies, biomarker research, and guideline recommendations on post-TAVI antithrombotic therapy. We evaluated the available evidence for antiplatelet and anticoagulant strategies after TAVI, predictors of bleeding and thrombotic complications, to identify emerging approaches using biomarkers for personalised risk stratification. Results: Thrombotic events after TAVI are predominantly early and procedural in origin, while new-onset atrial fibrillation (AF) leads to substantial late risk. Subclinical leaflet thrombosis is frequent, but its clinical significance remains uncertain, as anticoagulation reduces CT-detected leaflet abnormalities without improving clinical outcomes. Early bleeding within the first 30 days remains a principal contributor to mortality, influenced by frailty, vascular access, comorbidity, and intensity of antithrombotic therapy. Randomised evidence consistently supports a minimalist, indication-driven regimen: single antiplatelet therapy for patients without an oral-anticoagulation (OAC) indication, and OAC monotherapy for those with AF. Routine OAC use in unselected patients carries no advantage and exposes them to harm. Biomarkers and machine-learning models show promise for future individualised risk assessment. Conclusions: Antithrombotic strategies post-TAVI should prioritise minimising bleeding while maintaining adequate thromboembolic protection. Single antiplatelet therapy for patients without an indication for OAC and OAC alone for those with AF offer the best balance of safety and efficacy. Ongoing trials may clarify the role of imaging-guided therapy and biomarker-based risk stratification and refine antithrombotic strategies.