Abstract
A 61-year-old man developed atrial fibrillation 20 days after repair of a left ventricular rupture caused by acute myocardial infarction. Sinus rhythm was restored by cardioversion and maintained with pilsicainide (150 mg·day−1). Hyperkalemia appeared on postoperative day 47 and thus hemodialysis was scheduled. However, the patient was immediately transferred to the ICU for continuous hemodiafiltration (CHDF) before starting hemodialysis due to the development of ventricular tachycardia (VT). It could not be denied that the hyperkalemia might be related to the VT, but polymorphic VT persisted when the serum potassium concentration reached the normal range 12 hours after starting CHDF. These findings indicated that the proarrhythmic effect of pilsicainide was responsible for the sustained VT, which was accompanied by pilsicainide toxicity. The sinus rhythm was restored 36 hours after CHDF, when the serum pilsicainide concentration was 3.36 μg·ml−1, which was still substantially higher than the therapeutic range of 0.2–0.9 μg·ml−1. Despite the limited ability of hemodialysis to remove pilsicainide, CHDF clearly contributed to reducing the serum pilsicainide concentration, which apparently restored the sinus rhythm. These findings suggest that CHDF can help to treat arrhythmia caused by pilsicainide toxicity.
