[First experience of clinical use of new class III antiarrhythmic agent niferidil in patients with persistent atrial fibrillation and flutter].

The aim of the study was to evaluate the efficacy and safety of administered intravenously niferidil in doses 10, 20 and 30 mkg per kg in patients with persistent atrial fibrillation (AF) and flutter (AFL) for pharmacological cardioversion. The study included 30 patients (22 male) with persistent AF (n = 28) and AFL (n = 2) without structural heart diseases with median arrhythmia duration 6.1 +/- 4.

[Experimental and theoretical analysis of the role of cholinergically induced local non-excitability in atrial fibrillation and flutter].

Excitation of vagal nerves results in the emergence of temporarily inexcitable regions in atria. The fact is shown using microelectrode techniques and the mapping of excitation on frog atria isolated together with vago-sympathetic trunks. These regions serve as unidirectional block and functional obstacle provoking reentry-type arrhythmia.

[The role of atrial pressure in spontaneous initiation of atrial fibrillation in the dog.].

Atrial fibrillation (AF) frequently occurred under conditions associated with atrial dilatation (stretch) or vagal hyperactivity. To study possible role of atrial stretch in spontaneous initiation of vagal AF we compared changes of right atrial pressure (RAP) and activation patterns during AF beginning. In anesthetized open-chest dogs (n=45) AF was induced by stimulation of vagal nerves (VS) (30-60 Hz, 5-10 s train).

[Antiarrhythmic Efficacy of a New Class III Antiarrhythmic Drug RG-2.].

We studied effects of a new class III antiarrhythmic drug RG-2 in a canine model of vagally-mediated atrial fibrillation (AF). RG-2 was intravenously infused to anesthetized open-chest dogs in progressive doses (5, 10, 20 and 40 mg/kg, n=6) during vagally-induced AF. RG-2 significantly dose-dependently increased atrial effective refractory period (AERP) with and without vagal stimulation, but did not change conduction velocity.

[The role of stretching the sinus node artery in initiation of atrial fibrillation].

In anaesthetised dogs with open chest (n = 10), against the background of the Gd3+ (a blocking agent of mechano-sensitive ion channels), acetylcholine perfusion induced no significant changes either in probability of atrial fibrillation occurrence or in the paroxysm duration. The Gd3+ did not alter the deceleration of the sinus rhythm either. Therefore the mechanism of spontaneous occurrence of atrial cholinergic fibrillation seems not to be associated with the trigger activity induced by an increased blood pressure in the right atrium.