CHANGES OF HEART-RATE AND POWER SPECTRUM OF ITS FLUCTUATIONS INDUCED BY A SHORT-TERM COURSE OF QUINIDINE IN PATIENTS WITH VARIOUS ARRHYTHMIAS

The ability of quinidine to block alpha(1)-adrenoreceptors and M-2-cho linergic receptors suggests that in line with increasing heart rate th e drug is capable to decrease the power of both high-frequency (respir atory) variations of heart rate which is determined by parasympathetic influences on the sinus node and low-frequency (vasomotor) variations which are determined by combined influences of both divisions of the autonomic nervous system on this node. This suggestion was tested by a nalyzing 5-min ECG recordings from 22 patients (mean age 36+/-16 years ) with various arrhythmias but without organic heart disease. ECG was recorded in supine position during free and paced breathing and during active orthostatic test before and after 3 days of oral quinidine (1 g/day). Both at rest and during tests 60-70% of patients responded to quinidine by tachycardia while low-frequency variations power decrease d in 80-100% and high-frequency variations power decreased in 45-75% o f patients. A simultaneous spectral analysis of amplitudes of successi ve QRS complexes which allowed to estimate frequency, amplitude and re gularity of respiratory cycles showed that increase in low-frequency a nd/or high-frequency power was associated with respiratory changes. In some patients the rise in low-frequency power may result from increas ed power of so-called very slow variations of heart rate. There was no relationship between quinidine-induced decrease in low-frequency or h igh-frequency powers and age of patients or type of arrhythmia. Based on the literature analysis and our data we have concluded that the dec rease in heart rate induced by quinidine in 40% of patients with arrhy thmias is determined by tile predominance of direct inhibition by the drug of the sinus node automaticity over its tachycardia-inducing neur otropic action. The possibility that this action attenuates the neurot ropic component of the drug effect, i.e. stimulatory effect of the sym pathetic nervous system on the sinus node, which is caused by blockade of vascular alpha(1)-adrenoreceptors and reduction in blood pressure, can not be excluded.