[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.

[Clinico-neurophysiological features of the course of the disease in patients with paroxysmal atrial fibrillation].

The subjects of the study were 32 patients with paroxysmal atrial fibrillation (AF) and 19 ':ealthy individuals using a clinical and neurophysiological method of toposelective mapping of electroencephalogram (EEG). EEG was done during the inter-attack, pre-attack, and post-attack periods, as well as during a paroxysm. During the inter-attack period, the patients had a lower beta-rhythm power vs. the healthy controls, while there were no significant differences between them in the power of alpha- and beta-activity. Before an attack, the patients had a significant increase in beta, alpha-, and theta-range power, reflecting the intensification of the activity of the metaencephalic reticular formation, thalamocortical, and hypothalamosepto-hyppocampal systems, respectively. During an AF paroxysm, the activity of the thalamocortical and reticular systems was lowered, while the activity of the hypothalamo-hyppocampal system further increased. After an attack, the activity of all the mentioned systems went down to the initial state of the "optimal" brain functioning after an excessive excitation. It is assumed that generalized one-way direction of EEG changes before an attack reflects tensed functioning of practically all activation systems, which increases the probability of a "breakdown" in a form of an AF paroxysm. The data of the study evidence a cyclic character of the disease and stresses an important role in AF pathogenesis played by disturbances associated with the functional condition of non-specific temporal-limbic and reticular brain structures, especially in patients without organic myocardial alterations.