Opinion differs greatly about the value and risk of quinidine. The present communication attempts to demonstrate that more rational use of quinidine is possible by emphasis on serum quinidine concentration rather than on dose alone. Conversion of chronic atrial fibrillation and the appearance of myocardial toxicity are related more closely to the concentration of quinidine in the blood than to the dose. The serum concentration achieved with equal doses of the drug varied strikingly in different individuals; myocardial toxicity was infrequent at levels less than 6.0 ,g./ml. and increased proportionately as this level was exceeded. These levels could not always be predicted from the dose given. 2. Chronic cardiac "invalids" despite full cardiac therapy in whom it was thought that increased cardiac output associated with sinus rhythm might improve cardiac function.3. Those with atrial fibrillation and episodes of arterial emboli, in whom it was thought that restoration to sinus rhythm might decrease the likelihood of atrial thrombus formation.4. Those with chronic atrial fibrillation who had undergone a technically successful mitral valvulotomy.5. Those in whom atrial fibrillation persisted after successful treatment of hyperthyroidism.6. Those with atrial fibrillation of relatively recent origin (less than 6 months), regardless of symptoms and of the underlying disease.7. Those in whom disturbing palpitations and awareness of cardiac irregularity persisted despite full digitalization and a slow ventricular rate.As a general rule, conversion to sinus rhythm was not attempted in middle-aged or elderly patients with chronic atrial fibrillation who were entirely asymptomatic, who had been doing well on digitalis alone, and who had not experienced any cardiac difficulties or emboli over a period of months or years despite the arrythmia.Patients with paroxysmal atrial fibrillation are not considered in the present paper.Etiology
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