Summary: In addition to the role of the electrophysiological substrate, paroxysmal atrial fibrillation depends on the modulation of the atrial tissues by the autonomic nervous system. Experimentally, models of atrial fibrillation can be based on either adrenergic or vagal stimulations that provoke the arrhythmia by disturbing in a different way conduction and refractory periods of the atrium. Clinically, the role of the autonomic nervous system can be suspected from the clinical history, and paroxysmal attacks can typically be observed either at daytime or at night, at exercise or at rest. Careful attention should be paid to the changes of heart rate that occur in the minutes or tens of minutes prior to the attacks, and the trend of acceleration or slowing of cardiac frequency observed in Holter tracings provides reliable indications of the state of the vago-sympathetic balance in these patients. During the attacks, the electrocardiographic aspect of atrial flutter alternating with a pattern of atrial fibrillation is typical of vagally dependent arrhythmias, whereas atrial tachycardia is more frequently observed at the onset of adrenergic atrial fibrillation. When the paroxysmal forms of arrhythmia are resistant to usual pure antiarrhythmic therapy including type IA agents and flecainide or encainide, one should take into account the role of the autonomic nervous system. Propafenone, or beta-blockers combined with type I drugs, are very effective every time an adrenergic factor is involved, but prevent the benefi- cia1 role of other agents if a vagal mechanism is predominant. Amiodarone, a complex drug with multiple facets, can be active in many different situations but its use should be reserved to definitely resistant cases, in combination with other agents, in order to limit its potential long-term side effects. Digitalis and verapamil mainly address the tolerance to arrhythmias, rather than their prevention.

We performed atrial EP studies (atrial substrate evaluation) on 10 patients. These patients had evidence of paroxysmal, sustained, recurrent atrial arrhythmias (7 men and 3 women with a mean age of 64 +/- 15 years). All patients combined a brady-tachy syndrome; 7 patients had a sick sinus syndrome (SSS) and 3 patients a typical vagally induced atrial arrhythmia. No anti-arrhythmic drug was allowed in 3 patients with SSS, 1 drug failed in 4 patients and the combination of 2 drugs failed in 3 patients during the first to eighth years prior to pacemaker implantation. Atrial substrate evaluation was feasible in all these patients off anti-arrhythmic therapy and showed important abnormalities of atrial loco-regional conduction parameters and long refractory periods (RP). The remarkable point was, in 7 patients, a paradoxical improvement in intra-atrial conduction delay at rapid pacing rate. The DDD pacing mode was chosen in all patients. No technical problem occurred during implantation. Atrial pacing rate was programmed to be slightly higher than the mean diurnal heart rate calculated on Holter monitoring. After implantation, the mean follow-up period was 18 +/- 25 months with an average of one Holter every 4 months during the first 2 years. The 7 patients who improved intra-atrial conduction at rapid pacing rate were controlled without drugs, 2 patients were controlled with 1 drug, and 1 patient with 2 drugs. Atrial pacing in the DDD mode in a selected group of patients prevents paroxysmal and drug-resistant atrial arrhythmias. Atrial substrate evaluation is a sensitive tool for assuring the long-term benefit of atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

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Recent data suggest that a large proportion of ischemic strokes are due to embolic phenomena from the heart. Atrial fibrillation appears to be one of the principal causes of embolization. If electrophysiologic parameters are considered as determining factors, the existence of atrial hypervulnerability in patients with embolic strokes is significant, when arrhythmia has been excluded as an etiology. This study suggests that an aggressive approach to early diagnosis and management through electrophysiologic studies might aid in preventing future neurologic attacks.

Propranolol and nadolol were used in two groups of patients having ventricular arrhythmias. The two groups were characterised by differences in sympathetic drive. The 10 non-adrenergic patients had idiopathic, monomorphic extrasystoles (isolated with fixed coupling or in pairs or salvoes) arising from the right ventricle or the septum. These extrasystoles were chronic and benign, with a slightly increased daytime frequency (day:night = 1.6). They disappeared on exercise. The nine adrenergic patients had less frequent but more complex polymorphic ventricular extrasystoles, and rapid and irregular tachycardias which were resistant. They occurred predominantly during the day and were associated particularly with stress and exercise. They were either idiopathic, or coexisted with mitral valve prolapse (three cases) or hypertrophic subaortic stenosis (one case) in young patients (mean age, 32 years) who did not have coronary heart disease. Nadolol was more effective than propranolol in controlling the arrhythmia, heart rate, and variations in sinus rhythm in the adrenergic group, while the arrhythmia was not controlled in the non-adrenergic group. Using clinical variables, comparison of the frequency of extrasystoles by day and night, and assessment of the antiarrhythmic effect of beta-blockers, the role of the sympathetic tone in non-ischaemic ventricular arrhythmias may be elucidated.