Pramod Theetha Kariyanna¹, Leanna R. Smith¹, Karishma Patwa², Moro O. Salifu², Isabel M. McFarlane^2,

Marijuana is the most widely used recreational drug across the United States. Ongoing efforts to legalize marijuana, as well as the drug’s increasing popularity contribute to the marijuana’s reputation as having a low risk profile. Marijuana’s association with adverse cardiovascular events, such as arrhythmia and vasospasm is well-documented. We synthesized what is known about how marijuana use pertains to and is implicated endothelial cell damage and its effects on microcirculation. THC exerts effects through the cannabinoid receptors, CB1 and CB2. The downstream effects of CB1 activation point to a role for this receptor in atherogenesis and vasospasm, likely by precipitating oxidative stress. Endothelial cells, when exposed to reactive oxygen species, provide a stimulus for vasoconstriction with a diminished ability for vasodilation. This phenomenon has manifested itself in cases of coronary vasospastic angina, and coronary slow and no flow that have resulted from marijuana use, as confirmed by cardiac catheterization reports that showed no evidence of obstructive lesions that could otherwise be responsible for the patients’ symptoms. Marijuana users suffer from acute ischemic stroke at higher rates than non-users. Several theories have been proposed to support this observation, namely marijuana induced reversible cerebral vasoconstriction syndrome, and mitochondrial damage caused by oxidative stress that disproportionately affects cerebral vasculature. As marijuana use continues to grow, so does the important of elucidating the drug’s effect on endothelial cells and microcirculation. Further studies should investigate the temporal association between marijuana and endothelial damage, as well as the possibility of recovery from such injury, and whether there is therapeutic potential in cannabinoid receptors.

marijuana, microcirculation, endothelium, myocardial infarction, stroke, coronary vasospasm