Propafenone Disease Interactions

The use of propafenone is contraindicated in patients with bronchospastic disorders or severe obstructive pulmonary disease. Propafenone has beta-adrenergic blocking properties.

The use of propafenone is contraindicated in patients with uncontrolled congestive heart failure, cardiogenic shock, bradycardia, or marked hypotension. Propafenone can exacerbate congestive heart failure by beta blockade of sympathetic stimulation necessary for circulatory support. Propafenone also has negative inotropic activity that can depress cardiac output and cardiac index.

The use of propafenone is contraindicated in patients with conduction disorders such as second- or third-degree AV block, right bundle-branch block when associated with a left hemiblock(bifascicular block), sick sinus syndrome, or bradycardia-tachycardia syndrome in the absence of a functional artificial pacemaker.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

Reversible (+) ANA titers have been reported during administration of propafenone. Therapy with propafenone should be administered cautiously in patients with established systemic lupus erythematosus (SLE). Clinical monitoring, including ANA titers, is recommended. Patients without a previous history of (+) ANA titer or SLE who develop a (+) ANA while receiving propafenone should be evaluated and, if ANA titers persist or worsen, discontinuation of therapy should be considered.

Propafenone is extensively metabolized by the liver. The bioavailability of propafenone in patients with normal hepatic function is approximately 3% to 40%, but increases to approximately 70% in patients with severe hepatic impairment. Therapy with propafenone should be administered cautiously and the dosage reduced to 20% to 30% of that given patients with normal hepatic function. Clinical monitoring of cardiac function (ECG) and hepatic function is recommended.

Propafenone is partially eliminated by the kidney and approximately 50% of its metabolites are excreted in the urine. Therapy with propafenone should be administered cautiously in patients with renal impairment, monitoring for signs of overdosage.