Long-term antiarrhythmic drugs (AADs)

The choice of AAD for long-term maintenance of sinus rhythm and to prevent recurrent AF needs to account for comorbidities, cardiovascular risk factors, the potential for serious pro-arrhythmia and extra-cardiac toxic effects, patient preferences and symptom burden. For instance, amiodarone is more effective in preventing AF recurrences than other AAD, but extra-cardiac toxic effects are common and increase with the duration of treatment. As a result, the guidelines suggest considering other AADs before using amiodarone.5

The ESC/EHRA guidelines suggest (Figure 16):5

  • dronedarone, flecainide, propafenone or sotalol to prevent recurrent symptomatic AF in patients with normal left ventricular function and without pathological left ventricular hypertrophy
  • dronedarone to prevent recurrent symptomatic AF in patients with stable coronary artery disease and without CHF
  • amiodarone to prevent recurrent symptomatic AF in CHF patients
  • clinicians should periodically evaluate the AAD to confirm patients’ eligibility 
Initiation of long-term rhythm control in symptomatic atrial fibrillation patients

Figure 16. Initiation of long-term rhythm control in symptomatic atrial fibrillation patients.5

ECG recording during the initiation of an AAD should be considered to monitor heart rate, detect QRS and QT interval prolongation and AV block. The guidelines do not recommend AADs in people with a QT interval of more than 0.5 seconds or those with significant node disease or atrioventricular node dysfunction who do not have a functioning permanent pacemaker. If the patient does not want to undergo ablation or the approach is not indicated, clinicians could consider adding atrial-based bradycardia pacing to drug treatment that induces or exacerbates sinus node dysfunction to allow AAD treatment to continue. If recurrences seem likely, AAD could be considered following AF ablation to maintain sinus rhythm.5

Some non-AAD drugs have antiarrhythmic effects.5 As previously mentioned, the RAAS is implicated in the pathogenesis of some cases of AF.6 ACE inhibitors and ARB, both of which modulate this system, as well as beta-blockers may prevent new-onset AF in patients with CHF and reduced ejection fraction. ACE inhibitors and ARBs may also prevent of new-onset AF in patients with hypertension, particularly when associated with left ventricular hypertrophy. ACE inhibitors and ARBs are not recommended for the secondary prevention of paroxysmal AF in patients with little or no underlying heart disease.5

The next section summarises invasive management of atrial fibrillation

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