Metoclopramide as a Possible Cause of Prolonged QT Syndrome and Torsade de Pointes in a Patient With Heart Failure and Renal Insufficiency

摘要

Background: The long QT syndrome is a disorder of myocardial repolarization characterized by a prolonged QT interval and is associated with an increased risk for torsade de pointes. Metoclopramide is known to block ion channels, causing QT interval prolongation in experimental situations, but this has rarely been described in humans. nnObjective: To describe a patient with heart failure and renal impairment who was receiving metoclopramide and developed prolonged QT and torsade de pointes. nnCase Report: An 86-year-old man with a history of hypertension was admitted to the hospital after 6 weeks of shortness of breath. His history included gastroesophageal reflux disorder and hypothyroidism. His medications were l-thyroxine, metoclopramide, and lisinopril. On examination, he was in decompensated heart failure with an elevated jugular venous pulse, bibasilar rales, and pitting pedal edema. He had normal electrolyte levels (sodium, 136 mmol/L; potassium, 4.4 mmol/L; magnesium, 2.3 mmol/L [2.3 mEq/L]), thyroid function (thyroid-stimulating hormone level, 4.4 mU/L), and myocardial enzyme levels. The electrocardiogram (ECG) (Figure, A) on admission showed normal sinus rhythm and normal rate-corrected QT interval (QTc) (410 ms). He was given furosemide and continued receiving metoclopramide, 10 mg 4 times daily. The day after admission, his creatinine level increased from 14.92 μmol/L (1.3 mg/dL) to 167.96 μmol/L (1.9 mg/dL). A repeated ECG (Figure, B) showed prolongation of QTc (597 ms). In the next couple of hours, he developed torsade de pointes (Figure, C), which was successfully defibrillated. A repeated electrolyte check showed a magnesium level of 1.8 mmol/L (1.8 mEq/L), potassium level of 3.7 mmol/L, and troponin level of 0.00014 μg/L. He continued to have pause-dependent torsade de pointes on 3 more occasions, requiring defibrillation. After the events, the patient had coronary angiography, which showed normal coronary arteries. He received no further doses of metoclopramide, and the ECG showed reversion to a normal QT interval.