[Unwanted drug interaction between anti-arrhythmic drugs and drugs used for heart failure]

Abstract

The appearance of adverse drug reactions may depend on the category of used drugs as well as on the coexistence of a pathological stage. Clinically important are: interactions of digitalis glycoside drugs leading to the occurrence or intensification of toxic symptoms characteristic for those drugs; interactions of antiarrhythmic drugs which may cause proarrhythmic effects and hypotension, and also interactions of nitrates resulting in lowering of the blood pressure. Quinidine, verapamil, nitrendipine, amiodaron, propafenone, captopril, spironolactone decrease renal clearance of digoxin, and amilorid/triamteren lower the extrarenal clearance of this drug. Thus the outcome of those concommitant therapies is the increase of digoxin serum concentration and appearance of toxic symptoms. Clinically dangerous, in the course of the antiarrhythmic therapy, is the increased risk of the arrhythmia appearance when two or more antiarrhythmic drugs are applied concomitantly. Antiarrhythmic drugs class IA (quinidine, disopyramide), class III (sotalol, amiodarone), class IV (calcium channel blockers) used at the same time with potassium depleters diuretics or beta-blocking agents result in the inhibition of repolarization and the increased duration of activation potential with the risk of developing arrhythmia of the torsade de pointes types. Nitrates interactions are mainly of the pharmacodynamic character. Most common adverse drug reaction, observed during the concomitant nitrates and another circulatory drug therapy, is excessive lowering of the blood pressure. These may lead to the decrease in the therapeutic efficacy of these combinations. Interactions of circulatory drugs are numerous, sometimes difficult to predict and they may lead to the intensification of the adverse drug reaction and lowering of their therapeutic efficacy.