[The atrial arrhythmia syndrome of vagal origin].
Having observed 18 cases, the authors describe a syndrome of recurrent paroxysmal atrial arrhythmia which was very homogeneous from the clinical and ECG point of view. It was usually found in middle aged males, with no demonstrable underlying heart disease, whose disorder of intra-atrial conduction occurred during sinus rhythm. The condition developed slowly over the course of years towards a maximum incidence of several short daily attacks of an arrhythmia which alternated between an atrial fibrillation and atrial flutter. Vagal overactivity is the precipitating cause of these attacks which are usually not completely nocturnal. The condition never progressed to sino-atrial block nor to permanent fibrillation. The beginning of each attack, often heralded by atrial coupling with a long enough interval to cause re-entry, is accompanied by slowing of the sinus rate down to the threshold level. The vagal effect of shortening the action potential and refractory period is recognised to be non-homogeneous in the atrial wall, and suggests a re-entry mechanism rather than hyper-excitability. This would explain the usual resistance of atrial arrhythmias of vagal origin to digitalis, beta blockers and quinidine. Amiodarone alone is usually effective because of the prolongation of the action potential which it causes. In 5 particularly resistant cases a good clinical result was obtained by the insertion of an atrial pacemaker with a fairly rapid rate.
[The atrial arrhythmia syndrome of vagal origin]. Having observed 18 cases, the authors describe a syndrome of recurrent paroxysmal atrial arrhythmia which was very homogeneous from the clinical and ECG point of view. It was usually found in middle aged males, with no demonstrable underlying heart disease, whose disorder of intra-atrial conduction occurred during sinus rhythm. The condition developed slowly over the course of years towards a maximum incidence of several short daily attacks of an arrhythmia which alternated between an atrial fibrillation and atrial flutter. Vagal overactivity is the precipitating cause of these attacks which are usually not completely nocturnal. The condition never progressed to sino-atrial block nor to permanent fibrillation. The beginning of each attack, often heralded by atrial coupling with a long enough interval to cause re-entry, is accompanied by slowing of the sinus rate down to the threshold level. The vagal effect of shortening the action potential and refractory period is recognised to be non-homogeneous in the atrial wall, and suggests a re-entry mechanism rather than hyper-excitability. This would explain the usual resistance of atrial arrhythmias of vagal origin to digitalis, beta blockers and quinidine. Amiodarone alone is usually effective because of the prolongation of the action potential which it causes. In 5 particularly resistant cases a good clinical result was obtained by the insertion of an atrial pacemaker with a fairly rapid rate.