Abstract

Thirty-Three states in the US have passed laws to legalize marijuana usage, increasing its prevalence by 50% within the last year. Though society generally regards cannabis as safe, the exponential increase in users can evince dangerous side effects in patients presenting to physicians, such as the case presented below. A 37-year-old female presented to the ED with chest pain and an initial troponin of 24 that peaked at 29. The coronary arteries were found to be angiographically normal. She was discharged without any definitive diagnosis. Now 38, she again presented with complaints of crushing, substernal chest pain radiating down her left arm, unrelieved by nitro. Since the onset of pain, she progressively developed shortness of breath, nausea, diaphoresis, and anxiety, stating that she felt like she “was going to die.” Her presentation and impending sense of doom were ominous harbingers for a myocardial infarction; concerns that were validated with an initial troponin of 11.4. EKG showed normal sinus rhythm with nonspecific ST changes. CT Angiogram showed no evidence of pulmonary thrombo-embolism or dissection. Significant CAD leading to this extent of troponin elevation was not suspected as the patient had a normal angiogram a year prior. Stress-Induced Cardiomyopathy was unlikely based on the unremarkable echocardiogram findings. Coronary-Thrombus was considered, however, the hypercoagulable workup was negative along with lack of coronary thrombus on prior angiogram. Under these circumstances, the only explanation for the extent of troponin elevation was myocarditis. Viral infections are the most common cause of myocarditis, however the patient denied any associated symptoms. After ruling out viral etiologies, we subsequently evaluated and eliminated rheumatological disorders and medication-induced myocarditis. The patient’s history revealed that she led a healthy lifestyle, but had struggled with chronic back pain, which led to her cannabis use. By the time of her admission, she smoked up to 1.5 grams of cannabis a day, and stated that chest pain began immediately following smoking cannabis. Her previous episodes also correlated with her cannabis usage. Given the strong correlation of the patient’s symptoms with cannabis use, we theorized her cardiac stress was resultant from it, and recommended that she discontinue its use. To date there have been four reported cases of cannabis-induced myocarditis, making this a fifth case. Of note, the contaminants of marijuana may be variable and include substances like aluminum from soil or pesticides in grass that could traverse the marijuana plant. Inhaling such components has been correlated with an upregulation of cannabinoid receptors in platelets, vascular smooth muscle, and endothelium. CB1R activation has been observed to induce oxidative stress, inflammation, and fibrosis of the cardiomyocyte. With increased cannabis use, it is imperative that we document adverse events to definitively connect its use to cardiac damage.

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