[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.