Background Atrial fibrillation (AF) is frequently observed under conditions that are associated with atrial dilatation. The aim of this study was to investigate the effects of atrial dilatation on the substrate of AF. Methods and Results In 15 Langendorff-perfused rabbit hearts, the interatrial septum was perforated, and after occlusion of the caval and pulmonary veins, biatrial pressure was increased by raising the level of an outflow cannula in the pulmonary artery. Right and left atrial effective refractory periods (AERPs), monophasic action potentials (MAPs), and inducibility of AF by single premature stimuli were measured as a function of atrial pressure. Increasing the atrial pressure from 0.5±0.7 to 16.2±2.2 cm H ₂ O resulted in a progressive shortening of the right AERP from 82.2±9.8 to 48.0±5.1 ms. In the left atrium, an increase in pressure up to 7.4±0.3 cm H ₂ O had no effect on the AERP. At higher pressures, however, the left AERP also shortened, from 67.5±7.5 to 49.3±2.0 ms. The duration of MAPs also decreased by an increase in atrial pressure, showing a high correlation with the shortening in AERP ( r =.94, P <.01). All these changes were completely reversible within 3 minutes after release of the atrial stretch. Dilatation of the atria was a major determinant for the vulnerability to AF. The inducibility of AF increased from 0% at low pressures to 100% when the atrial pressure was >10 cm H ₂ O. Release of the atrial wall stress resulted in prompt cardioversion of AF. The increased vulnerability for AF was highly correlated with the shortening in AERP (logistic regression r =.97). No correlation was found with the spatial dispersion between right and left AERPs. Conclusions Increased atrial pressure in the isolated rabbit heart resulted in a significant increase in vulnerability to AF that was closely correlated to shortening of the AERP. These changes were completely reversible within 3 minutes after release of the atrial stretch, resulting in prompt termination of AF.

BackgroundThe aims of our study were to investigate the meaning of local atrial activation and its behavior during paroxysmal atrial fibrillation and to study the effect of overdrive pacing on local atrial activity.Methods and ResultsTwenty-five patients with lone paroxysmal atrial fibrillation underwent electrophysiological study. Functional and effective atrial refractoriness was determined. Mean and fifth percentile values of 100 consecutive atrial fibrillation intervals (FF) were evaluated at three atrial sites either at arrhythmia onset or at self-termination (or at minute 5). A high-voltage burst pacing was performed after 6 minutes of stable atrial fibrillation in 10 patients. Mean FF intervals were evaluated 5 seconds before and after atrial pacing. Forty-nine atrial fibrillation episodes were induced: 39 self-terminating within 5 minutes and 10 long-lasting. A significant correlation was found between mean FF and atrial functional refractory period (r=.73,P<.001) and between fifth percentile FF and atrial effective refractory period (r=.57,P<.005). Atrial fibrillation self-termination was associated with significant mean FF prolongation, whereas long-lasting fibrillation behaved the opposite. In 10 patients, burst pacing resulted in significant shortening of the mean FF at the stimulation site; no changes were observed in the two distant recording sites.ConclusionsThe analysis of the FF intervals demonstrates a strict correlation with atrial functional refractoriness. The self-termination of atrial fibrillation is related to a prolongation of the functional refractoriness (mean FF), whereas a shortening of both functional and effective refractoriness (fifth percentile) is associated with atrial fibrillation persistence. The provoked shortening of the mean FF at the stimulation site is consistent with the presence of a gap of excitability during atrial fibrillation in the human atria.

Although in physiological conditions RR interval and systolic arterial pressure (SAP) are likely to interact in a closed loop, the traditional cross-spectral analysis cannot distinguish feedback (FB) from feedforward (FF) influences. In this study, a causal approach was applied for calculating the coherence from SAP to RR ( K_s-r) and from RR to SAP ( K_r-s) and the gain and phase of the baroreflex transfer function. The method was applied, compared with the noncausal one, to RR and SAP series taken from 15 healthy young subjects in the supine position and after passive head-up tilt. For the low frequency (0.04–0.15 Hz) spectral component, the enhanced FF coupling ( K_r-s = 0.59 ± 0.21, significant in 14 subjects) and the blunted FB coupling ( K_s-r = 0.17 ± 0.17, significant in 4 subjects) found at rest indicated the prevalence of nonbaroreflex mechanisms. The tilt maneuver recovered FB influences ( K_s-r = 0.47 ± 0.16, significant in 14 subjects), which were stronger than FF interactions ( K_s-r = 0.34 ± 0.19, significant in 9 subjects). At the respiratory frequency, the RR-SAP regulation was balanced at rest ( K_s-r = 0.30 ± 0.18 and K_r-s = 0.29 ± 0.20, significant in 11 and 8 subjects) and shifted toward FB mechanisms after tilt ( K_s-r = 0.35 ± 0.19 and K_r-s = 0.19 ± 0.11, significant in 14 and 8 subjects). The causal baroreflex gain estimates were always lower than the corresponding noncausal values and decreased significantly from rest to tilt in both frequency bands. The tilt-induced increase of the phase lag from SAP to RR suggested a shift from vagal to sympathetic modulation. Thus the importance of nonbaroreflex interactions pointed out the necessity of accounting for causality in the cross-spectral analysis of the interactions between cardiovascular variables in healthy humans.

A new method for quantifying the organization of single bipolar electrograms recorded in the human atria during atrial fibrillation (AF) is presented. The algorithm relies on the comparison between pairs of local activation waves (LAWs) to estimate their morphological similarity, and returns a regularity index (/spl rho/) which measures the extent of repetitiveness over time of the detected activations. The database consisted of endocardial data from a multipolar basket catheter during AF and intraatrial recordings during atrial flutter. The index showed maximum regularity (/spl rho/=1) for all atrial flutter episodes and decreased significantly when increasing AF complexity as defined by Wells (type I: /spl rho/=0.75/spl plusmn/0.23; type II: /spl rho/=0.35/spl plusmn/0.11; type III: /spl rho/=0.15/spl plusmn/0.08; P<0.01). The ability to distinguish different AF episodes was assessed by designing a classification scheme based on a minimum distance analysis, obtaining an accuracy of 85.5%. The algorithm was able to discriminate among AF types even in presence of few depolarizations as no significant /spl rho/ changes were observed by reducing the signal length down to include five LAWs. Finally, the capability to detect transient instances of AF complexity and to map the local regularity over the atrial surface was addressed by the dynamic and multisite evaluation of /spl rho/, suggesting that our algorithm could improve the understanding of AF mechanisms and become useful for its clinical treatment.