Takotsubo Cardiomyopathy Associated With Severe Medetomidine Withdrawal: A Case Report

Takotsubo cardiomyopathy (TCM) is a transient syndrome of cardiac dysfunction with no occlusive coronary arterial disease, which may mimic an ischemic cardiac event. The pathogenesis of TCM is thought to be primarily driven by the effects of a temporary catecholamine surge on cardiac and vascular tissue. Medetomidine (an a2 agonist commonly found in the Philadelphia fentanyl supply) withdrawal is characterized by agitation and sympathetic hyperactivity that can precipitate a catecholamine surge. Though withdrawal from other Central Nervous System (CNS)-depressing substances such as opioids and clonidine have been found to be associated with TCM, there is little documentation of this phenomenon occurring from medetomidine withdrawal.

A 51-year-old woman with no reported medical history other than opioid use disorder presented to the emergency department due to concern for withdrawal from fentanyl and medetomidine. Her opioid withdrawal was well controlled with methadone and oxycodone. Shortly after coming off her dexmedetomidine infusion (started for medetomidine withdrawal), she developed acute ST-segment changes on electrocardiogram, elevated troponin levels on bloodwork, and regional wall-motion abnormalities on transthoracic echocardiogram. Her coronary angiography showed no occlusion and repeat cardiac laboratory workup days later had normalized with improvement in ejection fraction on cardiac echocardiography and magnetic resonance imaging. This signifies a temporary stress cardiomyopathy, likely from a2 agonist withdrawal.

This case describes TCM in a patient experiencing medetomidine withdrawal. This patient's cardiac dysfunction was transient, temporally correlating with the cessation of her dexmedetomidine infusion. This suggests an a2 agonist mediated withdrawal leading to sympathetic hyperactivity which can precipitate TCM.