Atrial defibrillation threshold in humans minutes after atrial fibrillation induction; "A stitch in time saves nine".

AIMS: To assess the effects of atrial fibrillation duration on the defibrillation threshold in atrial fibrillation patients seconds or minutes after initiation of the arrhythmia. METHODS AND RESULTS: Nineteen patients with recurrent symptomatic atrial fibrillation were evaluated. After programmed induction of atrial fibrillation, the defibrillation threshold was assessed after two sequential periods of arrhythmia in the same patient: an "ultrashort" period of 30 s duration and a "short" period, which lasted 10 min. After the specified period, internal cardioversion was attempted using a balloon-guided catheter that allows the delivery of biphasic shocks between one electrode array placed in the left pulmonary artery and a proximal electrode array on the lateral right atrial wall. The defibrillation threshold was assessed with energy steps of 0.5 J with a starting level of 0.5 J. Mean time from induction to successful defibrillation was 92+/-30 s after the "ultrashort" period of atrial fibrillation and 910+/-86 s after the short period. The defibrillation threshold was significantly greater after 10 min of atrial fibrillation than after 30 s of arrhythmia (2.32+/-0.61 J vs 1.31+/-0.66 J, P<0.001). Clinical data were not found to affect the defibrillation threshold. CONCLUSIONS: Prolongation of atrial fibrillation over minutes in patients with paroxysmal arrhythmia increases the energy requirements for successful defibrillation.

Sinus pacemaker function after cardioversion of chronic atrial fibrillation: is sinus node remodeling related with recurrence?

INTRODUCTION: The objective of this study was to investigate the temporal changes in sinus node function in postcardioversion chronic atrial fibrillation (AF) patients and their possible relation with the recurrence rates of AF. METHODS AND RESULTS: In 37 chronic AF patients, internally cardioverted to sinus rhythm, corrected sinus node recovery time (CSNRT), and the pattern of corrected return cycle lengths were assessed 5 to 20 minutes and 24 hours after conversion. The last 20 consecutive patients also were evaluated after autonomic blockade. Twenty subjects with normal atrial structure and no history of AF served as the control group. Patients were followed-up for 1 month for recurrence, and the density of supraventricular ectopic beats per hour was obtained during the first 24 hours after conversion. Fifteen patients (40.5%) relapsed during follow-up. CSNRT values at 600 msec (371 +/- 182 msec) and 500 ms (445 +/- 338 msec) were significantly higher than those of control subjects (278 +/- 157 msec, P = 0.050, and 279 +/- 130 msec, P = 0.037, respectively). Significant temporal changes in CSNRT also were observed during the first 24 hours after conversion (600 msec: 308 +/- 120 msec, P = 0.034; 500 msec: 340 +/- 208 msec, P = 0.017). No significant interaction and temporal effects were observed with regard to corrected return cycle length pattern. Similar data regarding CSNRT and corrected return cycle length pattern were obtained after autonomic blockade. Patients with abnormal CSNRT after cardioversion had higher recurrence rates (50%) than those with normal function (37%; P = NS). Patients who relapsed had a higher density of supraventricular ectopic beats per hour (159 +/- 120) compared with those who did not (35 +/- 37; P = 0.001). CONCLUSION: Depressed sinus node function is observed after conversion of chronic AF. Recovery from this abnormality and its independence from autonomic function suggest that AF remodels the sinus node. Our data do not support a causative role of sinus node function in AF recurrence, but they do indicate such a role for the density of atrial ectopic beats.