Mean Atrial Fibrillation Cycle Length Research Articles

New method of determining the atrial fibrillation cycle length during human atrial fibrillation.

The aim of this study was to investigate the usefulness of the autocorrelation function (reversed fast Fourier transform analysis) in determining the atrial fibrillation cycle length (AFCL) during human atrial fibrillation (AF). From 30 episodes of atrial electrograms recorded for 30 seconds from the high right atrium during type I AF in 16 patients, the mean, 5th percentile (p5), and 95th percentile (p95) of the AFCLs were measured by using a computer-picked activation time. The peak, minimum, and maximum AFCLs also were measured by using the autocorrelation function. The mean AFCL was retrieved at the point of the maximum peak of the coefficient of the first positive autocorrelogram. The minimum AFCL (min AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from negative to positive, and the maximum AFCL (max AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from positive to negative. There was a significantly strong correlation between the mean and peak AFCLs (r = 0.995, P < 0.0001), p5 and min AFCLs (r = 0.953, P < 0.0001), and p95 and max AFCLs (r = 0.98, P < 0.0001). The autocorrelation function was useful in determining the AFCLs, at least during type I AF. The min AFCL may be used as an index of the refractory period during AF when the p5 AFCL approximates the refractory period.

Nonreentrant focal activations in pulmonary veins in canine model of sustained atrial fibrillation.

Repetitive rapid activities are present in the pulmonary veins (PVs) in dogs with pacing-induced sustained atrial fibrillation (AF). The mechanisms are unclear. We induced sustained (>48 h) AF by rapidly pacing the left atrium (LA) in six dogs. High-density computerized mapping was done in the PVs and atria. Results show repetitive focal activations in all dogs and in 12 of 18 mapped PVs. Activation originated from the middle of the PV and then propagated to the LA and distal PV with conduction blocks. The right atrium (RA) was usually activated by a single large wavefront. Mean AF cycle length in the PVs (left superior, 82 +/- 6 ms; left inferior, 83 +/- 6 ms; right inferior, 83 +/- 4 ms) and LA posterior wall (87 +/- 5 ms) were significantly (P < 0.05) shorter than those in the LA anterior wall (92 +/- 4 ms) and RA (107 +/- 5 ms). PVs in normal dogs did not have focal activations during induced AF. No reentrant wavefronts were demonstrated in the PVs. We conclude that nonreentrant focal activations are present in the PVs in a canine model of pacing-induced sustained AF.

Atrial fibrillation produced by prolonged rapid atrial pacing is associated with heterogeneous changes in atrial sympathetic innervation.

Structural and electrophysiological changes of the atria occur with prolonged rapid rates; however, the effects of sustained atrial fibrillation (AF) on autonomic innervation of the atria are unknown. We hypothesized that electrophysiological remodeling from rapid atrial rates is accompanied by altered atrial autonomic innervation. Six dogs (paced group) underwent atrial pacing at 600 bpm; 9 dogs (control animals) were not paced. All paced dogs developed sustained AF by week 4 of pacing. All 15 animals underwent positron emission tomography imaging of the atria with [C-11] hydroxyephedrine (HED) to label sympathetic nerve terminals. HED retention in the atria was significantly greater in paced dogs compared with control animals (P=0.03). Tissue samples from the atrial appendages had a greater concentration of norepinephrine in paced animals than in control animals (P=0.01). The coefficient of variation of HED retention was also greater in paced animals (P=0.05) and was greater in the right atrium than in the left atrium (P=0.004). Epicardial activation maps of AF were obtained in the paced animals at baseline and with autonomic manipulation. Mean AF cycle length was longer in the right atrium (109.2+/-5 ms) than in the left atrium (85.8+/-5.5 ms) at baseline (P=0.005). AF cycle length did not vary significantly from baseline (97.6+/-13.4 ms) with stellate stimulation (100.5+/-6 ms) but lengthened with propranolol (107.5+/-6.1 ms, P=0.03). Rapid rates of AF produce a heterogeneous increase in atrial sympathetic innervation. These changes parallel disparate effects of rapid pacing-induced AF on atrial electrophysiology.

Functional mechanisms underlying tachycardia-induced sustained atrial fibrillation in a chronic dog model.

Rapid atrial activation causes electrical remodeling that promotes atrial fibrillation (AF), but underlying mechanisms are incompletely understood. We applied epicardial mapping to evaluate atrial electrophysiology and AF duration in dogs subjected to rapid atrial pacing (400/min). Dogs paced for 1 (P1, n=7), 7 (P7, n=13), or 42 (P42, n=7) days were compared with sham dogs (P0, n=13). Atrial pacing progressively increased AF duration. Atrial effective refractory period (ERP) and ERP accommodation to rate were significantly decreased by pacing, with near-maximal changes within 7 days. Atrial conduction velocity decreased more slowly, with maximum changes at 42 days, contributing to increases in AF duration after ERP stabilized. Stepwise multilinear regression indicated that both wavelength (P=.02) and duration of pacing (P=.0001) were independent determinants of changes in AF duration. Mean atrial fibrillation cycle length (AFCL) at 112 recording sites decreased with increased duration of rapid pacing (P<.001), and the SD of AFCL increased progressively (P<.0001), together accounting for 72% of the variance in AF duration. Increases in AFCL variability were due to regionally determined differences in AFCL changes caused by rapid pacing. The number of zones of reactivation per cycle of AF increased as AF became more sustained, consistent with multiple-wavelet reentry. Rapid atrial activation causes time-dependent decreases in ERP, conduction velocity, and wavelength, which, along with increased regional heterogeneity, provide a substrate for AF. The conduction abnormalities and increased regional heterogeneity previously noted in patients with AF may be a consequence, as well as a cause, of the tachyarrhythmia.

Simple Left Atrial Procedure for Chronic Atrial Fibrillation Associated With Mitral Valve Disease

Background. A computerized 48-channel mapping system was used to investigate the characteristics of an atrial epicardial electrogram during chronic atrial fibrillation (AF) in patients with solitary mitral valve disease. We have devised a simple left atrial procedure to eliminate the chronic AF during a mitral valve operation. Methods. Using this mapping system, we performed intraoperative atrial mapping in 11 patients with chronic AF associated with mitral valve disease. The AF duration ranged from 0.4 to 15 years (mean, 8.0 ± 4.5 years). A simple surgical ablation of the AF on the left atrium only was performed during the mitral valve operation. Results. The mean AF cycle length of the atria ranged from 129 to 169 milliseconds in the right atrium and from 114 to 139 milliseconds in the left atrium. The mean AF cycle length of the left atrium was shorter than that of the right atrium. Regular and repetitive activation was found in the left atria of 7 of 11 patients. The AF disappeared in all patients immediately after the operation, and 10 of these patients continued to have a sinus rhythm postoperatively (AF-free rate, 91%). Conclusions. Computerized intraoperative mapping revealed a shorter mean AF cycle length in the left atrium. A simple left atrial procedure was effective in eliminating chronic AF associated with solitary mitral valve disease.

Response of type I atrial fibrillation to atrial pacing in humans.

High-density mapping studies of atrial fibrillation (AF) have suggested the presence of an excitable gap. The purpose of this study was to assess the local and left atrial response to pacing at the high right atrium during type I AF in humans. Pacing was performed at the high right atrium during type I AF in 24 patients in the electrophysiology laboratory. The response to pacing was assessed at cycle lengths 10, 20, 30, 40, and 50 ms less than the mean baseline atrial cycle length. Digitized tracings of the baseline tachycardia and the response to pacing were recorded from the high right atrium and from the distal coronary sinus. Computer analysis of these signals was used to calculate a left atrial electrogram density before, during, and after pacing. Two hundred eight-eight segments of AF with a duration of 3.9 +/- 0.5 seconds (mean +/- SD) were analyzed. Local capture of the right atrium during AF was demonstrated for at least one pacing cycle length in each patient. The left atrial electrogram density was significantly greater than baseline at each pacing cycle length that resulted in local capture, except when pacing at 50 ms less than the mean AF cycle length. There was no significant change in the baseline left atrial electrogram density compared with baseline when pacing did not result in local capture of AF. Local right atrial capture is often possible by pacing during type I AF and consistently influences the left atrial electrograms recorded in the coronary sinus. These results confirm the presence of excitable tissue in the right and left atria in type I AF.

977-73 Observations During Induced Atrial Fibrillation and its Spontaneous Termination in the Sterile Pericarditis Model

Atrial fibrillation (AF) is thought to be due to circulating multiple reentrant wavelets, but it is not known how interatrial activation acts to sustain AF. To test the hypothesis that the exchange of reentrant wave fronts between the right and left atria via the intercaval region, septum, and Bachmann's bundle plays a role in the self-sustaining mechanism of AF, we studied activation of both atria during induced AF and during its spontaneous termination. Three hundred seventy-two unipolar electrograms were recorded simultaneously from an electrode array placed on both atrial free walls by using a multiplexing system during 10 induced AF episodes lasting up to 7 minutes in 5 dogs with sterile pericarditis. Activation maps were analyzed during sustained AF and just before termination of AF for 5 consecutive beats, respectively. The mean number of the lines of functional block (LFB) par beat in each atrium, the mean AF cycle length, and the mean number of wave fronts passing between the atria per beat were compared in during sustained AF and before termination of AF in the same AF episode. Complete reentrant circuits were rarely detected in either atrium during AF. Wave fronts traveling in part around LFBs were observed, and the location and length of the LFBs changed from beat-to-beat. The mean number of LFBs detected in the right atrium did not change during sustained AF compared with AF termination (1.7 ± 0.5 vs. 1.8 ± 0.8, NS). However, the mean numberof LFBs in the left atrium significantly decreased from 1.4 ± 1.2 during sustained AF to 0.4 ± 0.6 before AF termination (p &lt; 0.05). The mean AF cycle length significantly prolonged from 107 ± 19 ms during sustained AF to 151 ± 34 ms before AF termination (p &lt; 0.0001). In the beats before AF termination, wave fronts going from left-to-right significantly decreased (1.4 ± 0.5 during AF to 0.4 ± 0.4 before AF termination, p &lt; 0.05). so that the left atrium was activated by right atrial wave fronts. The presence of LFBs associated with partial reentrant circuits in the left atrium and exchange of wave fronts between the atria play an important role in sustaining AF. Spontaneous termination of AF is preceded by prolongation of AF cycle length, decreasing number of LFBs in the left atrium, and a marked decrease in left-to-right activation wave fronts.