Anticoagulation and thromboembolic risk management in pharmacological and electrical cardioversion of atrial fibrillation: State of the evidence and knowledge gaps.

Pharmacological and electrical cardioversion of atrial fibrillation (AF) is associated with markedly increased (>10-fold) risk of thromboembolic events clustering within 7 days following sinus rhythm restoration. Current evidence indicates that post-cardioversion thrombus formation from atrial stunning, rather than preexisting thrombus, causes most thromboembolic complications. Risk factors include traditional CHA2DS2-VASc components (particularly heart failure), AF duration ≥12 h, mitral valve stenosis, cardiac amyloidosis and hypertrophic cardiomyopathy. While placebo-controlled randomized trials are lacking, there is overwhelming observational evidence that oral anticoagulation (OAC) reduces post-cardioversion thromboembolism by 60-80 % to a residual risk of approximately 0.5 %. This benefit seems independent of CHA2DS2-VASc and AF duration (including <48 h). Current guidelines recommend OAC for ≥3 weeks before and ≥4 weeks after cardioversion, or to rule out intracardiac thrombus by imaging, with OAC immediately before cardioversion and for ≥4 weeks. The safety of this strategy was validated in large prospective trials. However, alternative durations of pre-/post-cardioversion OAC have never been tested in randomized trials. The optimal duration of pre-cardioversion OAC remains unclear. Shorter pre-cardioversion delay is associated with increased success of cardioversion, reduced AF recurrence, reduced severity and duration of atrial stunning, and possibly reduced thromboembolic complications. Likewise, antiarrhythmic drug (AAD) pre-treatment improves cardioversion outcomes but is sometimes withheld by fear of early sinus rhythm restoration and associated thromboembolic risk. Randomized data from the ACUTE trial have shown that early AAD introduction was safe. Given the short-lived but dramatic increase in thromboembolic risk post-cardioversion, intensifying OAC immediately before cardioversion might further reduce risk, as suggested by observational studies.