N-Acetylprocainamide, Torsades de Pointes, and Hemodialysis

  1. KHIEM P. V. NGUYEN, M.D.;
  2. GEORGE THOMSEN, M.D.;
  3. BING LIEM, D.O.;
  4. CHARLES D. SWERDLOW, M.D.; and
  5. MICHAEL R. FRANZ, M.D.
  1. Stanford University School of Medicine;
    Stanford, CA 94305

    Excerpt

    To the editor: N-acetylprocainamide (acecainide; NAPA) is the principal metabolite of procainamide. We report a case of N-acetylprocainamide-induced torsade de pointes that was resistant to overdrive pacing, but that responded dramatically to hemodialysis.

    A 34-year-old woman with chronic glomerulonephritis had mitral valve replacement. Her admission electrocardiogram showed a QT of 0.35 seconds (QTc, 0.40). The blood urea nitrogen level was 65 mg/mL and the creatinine level was 2.6 mg/dL. On the fourth postoperative day, treatment was begun with procainamide for ventricular bigeminy. The ventricular bigeminy was suppressed at procainamide concentrations ranging from 2.7 to 5.6 µg/ mL for the next

    This 100-word excerpt has been provided in the absence of an abstract.

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