Quinidine Therapy after Mitral Valvotomy

Nearly half a century has passed since quinidine was first used to convert atrial fibrillation to regular sinus rhythm in man (Frey, 1918). There is general agreement nowadays that the cardiorespiratory benefits resulting from the successful reversion of long-standing atrial fibrillation to sinus rhythm are worth the risk of quinidine therapy (Hay, 1924; Stroud, LaPlace, and Reisinger, 1932; Kohn and Levine, 1935). However, the published indications, results, and incidence of toxic effects from the use of quinidine in heart disease still vary considerably (Viko, Marvin, and White, 1923 ; Wolff and White, 1929; McMillan and Welfare, 1947; Gold, 1950; Hecht, Osher, and Samuels, 1951; Holzman and Brown, 1951; Yount, Rosenblum, and McMillan, 1952; Freeman and Wexler, 1960). Several attempts have been made to assess the value of this drug in specific forms of heart disease, but opinions differ on factors influencing the response of long-standing atrial fibrillation to quinidine. The age of the patient, the aetiology of the heart disease, the presence of cardiac failure or cardiomegaly, and the duration of the arrhythmia have all been considered (Viko et al., 1923; Wolff and White, 1929; Harris, 1929; McMillan and Welfare, 1947; Holzman and Brown, 1951; Sokolow and Ball, 1956). In recent years atrial fibrillation has been found to be one of the most frequent post-operative complications following mitral valvotomy in patients previously in sinus rhythm (Logan and Turner, 1953; Sellors, Bedford, and Somerville, 1953; Dimond and dos Santos, 1954; Wood, 1954; Goodwin, Hunter, Cleland, Davies, and Steiner, 1955; Heinz and Hultgren, 1957). Reasons for the development of this are still uncertain. Trauma to the left atrium, traumatic pericarditis, associated or surgically induced mitral incompetence, active rheumatic myocarditis, and electrolytic alterations have all been considered but not proven. There is some evidence to suggest that adequate use of digitalis and quinidine after operation helps to prevent arrhythmia developing (Kittle and Crockett, 1959). Fortunately, reversion to sinus rhythm can be accomplished with quinidine therapy in a very high percentage of these patients (Logan and Turner, 1953; Dimond and dos Santos, 1954; Wood, 1954: Goodwin et al., 1955; Heinz and Hultgren, 1957). On the other hand, postoperative attempts to revert and maintain sinus rhythm in patients who developed arrhythmia before valvotomy have met with very little success (Sellors et al., 1953; Wood, 1954; Kittle and Crockett, 1959). The present investigation was designed to study the immediate and long-term effects of quinidine on both chronic and recently established atrial fibrillation in patients with dominant mitral stenosis who have had a recent mitral valvotomy. In addition, an attempt has been made to predict the likelihood of achieving reversion to sinus rhythm in both these groups of patients from (a) the electrocardiographic pattern of atrial activity, and (b) the radiological size of the left atrium.