Synthetic cannabinoids (SC), though not detected with routine urine toxicology screening, can cause severe metabolic derangements and widespread deleterious effects in multiple organ systems. The diversity of effects is related to the wide distribution of cannabinoid receptors in multiple organ systems. Both cannabinoid-receptor-mediated and non-receptor-mediated effects can result in severe cardiovascular, renal, and neurologic manifestations. We report the case of a 45-year-old African American male with ST-elevation myocardial infarction, subarachnoid hemorrhage, reversible cardiomyopathy, acute rhabdomyolysis, and severe metabolic derangement associated with the use of K2, an SC. Though each of these complications has been independently associated with SCs, the combination of these effects in a single patient has not been heretofore reported. This case demonstrates the range and severity of complications associated with the recreational use of SCs. Though now banned in the United States, use of systemic cannabinoids is still prevalent, especially among adolescents. Clinicians should be aware of their continued use and the potential for harm. To prevent delay in diagnosis, tests to screen for these substances should be made more readily available.

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Background: Recreational marijuana use is rising, especially among young adults. The cardiovascular (CVD) effect of marijuana remains mostly unknown.Methods: This is a retrospective study of 14,490 patients admitted to our hospital between 2012 and 2014 who had urine toxicology done for various reasons. Patients with a primary diagnosis of acute coronary syndrome (ACS) were queried in both the marijuana-positive group (n = 59) and the marijuana-negative group (n = 195). The risks of having ACS were compared in both groups.Results: There was no difference in the risk of having ACS between the two groups in the population < 54 years of age (OR: 0.90, 95% CI: 0.67-1.20, p = 0.48). However, there was a significant difference in the risk of having ACS in the 18-36 age group (OR: 2.84, 95% CI: 1.14-7.07, p = 0.01). Multivariate analysis performed to adjust for the potential confounding effects of smoking and cocaine use showed that marijuana use (OR: 0.93, 95% CI: 0.68-1.25, p = 0.65) did not increase the likelihood of ACS for patients ≤ 54 years or for those in the 37-54 age group (OR: 1.11, 95% CI: 0.79-1.53, p = 0.50). However, among the 18-36 age bracket, marijuana use was independently associated with a higher risk of ACS (OR: 5.24, 95% CI: 1.84-16.93, p = 0.002). Conclusion:In younger patients (age 18-36 years), marijuana use is independently associated with a fivefold higher risk of ACS.

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