Atrial fibrillation

Heart failure and atrial fibrillation promote each other in a vicious circle. The prevalence of atrial fibrillation among candidates for BiV resynchronization is high and increases with the severity of symptoms, from 5% among patients in NYHA functional class I, 10 to 25% among patients in class II and III, and 50% among patients in class IV. The presence of atrial fibrillation lowers the likelihood of response to resynchronization. Complete and consistent BiV capture, essential for a reliable response, is compromised in presence of atrial fibrillation. A proportion of patients in atrial fibrillation present with a rapid and irregular ventricular rate, which prevents a consistent capture. In addition, they cannot benefit from AV resynchronization, which contributes to the results obtained in presence of sinus rhythm. In resynchronized patients, sinus rhythm must be maintained and heart rate controlled meticulously for as long as possible, using drug therapy, if necessary. The various choices include 1) the administration of a loading dose of amiodarone and performance of cardioversion to restore sinus rhythm; 2) treatment with amiodarone or ablation of the pulmonary veins and left atrial arrhythmogenic substrate to maintain sinus rhythm; 3) the administration of a rate-controlling treatment to facilitate BiV stimulation; 4) the programming of a specific algorithm, which triggers stimulation upon sensed ventricular events; and 5) the ablation of the His bundle to eliminate the competition between spontaneous and paced rhythm.

The ablation of the AV junction by radiofrequency is a validated treatment which, when combined with the programming of a rate response, maintains the heart rate adapted to rest as well as effort and consistent BiV stimulation by eliminating the competition with spontaneous rhythm. The programming of algorithms triggering stimulation (pseudo-VVT) in patients in atrial fibrillation may be ineffective since the rate remains rapid and fusion between spontaneous activation and ventricular stimulation is often incomplete, if not absent (pseudo-fusion). Ablation of the pulmonary veins and of the left atrial substrate has been performed, although the results in patients in heart failure, whose left atrium is dilated, are suboptimal. Therefore, as a first step, attempts must be made to maintain sinus rhythm with a view to preserve the atrial contribution to ventricular filling and a range of physiologic rates at rest as well as during effort. When this strategy is unsuccessful, rate must be controlled with beta-adrenergic blockade, though ablation of the His bundle should be liberally offered in case of incomplete result, since patients in whom AV conduction is preserved and whose percentage of stimulation is low derive no benefit from this treatment.

Several algorithms can also be programmed to prevent the development of atrial fibrillation, based on various mechanisms, including increase in the percentage of atrial stimulation, decrease in the duration of post-PVC pauses, or non-competitive atrial stimulation. There is currently no proof of the efficacy of this type of algorithms in patients undergoing CRT.

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