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.
A 32-year-old female with a past medical history of chronic back pain, fibromyalgia, chronic pain syndrome, and past opioid usage presented to our ED with atypical chest pain, palpitations, and shortness of breath. She also gave a history of near-syncopal episodes in the past. The day before she presented to the ED, the patient had a syncopal episode and "turning purple" at home, prompting her daughter to call the emergency medical services (EMS), but the patient canceled the EMS after she awakened from this episode (likely due to Torsade’s de Pointes). On arrival to the ED, she had an episode of polymorphic ventricular tachycardia, which was sustained, and the patient spontaneously self-converted to sinus rhythm with frequent premature ventricular contractions and ventricular bigeminy (Figure ). She had a persistently prolonged QT interval, and nonspecific ST changes were noted. She was put on telemetry, where 19 beats of Torsade’s were noted. The patient denied any known personal or family history of heart disease or any congenital QT syndrome. She is an everyday cigarette smoker and denied any alcohol or any other illicit drug use. Toxicology studies were unremarkable.\nLabs were normal except for hypokalemia, which was replaced. Her serial cardiac enzymes were normal imaging of the chest, abdomen, and pelvis was unremarkable. The patient received amiodarone and magnesium in the ED and was put on continuous telemetry. Despite this intervention the patient continued to show ventricular bigeminy and short runs of polymorphic ventricular tachycardia (Figure ). The patient was upgraded to the intensive care unit (ICU), for closer monitoring and evaluation. The electrophysiology and cardiology services were consulted. The patient underwent an echocardiogram, which showed a normal ejection fraction, normal right and left ventricular functions, and no valvular abnormalities. The patient later endorsed that she was on oxycodone, fentanyl patch, and hydrocodone for her chronic pain issues. Her primary care had weaned her off the medications, and she was not getting any more opioid prescriptions. She also confided that she had been consuming 200 tablets of 2 mg over-the-counter (OTC) loperamide every week to "extend her opioid analgesic prescription for her chronic pain issues" and that she had taken one high dose of 200 tablets of 2 mg all at once before today's ED visit. Due to the long half-life of loperamide, the patient was advised to continue admission to the ICU till the QT interval stabilizes. Further plan was made to send her home on life vest with outpatient follow-up for implantable cardiac defibrillator (ICD) therapy. She did not seem interested in any of the above-stated therapies and adamantly refused any outpatient or inpatient opiate rehabilitation. While all these discussions were taking place, the patient left the hospital against medical advice (AMA).\nThe patient again presented to our ED with chest pain, shortness of breath, nausea, and vomiting on the following day. She was still bradycardic in the '50s along with persistent, prolonged QT interval and ventricular bigeminy (Figure ). Electrophysiology and cardiology services were again consulted, and the patient also underwent coronary angiography, which did not show any significant blockage or evidence of structural heart disease. It was again reiterated to her about the importance of considering life vest versus ICD versus medical management. She was also advised to refrain from loperamide use entirely and to quit cigarette smoking. Despite all the advice and education from several physicians and hospital staff, the patient again left the hospital AMA and was unfortunately lost to follow up.