Title:
Opioid Intoxication Precipitating Takotsubo Cardiomyopathy: An Atypical Presentation of Opioid Use Disorder
Introduction:
With the escalating prevalence of opioid use disorder (OUD) over recent decades, there has been a parallel rise in associated complications. One such complication that has been relatively underreported is the connection between OUD and stress-induced cardiomyopathy, commonly referred to as Takotsubo cardiomyopathy (TTC). Takotsubo cardiomyopathy is characterized by transient left ventricular (LV) dysfunction featuring apical ballooning, elevated cardiac enzyme levels, and electrocardiogram (EKG) findings resembling myocardial infarction (MI), all in the absence of mechanical obstruction in the coronary vasculature. This report presents a compelling case of opioid withdrawal precipitating TTC.
Clinical Case:
A 62-year-old male, known to have a history of opioid use disorder, presented with complaints of exertional dyspnea, generalized weakness, vomiting, and diarrhea. The patient disclosed a daily history of snorting ten bags of heroin over 37 years, with the last use occurring one day before admission. Physical examination revealed diminished breath sounds in the right lung and mild wheezes in the right middle lobe. Vital signs were within normal limits. Laboratory results indicated a rising troponin level, increasing from 1803 to 2873 pg/mL, B-type natriuretic peptide (BNP) at 981 pg/mL, and creatine kinase-MB (CK-MB) at 18.6 ng/mL. Chest X-ray findings were unremarkable, with no signs of consolidation, congestion, or effusion. The initial EKG showed nonspecific ST and T wave abnormalities, while a subsequent EKG demonstrated new diffuse T wave inversions. Echocardiography revealed an acute reduction in left ventricular ejection fraction (LVEF) to 30-35%, along with mild mitral regurgitation and hypokinetic wall motion at the cardiac apex. Cardiac catheterization excluded coronary artery disease and confirmed the presence of TTC, characterized by a reduced LVEF of 25-30% and ballooning of the mid- distal anterior apex and mid-distal inferior wall. Elevated troponin levels, BNP, EKG changes, and catheterization findings corroborated the patient's TTC diagnosis. The patient was discharged in stable condition, with plans for rehabilitation focused on addressing opioid abuse and instructions for outpatient follow-up, including a repeat echocardiogram.
Discussion:
Although opioid withdrawal induced TTC has been sporadically documented in previous cases, the exact mechanism remains a subject of speculation. It is postulated that the hyperactivity of the adrenergic system, which typically arises around 72 hours after opioid discontinuation, may contribute to this phenomenon. However, in this specific case, no concrete evidence suggests that the patient ceased opioid use prior to symptom onset. Consequently, this case could be attributed to opioid intoxication, an aspect rarely explored in the literature as a potential trigger for TTC. Alternatively, emotional stress or other risk factors may be at play, highlighting the necessity of obtaining a comprehensive psychological history for all TTC patients. This case serves as a reminder of the atypical triggers for TTC in individuals with a history of opioid use disorder, emphasizing the importance of maintaining a high index of clinical suspicion for TTC in cases with suspected opioid abuse.