A 32-year-old male presented with severe palpitations and syncope. He had a history of prior alcohol, opiate, and methamphetamine abuse, but otherwise no known medical conditions. He admitted to taking, over the prior 10 days, up to 200 mg daily of loperamide (maximum recommended dosage 16 mg per day) and multiple doses of famotidine daily (estimated up to 500 mg per day). Both medications were obtained over the counter. He did not take any other medications, supplements, or recreational substances.\nHis initial vital signs were as follows: blood pressure 121/76 mmHg; pulse 62 beats/min; temperature 98 F; and oxygen saturation 97%, breathing ambient air. He appeared disheveled, but otherwise had no abnormal physical exam findings. His presenting electrocardiogram (ECG) showed sinus tachycardia at 101 beats/min, first-degree atrioventricular (AV) block, nonspecific intraventricular conduction delay, and prolonged QT interval (Fig. ). Serum electrolytes, blood counts, cardiac troponin (I), renal, liver, and thyroid function were normal. Transthoracic echocardiogram showed normal chamber size and function and normal valves.\nShortly after admission, he had recurrent symptoms (syncope preceded by palpitations) that occurred during sustained monomorphic VT (Fig. ). VT terminated spontaneously. Loperamide and famotidine were discontinued, and he was treated with intravenous magnesium and supportive care. During hospitalization, he had frequent multifocal premature ventricular complexes and runs of both monomorphic and polymorphic VT. After 5 days, his PR interval, QRS duration, and QT interval normalized and VT resolved. He was discharged and strongly encouraged to abstain from recreational drug use. At 6 months follow-up, he had maintained abstinence from recreational drugs and his ECG continued to be normal (Fig. ).
46-year-old male was presented in the ER after cardiac arrest. Patient had two-hour flight before he started feeling light-headed and passed out at the airport. The airport emergency services found him in ventricular fibrillation and provided him with two shocks before he regained consciousness. Subsequent EKG showed normal sinus rhythm and prolonged QT (QTc-589 msec); EKG is not available. Upon arrival to ER, patient was alert and oriented but amnesic about past events. Patient was taken for cardiac catheterization which revealed nonobstructive coronaries and normal ejection fraction. Electrolytes were unremarkable except potassium of 3.1 which was replaced. Complete blood counts, renal function, serum troponin, and serum magnesium were within normal limits. MRI of brain revealed no significant abnormalities. Shortly after coronary angiogram, patient again went to cardiac arrest and resuscitated with one shock. Cardiac monitor showed torsades de pointes ventricular tachycardia () with hemodynamic instability. Patient was intubated for airway protection and received IV magnesium and IV amiodarone. Toxicology screen was unremarkable except benzodiazepine he received during intubation (midazolam) for sedation. EKG showed normal sinus rhythm, nonspecific ST-T wave abnormality, and prolonged QT (QTc-620 msec) (). Echocardiogram revealed structurally normal heart. Acute pulmonary embolism was also ruled out with computed tomography pulmonary angiogram. Patient's spouse reported that patient has been taking large amount of Loperamide for irritable bowel syndrome for more than 5 years. However, she was not able to quantify the amount of Loperamide. Patient persistently experienced multiple episodes of sustained ventricular tachycardia requiring multiple defibrillation in setting of significantly prolonged QTc (>600 msec) on multiple serial EKGs. Patient was treated with metoprolol, lidocaine, and magnesium infusion. Over the period of 7 days, patient stopped having sustained ventricular tachycardia. Frequency of nonsustained ventricular tachycardia was also reduced and patient was extubated after several days of CCU monitoring. Lidocaine and magnesium were discontinued and metoprolol was continued. Loperamide levels were not obtained. After extubation, patient denied having similar episode in the past, chest pain, palpitations, syncope, shortness of breath, and any family history of sudden cardiac death or cardiac diseases. However, patient admitted that he has been self-medicating with over-the-counter 2 mg Loperamide approximately 50 tablets a day for diarrhea predominant irritable bowel syndrome for more than 5 years. He also admitted having approximately 100 pills of Loperamide daily for the last 2 days before admission. Since patient was buying over-the-counter Loperamide from different pharmacy; we could not determine exact frequency of purchase. Patient denied using illicit drug use, herbal supplements, or concurrent p-glycoprotein inhibitors. Serial EKG monitoring showed gradual decrease in QTc. However, serial EKG monitoring off Loperamide for several days revealed normal sinus rhythm and QTc of 472 msec () and 456 msec (). Only one EKG revealed QTc of 432 msec (). Thus, patient's QTc interval did not completely normalize after several days off all QTc prolonging medications and subsequently he received dual chamber automated cardioverter defibrillator (AICD) before discharge for secondary prevention of cardiac arrhythmia related death. Since majority of patient's QTc interval was >440 msec even after a week of stopping all QT prolonging medications, at this time, we think that patient may have subclinical long QT syndrome which was unmasked by Loperamide. However, electrophysiological studies were not performed to verify the diagnosis. Patient was instructed not to use Loperamide again.