Abstract
Each of four basic theories for the genesis of auricular fibrillation and flutter is supported by experimental procedures using laboratory animals. These procedures were used to evaluate certain compounds felt to have antifibrillatory properties. Drugs with high experimental antifibrillatory potency did not necessarily exhibit therapeutic action when subjected to clinical test. No basic theory as yet has sufficient experimental proof to explain completely the mechanism of auricular fibrillation. Hypervagotonia is undoubtedly an important factor in the initiation of auricular fibrillation but not in the maintenance of the arrhythmia. An unknown factor (or factors) appears to be responsible for the maintenance of auricular fibrillation. Diphenhydramine hydrochloride (Benadryl) may be added to the list of successful therapeutic agents for clinical auricular fibrillation. Although our results do not indicate it for routine use in place of quinidine, its use may prove valuable in selected patients. Banthine, while possessing the ability to prolong the myocardial refractory period and to prevent or reverse auricular fibrillation in experimental animals, did not prove effective in the treatment of auricular fibrillation in humans.
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