CLINICAL APPROACH TO PAROXYSMAL ATRIAL-FIBRILLATION

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 en‐cainide, 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 beneficial 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. Copyright © 1990 Wiley Periodicals, Inc.