Fatal Cannabis-Associated Cardiovascular Toxicity Following High-Potency Cannabis Use: An Integrated Clinicopathologic Investigation.

von Both I.; Chatterton C.; Balachandra T. · The American journal of forensic medicine and pathology · 2026

**Background & Methods** This is a clinicopathologic case report of a fatal cardiovascular event in a 28-year-old male following consumption of a legally purchased high-potency cannabis product. The investigation integrated clinical presentation, serial electrocardiography, cardiac biomarkers, autopsy findings, toxicology, and comprehensive cardiac genetic testing. **Key Findings** • A previously healthy 28-year-old experienced witnessed ventricular fibrillation during cannabis use; spontaneous circulation was restored after approximately 50 minutes of resuscitation, but severe hypoxic-ischemic encephalopathy developed, resulting in death 6 days later after withdrawal of life support. • Serial ECGs revealed evolving ischemic abnormalities with dynamic elevation of cardiac biomarkers; autopsy demonstrated structurally normal heart with patent coronary arteries but patchy acute subendocardial myocardial infarction. • Antemortem toxicology confirmed cannabis exposure (Δ9-THC and 11-nor-9-carboxy-Δ9-THC detected); comprehensive cardiac genetic testing identified no pathogenic variants, and clinical findings support acute cannabis-associated cardiovascular toxicity rather than underlying structural or genetic cardiac disease. **Dosage & Administration** The cannabis product was labeled as containing 29.9% Δ9-THC. Specific dose consumed and exact administration method details are not quantitatively reported. **Safety & Adverse Effects** Acute cannabis-associated cardiovascular toxicity manifested as ventricular fibrillation, myocardial ischemia, and myocardial infarction. The authors propose transient myocardial ischemia secondary to coronary vasospasm as the primary mechanism, though primary ventricular arrhythmia with secondary global ischemia-reperfusion injury cannot be excluded. Secondary complications included severe hypoxic-ischemic encephalopathy. **Evidence Quality** This is a single case report with level of evidence C, representing the lowest tier of clinical evidence hierarchy. The study lacks control groups, comparative data, and cannot establish causality with certainty. Limitations include the retrospective inability to definitively exclude primary arrhythmia as the initiating event and inability to generalize findings to broader populations. However, the integrated multidisciplinary investigation (clinical, electrocardiographic, pathologic, toxicologic, and genetic) strengthens the clinicopathologic findings. The case is notable for comprehensive evaluation and highlights need for further mechanistic research into cannabis-associated acute cardiovascular complications, particularly with high-potency products in young, previously healthy individuals.

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