American Journal of Preventive Cardiology (Sep 2023)

PHENTERMINE-INDUCED VENTRICULAR TACHYCARDIA

  • Ronak Bharucha,
  • Sawyer Bawek,
  • Muhaimen Rahman,
  • Khaled Abdulla

Journal volume & issue
Vol. 15
p. 100531

Abstract

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Therapeutic Area: Pharmacologic Therapy Background: Phentermine, a common appetite suppressant, functions as a central nervous system stimulant through activation of the noradrenergic pathway of the sympathetic nervous system. Its use has been associated with reports of tachyarrhythmias as well as QT prolongation. Here, we present a case of phentermine-induced QT prolongation and associated VF. Methods: N/A Results: The patient is a 41-year-old-female with a past medical history of obesity, polysubstance abuse (alcohol and tobacco), and depression/anxiety who presented to the Emergency Department via EMS after she collapsed at home and was found to be in VF. She received bystander CPR in addition to defibrillation with return of spontaneous circulation. The patient had no previous cardiac history and was taking no medications other than clonazepam and phentermine. There was no significant family history of cardiovascular disease.Upon admission, the patient was hemodynamically stable. Her initial EKG revealed normal sinus rhythm with nonspecific ST/T-wave abnormality as well as QT prolongation, with a QTc 520 ms, which persisted. Blood work showed a peak troponin I level of 0.10. Electrolytes were all within normal limits, including potassium (4.4) and magnesium (2.4). Toxicology workup was positive for amphetamines. Coronary angiography soon after admission revealed patent coronary arteries with preserved LV function and LVEDP 14 mmHg. A transthoracic echocardiogram revealed a left ventricular ejection fraction of 60-65% with no structural or wall motion abnormalities. Therefore, it was determined that the likely mechanism of her cardiac arrest through QT prolongation was from phentermine use. While she received IV amiodarone per ACLS protocol, which could have confounded her presenting EKG, such a modest dose would not be expected to cause significant QT prolongation. A secondary prevention ICD was placed and she was discharged home with instructions to discontinue phentermine indefinitely. Conclusions: The increased prevalence of obesity has seen with it a rise in the use of pharmacotherapy directed at promoting weight loss. Our case demonstrates that the popular appetite-suppressant, phentermine, may have the ability to promote potentially fatal cardiac arrhythmias through QT prolongation. Patients and physicians should both be cognizant of the potential for these medications to exert significant adverse cardiovascular effects.