24-year-old with history of smoking tobacco and cannabis • dyspnea • chest tightness

A toxicology screen was positive for tetrahydrocannabinol (THC) and negative for other substances. Hypercoagulable laboratory studies were normal, including anticardiolipin antibody IgG and IgM, factor V Leiden, prothrombin G20210A mutation, thrombin time, antithrombin III, and protein C and S activity. It was therefore believed that the AMI was due to in-situ coronary artery thrombus formation precipitated acutely by smoking cannabis—possibly with an underlying hypercoagulable state, even though no laboratory abnormalities were detected.

A registry of patients with coronary thrombosis without coronary atherosclerosis, especially in states where cannabis is legal, would be useful.

Our patient was discharged on lifelong aspirin 81 mg/d and oral rivaroxaban (maintenance dose of 20 mg/d). Metoprolol succinate 12.5 mg/d and lisinopril 2.5 mg/d were also initiated due to LV systolic dysfunction (and to be used indefinitely). Cannabis and tobacco smoking cessation was strongly emphasized, as both have independently been shown to increase cardiovascular events; the overall effects of using both substances, however, are currently unknown. At 6-month follow-up, the patient was doing well; an echocardiogram demonstrated an improvement in LV systolic function with an LVEF of 45%.

THE TAKEWAY

Coronary thrombosis can result in an AMI, even without underlying coronary atherosclerosis. Smoking cannabis may predispose individuals to in-situ coronary thrombosis and subsequent AMI. Although not often encountered in clinical practice, providers must be aware of this phenomenon in the differential diagnosis for AMI—particularly in young patients without traditional risk factors.

CORRESPONDENCE
Konstantinos Dean Boudoulas, MD, The Ohio State University Davis Lung and Heart Research Institute, 473 W. 12th Avenue, Suite 200, Columbus, Ohio 43210; kdboudoulas@osumc.edu