N‑acetylprocainamide (NAPA) Unit Conversion

N‑acetylprocainamide (NAPA), the primary active metabolite of the antiarrhythmic drug procainamide, results from acetylation of procainamide in the liver. NAPA is a less potent antiarrhythmic agent than procainamide and has qualitatively different cardiac actions. In slow acetylators, approximately 25 % of the procainamide dose is converted to NAPA; in rapid acetylators, up to 40 % of the dose may be converted to NAPA. Both procainamide and NAPA are chiefly eliminated by the kidneys. NAPA has a slower rate of renal elimination than procainamide and can accumulate rapidly in the presence of renal or circulatory impairment. In that case, NAPA concentrations may reach toxic levels, a circumstance that is exacerbated in rapid acetylators. Because of the variable hepatic conversion and renal elimination of procainamide and NAPA and the attendant possible toxic effects, both compounds should be monitored in patients on chronic procainamide therapy.

The commonly accepted therapeutic range for the sum of N‑acetylprocainamide and procainamide is 5‑30 μg/mL (18.1‑108.3 μmol/L). For effective treatment, some patients may require serum or plasma levels outside this range. The range, therefore, is provided only as a guide for interpretation along with other clinical symptoms and clinical history. The factors that can influence the relationship between N‑acetylprocainamide serum or plasma concentrations and clinical response include renal and circulatory function, rate of acetylation, the severity and type of cardiac arrhythmia, general state of health, and use of other drugs. The concentration of N‑acetylprocainamide in serum or plasma depends on the time of the last procainamide dose; mode of administration; concomitant drug therapy; sample condition; timing of sample collection; and individual variations in absorption, biotransformation, distribution, and excretion. These parameters must be considered when interpreting results.