Abstract 16368: Opioid Withdrawal-Induced Takotsubo Cardiomyopathy in Hypertrophic Cardiomyopathy

Abstract

Introduction: This case highlights opioid withdrawal-induced Takotsubo cardiomyopathy (TCM) in a patient with pre-existing hypertrophic cardiomyopathy (HCM) and discusses the concurrent management. Clinical Presentation: An 85-year-old female with HCM, depression, and chronic back pain presented with generalized weakness five days after opioid discontinuation. She exhibited elevated troponin levels and ST elevation in anteroseptal leads, concerning for STEMI. Coronary angiogram revealed nonobstructive coronary artery disease. Transthoracic echocardiogram revealed newly reduced EF 45%, hyperdynamic basal left ventricle, and akinetic mid-distal left ventricle, consistent with TCM. Notably, marked basal anteroseptum thickness and systolic anterior mitral valve motion with left ventricular outflow tract obstruction (LVOTO) and a peak gradient of 92 mmHg. Presentation was complicated by hypotension, pulmonary edema and cardiorenal syndrome. β-blocker use initially deferred, opting for phenylephrine and diuresis until stabilization permitted β-blocker introduction. Discussion: We present a unique case of TCM precipitated by opioid withdrawal in a patient with existing HCM. Standard critical care management for TCM involves hemodynamic support until cardiac function recovers, though the use of vasopressors and inotropes remains controversial. Importantly, this case demonstrates severe provoked LVOTO, mimicking acute myocardial ischemia. Recognizing such scenarios is vital, as inappropriate use of vasodilators or inotropes can be fatal. Class I-IIa recommendations endorse β-blockers and vasoconstrictors for severe provoked LVOTO with hypotension and pulmonary edema. Phenylephrine, a selective α-agonist, maintains LVOT turgidity through preload enhancement, while β-blockers facilitate ventricular filling and reduce LVOT pressure gradient. Further research is warranted as current evidence level remains class C.