Edward B. Leahey

The Effect of Quinidine and Other Oral Antiarrhythmic Drugs on Serum Digoxin: A Prospective Study

We compared the effects of quinidine and three alternate antiarrhythmic drugs on serum digoxin concentration in 63 patients before and during administration of quinidine, procainamide, disopyramide, or mexiletine. Quinidine increased digoxin concentration by at least 0.5 nmol/L in 21 of 22 patients: Mean serum digoxin rose from 1.2 nmol/L to 2.4 nmol/L (P less than 0.001). Procainamide, disopyramide, or mexiletine increased serum digoxin by 0.5 nmol/L in one of 41 patients. Anorexia, nausea, and vomiting develop soon after starting quinidine therapy in 10 of the 22 patients who received quinidine but in only five of the 41 patients who received procainamide, disopyramide, or mexiletine (P less than 0.01). Quinidine prolonged the PR intervals from 160 +/- 14 ms to 183 +/- 26 ms, but procainamide, disopyramide, and mexiletine did not change the PR interval (P less than 0.005). In digitalized patients, quinidine increases serum digoxin concentration, increases digoxins effect on atrioventricular conduction, and produces more adverse gastrointestinal effects than procainamide, disopyramide, or mexiletine.

Quinidine and Digoxin

SummaryAn increase in serum digoxin concentration occurs in 90% of patients given quinidine. On average, the serum digoxin doubles during treatment with therapeutic doses of quinidine. Almost every patient treated with quinidine will have a decrease in the renal clearance of digoxin and many will have a decrease in the volume of distribution of digoxin. Whether changes in the inotropic effect of digoxin occur during concurrent quinidine administration is an unsettled area. However, gastrointestinal and cardiac toxicity, which closely resemble digitalis toxicity, often occur when quinidine causes the serum digoxin concentration to rise. These effects subside when the digoxin dose is reduced. Therefore it is prudent to monitor serum digoxin concentrations during concomitant quinidine treatment and to adjust the digoxin dose according to the results. When the toxicity is severe or dose adjustment is difficult, another antiarrhythmic drug should be selected.An increase in serum digoxin concentration occurs in 90% of patients given quinidine. On average, the serum digoxin doubles during treatment with therapeutic doses of quinidine. Almost every patient treated with quinidine will have a decrease in the renal clearance of digoxin and many will have a decrease in the volume of distribution of digoxin. Whether changes in the inotropic effect of digoxin occur during concurrent quinidine administration is an unsettled area. However, gastrointestinal and cardiac toxicity, which closely resemble digitalis toxicity, often occur when quinidine causes the serum digoxin concentration to rise. These effects subside when the digoxin dose is reduced. Therefore it is prudent to monitor serum digoxin concentrations during concomitant quinidine treatment and to adjust the digoxin dose according to the results. When the toxicity is severe or dose adjustment is difficult, another antiarrhythmic drug should be selected.

Digoxin-Quinidine Interaction: Current Status

Excerpt Quinidine has been the prototype of antiarryhthmic drug since it was introduced into clinical practice in 1918, and it is widely used for treatment of both atrial and ventricular arrhythmia...

Mexiletine: a new antiarrhythmic drug.

Excerpt The treatment of ventricular arrhythmias remains a major challenge. Ventricular arrhythmias may be symptomatic; ventricular arrhythmias after myocardial infarction have recently been correl...

Therapy of Cardiac Arrhythmias and Conduction Abnormalities in Coronary Artery Disease

Two of the most important treatable causes of death in patients with coronary artery disease are the cardiac arrhythmias and conduction abnormalities. They may be associated with acute myocardial infarction (AMI) or chronic ischemia. Detection of such rhythm and conduction abnormalities has been discussed in chapter 5, and their pathophysiology was commented on in chapter 2. For the purpose of discussing therapeutic approaches, AMI can be divided into four phases: (1) the prehospital phase, (2) the CCU phase, (3) the post-CCU phase, and (4) the post-hospital phase. The cardiac arrhythmias and conduction defects encountered in each of these phases will be discussed, as will their therapy. The management of arrhythmias encountered in the setting of chronic ischemic heart disease will also be discussed.

Quinidine-Digoxin Interaction-Reply

We would like to reply to the comments by Matzke and Burkle and those by Cisneros. Matzke and Burkle have reservations regarding the incidence of the interaction. We have made no attempt to state the actual incidence of this interaction; a retrospective study of hospitalized cardiac patients cannot possibly establish a true incidence. We have simply reported the finding of 25 cases in a single medical center in a single year, which suggests to us that the interaction must be common. Based on their mathematical model, Drs Matzke and Burkle expected higher serum digoxin concentrations than we found. The implication of this comment is that serum digoxin concentration may have risen merely from institution of a higher dose, enforced patient compliance in the hospital, or increased absorption from changes in other medications. We do not belive this to be the case for the following reasons: First, the baseline