[New facts about pathogenesis of atrial fibrillation: correlation between changes in bioelectric brain activity and recurrence of atrial fibrillation paroxysms].

AIM: Determination of neurophysiological features of the disease course in patients with paroxysmal atrial fibrillation (AF); pathogenetic validation of use and assessment of therapeutic efficacy of clonazepam (an atypical agonist of benzodiazepine receptors) in combined antiarrhythmic therapy.

MATERIAL AND

METHODS

The study group consisted of 31 patients with paroxysmal AF free of severe organic changes of the myocardium with twice a week paroxysms, on the average, treated ineffectively with beta-adrenoblockers, amiodaron, sotalol, etacisine, allapinin or combination of the above drugs. A comparative group consisted of 10 patients with perpetual arrhythmia. Fifteen healthy subjects entered the control group. Electroencephalograms were made on the unit Brain Surfing (Russia). Compression-spectral analysis was conducted with utilization of Fourier's algorithm in different periods of the disease for calculation of the absolute (mcV2/Hz) spectral power of the teta- (4.0-7 Hz), alpha (8-13 Hz) and beta-rhythm (14-18 Hz). Clonazepam was given in a dose 1.5 mg/day in addition to insufficiently effective anti-arrhythmic therapy. Holter ECG monitoring was carried out initially and in therapy with clonazepam.

RESULTS

The spectral power of alpha-, beta- and teta-rhythm of patients with paroxysmal AF exhibits significant cyclic fluctuations depending on the disease course period. In attack-free period AF patients differ from healthy subjects by a significant fall of spectral power of beta-rhythm indicating functional deficiency of the reticular formation in this disease. 0-24 hours before AF paroxysm spectral power of all the rhythms rose greatly reflecting marked functional disintegration of nonspecific brain systems realizing psychovegetative regulation. At AF paroxysm spectral power of alpha- and beta-rhythm significantly decreased while that of teta-rhythm grew (activation of the lymbic complex). 0-24 h after paroxysm spectral power of alpha- and beta-rhythm continued to fall, of teta-rhythm--sharply fell. Spectral EEG characteristics in this period maximally approached those of the control group. Clonazepam treatment decreased the paroxysms two times and more in 58.1% patients. Holter ECG showed associated reduction in the number of supraventricular extrasystoles by 81.9%. The compression-spectral ECG analysis revealed a 12% enhancement of beta-rhythm spectral power showing lessening of functional disintegration of nonspecific brain systems.

CONCLUSION

The course of paroxysmal AF is characterized by functional disintegration of nonspecific brain systems (thalamo-cortical, lymbic and mesencephalic reticular formation) which is maximally evident before AF paroxysm and attenuates after it. Cyclic changes in functional activity are a neurogenic factor realizing readiness of the atria to fibrillation. An atypical agonist of benzodiazepine receptors clonazepam effectively influences neurogenic mechanisms provoking AF paroxysms.