Is there evidence supporting the practice of discontinuing digoxin three days before electrical car

Fråga: Is there evidence supporting the practice of discontinuing digoxin three days before electrical cardioversion of atrial fibrillation and atrial flutter?

Sammanfattning: In conclusion the notion to discontinue digoxin for at least 24 hours before elective cardioversion of atrial arrhythmias is based on the finding from the mid-sixties where patients with digitalis toxicity developed ventricular arrhythmias after electrical cardioversion. The support for avoiding cardioversion in patients without digitalis toxicity must be considered sparse. The patients included in this study differ substantially from patients being subjected to electrical cardioversion today. There are at least three studies where cardioversion in patients with therapeutic digoxin levels have not been associated with serious ventricular arrhythmias. All studies have one or more limitations making it difficult to give specific recommendations, but in patients without acute myocardial ischemia, electrolyte disturbances and no clinical signs of digitalis toxicity elective electric cardioversion seems safe.

Svar: The use of direct current cardioversion in patients with atrial arrhythmia and on maintenance doses of digitalis is usually discouraged because of the danger of precipitating lethal ventricular arrhythmias. As a consequence it is widely recommended that digoxin and other digitalis glycosides be withheld for 24 hours or more before elective electrical cardioversion. This is based on the finding from the mid-sixties where patients with digitalis toxicity develop ventricular arrhythmias after electrical cardioversion (1). In this study the patients shown to be more susceptible to develop serious arrhythmias had clinical and ECG signs of digitalis toxicity. They also received comparatively high doses of digoxin (40 % received 0.5 mg/day or more) (1). The majority of patients included suffered from rheumatic heart disease.

In an extensive search in databases we found a few studies that addressed this particular problem (2,3,4). In a study by Ditchey el al. 21 patients with supraventricular arrhythmias were monitored by ECG one hour before and one hour after direct current cardioversion (2). All patients were treated with digoxin in concentrations considered "non-toxic" (0.13-3.8 nmol/L, mean 2.0 nmol/L), but no data regarding when in the dose interval these samples were taken were provided. Seventeen of these patients received additional antiarrhythmic therapy with oral quinidine, two of these patients also received oral propranolol and a single dose lidocaine immediately before cardioversion. No patient developed serious ventricular arrhythmia after cardioversion, and all patients with serum digoxin levels greater than 2.6 nmol/L had the same or fewer ectopic beats per hour after cardioversion. In general serum digoxin levels correlated poorly with signs of ventricular ectopy. This study had limitations whereas a majority of patients received additional antiarrhythmic therapy.

In a study by Ali et al. 50 patients with either atrial fibrillation (52%), atrial flutter (32%), supraventricular tachycardia (10%) or ventricular tachycardia (6%) were studied (3). The effectiveness of low dose cardioversion and the incidence of post-cardioversion arrhythmias were studied. All patients were treated with digoxin but concentrations were measured in only 11 patients. Concentrations in these patients ranged from 0.9-3.1 nmol/L, (mean 2.0 nmol/L) but no data regarding when in the dose interval these samples were taken were provided. Six of these patients were clinically found to have toxicity symptoms on the basis of cardiac arrhythmia, GI-symptoms and digoxin blood levels of 1.8-3.1 nmol/L. All patients were monitored in an intensive care unit for at least 12 hours following the procedure and only one patient developed ventricular tachycardia, which was successfully treated with a bolus of lidocaine. An additional 12 patients had occasional premature beats. This study has limitations whereas digoxin concentration is unknown in a majority of patients and there is a strong heterogeneity in arrhythmia etiology.

In a more recent study by Mann et al. the incidence of cardioversion-induced ventricular arrhythmias in 19 patients with therapeutic serum levels of digoxin were studied (4). Only patients with therapeutic serum digoxin levels were included (0.64-2.4 nmol/L, mean 1.4 nmol/L), but no data regarding when in the dose interval these samples were taken were provided. No patient developed malignant ventricular arrhythmias in the immediate 3-hour period after cardioversion. No relation between either serum digoxin level nor applied energy level and change in frequency of single premature ventricular beats after cardioversion were found. Also this study has limitations as patients with acute myocardial ischemia, serious electrolyte disturbance and requiring class 1 antiarrhythmic agents were excluded.