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Background: Atrial fibrillation (AF) causes electrical, functional, and structural changes in the atria. We examined electrophysiologic remodeling caused by AF and its reversal noninvasively by applying a new atrial signal analysis based on magnetocardiography (MCG). Methods: In 26 patients with persistent AF, MCG, signal-averaged electrocardiography (SAECG), and echocardiography were performed immediately after electrical cardioversion (CV), and repeated after 1 month in 15 patients who remained in sinus rhythm (SR). Twenty-four matched subjects without history of AF served as controls. P-wave duration (Pd) and dispersion (standard deviation of Pd values in individual channels) and root mean square amplitudes of the P wave over the last 40 ms portions (RMS40) were determined. Results: In MCG Pd was longer (122.8 ± 18.2 ms vs 101.5 ± 14.6 ms, P < 0.01) and RMS40 was higher (60.4 ± 28.2 vs 46.9 ± 19.1 fT) in AF patients immediately after CV as compared to the controls. In SAECG Pd dispersion was increased in AF patients. Mitral A-wave velocity and left atrial (LA) contraction were decreased and LA diameter was increased (all P < 0.01). After 1 month, Pd in MCG still remained longer and LA diameter greater (both P < 0.05), while RMS40 in MCG, Pd dispersion in SAECG, mitral A-wave velocity, and LA contraction were recovered. Conclusions: Magnetocardiographically detected atrial electrophysiologic alterations in persistent AF diminish rapidly although incompletely during maintained SR after CV. This might be related to the known early high and late lower, but still existent tendency to AF relapses. [ABSTRACT FROM AUTHOR]

KETTUNEN, E., et al.: Atrial Refractoriness and Action Potential Duration After Sudden Reversal of Atrioventricular Sequence. To address the potential of atrioventricular (AV) asynchrony to provoke cardiac arrhythmias, atrial electrophysiology was examined during normal and reversed AV interval in anesthetized pigs. A new automatic stimulation technique was adapted to monitor rapid changes in the effective refractory period (ERP), using continuous AV sequential pacing, incremental extrastimulus interval scanning, and automatic detection of capture. Right atrial ERP using 2–8 ms stimulus interval increments and right atrial and ventricular monophasic action potential (MAP) duration were determined simultaneously when the AV interval was changed from normal (+80 ms) to reversed (−40 ms) and back. During reversed AV interval the peak right atrial pressure increased from 8 ± 3 to 14 ± 4 mmHg (P < 0.001) and mean arterial pressure decreased from 86 ± 18 to 65 ± 21 mmHg (P < 0.001). At new steady state, atrial ERP and MAP duration at 90% level of repolarization were lengthened by 22 ± 16 and 42 ± 12 ms respectively (P < 0.001). Ventricular MAP duration did not change. A statistically significant lengthening in atrial ERP could be demonstrated in 5–10 seconds. After reversion of the AV sequence, the ratio of atrial ERP to MAP duration decreased from 1.27 to 0.94 (P < 0.001) on average for 15 seconds, the change being thought to favor reentry. Thus atrial wall stress from contraction during ventricular systole even for a short period of time modifies atrial electrophysiology. Deficient AV synchrony may immediately contribute to the development of atrial arrhythmias. (PACE 2004; 27:10–18) [ABSTRACT FROM AUTHOR]

Conventional determination of the ventricular effective refractory period (VERP) is unsuitable for detection of rapid fluctuations in the effective refractory period (ERP). A programmed stimulation system was developed that adapts continuous atrioventricular sequential pacing, incremental extrastimulus interval (S1S2) scanning, and automatic detection of extrastimulus capture which is followed by shortening of S1S2 to execute repeated scanning. The accuracy of ERP determination was tested using variable incremental (2 and 4 ms) and decremental (4-16 ms) steps of the S1S2 interval. Based on a mean of 82 determinations in eight patients, the average VERP values stayed at 249.8-251.0 ms except during the highest capture frequency. Standard deviation of ERP values ranged from 1.1 to 2.5 ms on average at the tested incremental and decremental steps. One determination was accomplished within 7.8-15.6 seconds on average. The ability to track changes in ERP was tested by changing the drive cycle length. Time constants for the adaptation rate of VERP and ventricular monophasic action potential duration at a 90% level of repolarization were determined from each test, and were similar, 51 ± 8 seconds (mean ± SEM) for ERP and 51 ± 6 seconds for the action potential duration. Thus, the developed method provides accurate ERP measurements during rapid variation in ventricular refractoriness. It allows studying the recovery of excitability and the action potential duration simultaneously, and would be valuable particularly in pathological conditions and pharmacologic interventions where these electrophysiological variables become dissociated. [ABSTRACT FROM AUTHOR]