Pantoprazole (Proton Pump Inhibitor) Contributing to Torsades de Pointes Storm

Abstract

P roton pump inhibitors (PPI), commonly used medications for peptic ulcer prophylaxis, have been recently described to cause hypomagnesemia through both urinary and gastrointestinal losses. Very few reports have linked hypomagnesemia with life-threatening ventricular arrhythmias. However, these reports included patients with other complex medical problems that may have also contributed to these arrhythmias. To our knowledge, ventricular arrhythmias associated with hypomagnesemia induced by proton pump inhibitors have never been reported. We present a case of a 53-year-old chronic alcoholic male patient, who was started on a proton pump inhibitor for peptic ulcer prophylaxis, which resulted in resistant hypomagnesemia associated with a storm of life-threatening arrhythmias, namely Torsades de Pointes (TdP). Case ReportA 53-year-old man with no previous cardiac history was brought by Emergency Medical Services with a chief complaint of palpitations and dizziness for 1 day. His only significant medical history was chronic alcohol abuse and was not taking any medications before his admission. His physical examination was normal, except for an irregularly irregular rapid pulse and a blood pressure of 157/104 mm Hg. The ECG on admission showed atrial fibrillation with rapid ventricular response at an average of 190 beats per minute. Admitting routine labs showed normal complete blood counts. Electrolyte laboratory values revealed 136 mEq/L of sodium, 4.6 mmol/L of potassium, 100 mEq/L of chloride, 16 mEq/L of bicarbonate, 11 mg/dL of blood urea nitrogen, 0.68 mg/dL of creatinine, 9 mg/dL of calcium, and 1.5 mg/ dL of magnesium. He was started on intravenous diltiazem for rate control and intravenous heparin for anticoagulation. Routine oral pantoprazole 40 mg once daily was also prescribed for peptic ulcer prophylaxis. Seven hours later, while on telemetry, the patient became unresponsive. The telemetry rhythm strip showed sustained polymorphic ventricular tachycardia (pVT; Figure 1A). The patient was treated with 1 g of IV magnesium sulfate, IV lidocaine bolus of 100 mg, and maintenance of 1 mg/min infusion, followed by 3 successive cardioversions, which eventually restored sinus rhythm. Another 2 g of magnesium sulfate was administered intravenously, and the patient was intubated for airway protection. After successful cardioversion, a 12-lead ECG showed sinus rhythm at 95 beats per minute, with T wave alternans. The measured QT was 0.62 s (QTc = 0.65 s), alternating with 0.46 s (QTc = 0.51 s; Figure 2). (All QTc's were calculated using Bazett formula on 2 separate leads.)During his hospital stay (41 days), the patient was maintained on IV lidocaine at 2 mg/min, as well as IV magnesium for replacement (up to 6 g of magnesium sulfate per day). Despite the daily high doses of magnesium administered, the serum level fluctuated from 1.5 mg/dL to 2.7 mg/dL, and the QTc remained prolonged varying from 0.47 to 0.72 s (average of 0.538±0.062 s). Incessant sustained and nonsustained episodes of pVT and TdP continued to occur...

Micafungin and a case of polymorphic ventricular tachycardia

“…Other than amiodarone and fluconazole, pantoprazole was the only drug the patient was receiving at the time of arrhythmia that has been linked to QTc prolongation . That case was recently reported in a patient with chronic alcohol abuse and resistant hypomagnesaemia . This scenario does not appear likely in our patient as his magnesium concentration was within normal limits and he was not dependent on alcohol.…”

Potential Cardiovascular Risks of Proton Pump Inhibitors in the General Population

“…Subsequently, Bibawy, et al presented the case of a 53-year-old chronic alcoholic male patient with numerous life-threatening arrhythmias associated with PPI-induced hypomagnesemia. 44) In their study, the patient had no history of cardiovascular diseases and was not taking any medications before admission. Routine oral pantoprazole was prescribed for peptic ulcer prophylaxis.…”

Polymorphic ventricular tachycardia due to change in pacemaker programming

“…Although pantoprazole could cause QT prolongation, 5 she had been on it for a long time, and she was not on any other QT-prolonging drugs. Potassium and magnesium supplementation did not stop the polymorphic VT. Coronary angiogram excluded flow-limiting coronary artery disease, making ischemia an unlikely cause of presentation.…”