Procainamide Disease Interactions

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

Bone marrow suppression inducing granulocytopenia, anemia, and thrombocytopenia has occurred during administration of procainamide. Most event occurred at recommended dosages and within twelve weeks of initiation of procainamide therapy. Agranulocytosis has resulted in death in 20% to 25% of reported cases. Therapy with procainamide should be administered cautiously in patients with or predisposed to myelosuppression or any type of cytopenia. Clinical monitoring of hematopoietic function including complete blood counts prior to initiation of therapy and at weekly intervals for the first 3 months of therapy and periodically after that is necessary.

The use of procainamide is contraindicated in patients with complete AV node block because of its effects in suppressing nodal or ventricular pacemakers and the hazard of asystole. Therapy with procainamide should be avoided in patients with second-degree AV block or various hemiblocks in the absence of a functional artificial pacemaker.

The use of procainamide is contraindicated in patients with established systemic lupus erythematosus (SLE), since aggravation of the symptoms is highly likely. A positive antinuclear antibody test (+ANA), with or without symptoms of SLE, often results from chronic therapy with procainamide in patients without SLE. An SLE-like syndrome, rarely involving pathologic renal changes, can occur following prolonged procainamide therapy. The benefit versus risk should be evaluated in the presence of a +ANA in a patient without a history of or predisposition to SLE.

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.

Procainamide decreases the release of acetylcholine from skeletal muscle motor nerve endings. Procainamide can worsen the symptoms of myasthenia gravis. Therapy with procainamide should be administered cautiously in patients with myasthenia gravis.

Procainamide is primarily eliminated by the kidney. The serum concentration of procainamide is increased and the half-life prolonged in patients with renal impairment. Therapy with procainamide should be administered cautiously in patients with renal dysfunction and dosage modifications should be made based on the degree of renal impairment.