Key points
- 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 effects
- The 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 mechanisms
- The composition of marijuana (THC–cannabidiol ratio, terpenoids) can influence its therapeutic and cardiovascular adverse effects, with marijuana smoke being as harmful as tobacco smoke
- Most 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 effects
- In 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 increased
- Clinicians 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 (Also see Handbook of Cannabis and Related Pathologies – 1st Edition (elsevier.com)
