Polysubstance abuse in a 23-year-old male caused concurrent opioid-induced CHANTER syndrome and cocaine-induced coronary vasospasm with a peak troponin of 3700 ng/L, requiring cautious management.
Case Report (n=1)
This case highlights the diagnostic and management challenges of concurrent CHANTER syndrome and cocaine-induced type II NSTEMI, emphasizing that the risks of anticoagulation may outweigh the benefits in such complex polysubstance abuse presentations.
Abstract Introduction Polysubstance abuse can cause complex multi-organ dysfunction, including rare neurologic and cardiac complications. CHANTER syndrome—Cerebellar, Hippocampal, and Basal Nuclei Transient Edema with Restricted Diffusion—is a reversible cerebellar syndrome linked to opioid toxicity. Cocaine-induced coronary vasospasm causing myocardial injury is another serious but uncommon outcome. We present a case involving both in a young adult, emphasizing diagnostic and management challenges. Case Presentation A 23-year-old male with a history of polysubstance abuse was found unresponsive by his father. EMS noted pinpoint pupils, respiratory depression, and hypoxia. Naloxone was given with partial improvement, followed by seizure-like activity and foaming at the mouth, aborted with IV benzodiazepines. He was intubated for airway protection and transferred to the ED. On arrival, he was febrile, tachycardic, mildly hypotensive, and had lower extremity ataxia. Labs showed elevated lactate and troponins (peak 3700 ng/L). Urine drug screen was positive for cocaine, benzodiazepines, marijuana, and fentanyl. CT head showed a right cerebellar lesion concerning for mass. Serial ECGs revealed sinus tachycardia, Q waves in leads III/aVF, and evolving T wave inversions in V1-V5, concerning for NSTEMI. Anticoagulation was withheld due to neurologic concerns. Echocardiogram was unremarkable. Troponins down trended without intervention. Cardiology diagnosed a type II NSTEMI, suspected from cocaine-induced coronary vasospasm. MRI showed restricted diffusion in cerebellar folia with high signal on DWI, T2, and FLAIR, low ADC values, and minimal enhancement—findings suggestive of CHANTER syndrome. PICA vasospasm was less likely due to non-territorial pattern. EEG showed mild encephalopathy without epileptiform activity. Keppra was initiated, then discontinued as seizures were deemed toxic-metabolic. The patient improved, was extubated, and discharged stable with outpatient MRI follow-up. Discussion This case highlights the dual burden of neurologic and cardiac issues in polysubstance abuse. CHANTER syndrome, though reversible, can mimic infarcts on imaging, complicating diagnosis. In suspected cocaine-induced myocardial injury, where Type II MI is likely and no thrombus is evident, the risks of anticoagulation—especially with concurrent neurologic concerns such as CHANTER syndrome and seizures—often outweigh the benefits. A multidisciplinary, cautious approach is essential. This abstract is funded by: None
Alali et al. (2026) conducted a case report in Polysubstance abuse, CHANTER syndrome, cocaine-induced coronary vasospasm (n=1). Polysubstance abuse in a 23-year-old male caused concurrent opioid-induced CHANTER syndrome and cocaine-induced coronary vasospasm with a peak troponin of 3700 ng/L, requiring cautious management.