Cardiovascular effects of marijuana and synthetic cannabinoids: the good, the bad, and the ugly

Activation of cannabinoid receptor 1 (CB1R) by endocannabinoids or synthetic ligands mediates acute haemodynamic effects and might contribute to pathology in cardiovascular disease; activation of cannabinoid receptor 2 (CB2R) exerts anti-inflammatory effectsThe psychoactive constituent of marijuana, Δ9-tetrahydrocannabinol (THC), exerts its cardiovascular effects via CB1R activation; at low doses it might have beneficial properties via partial activation of CB1R and CB2R, and unrelated mechanismsThe composition of marijuana (THC–cannabidiol ratio, terpenoids) can influence its therapeutic and cardiovascular adverse effects, with marijuana smoke being as harmful as tobacco smokeMost synthetic cannabinoids used for recreational use are full agonists of CB1R (THC is a partial agonist) with up to several hundred-fold higher potency and efficacy than THC, causing more dangerous adverse effectsIn parallel with a tenfold increase in the THC content of marijuana and the widespread availability of synthetic cannabinoids for recreational use, the number of serious cardiovascular adverse effects reported has markedly increasedClinicians should be vigilant to recognizing potential cardiovascular effects of marijuana and synthetic cannabinoids; controlled clinical trials should determine the long-term consequences of the use of medical marijuana on cardiovascular morbidity and mortality