Review finds cardiovascular concerns, but causation remains unproven

Expanded Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) use have prompted increasing interest in their risk for cardiovascular complications. This narrative review synthesizes mechanistic, experimental, and epidemiologic evidence on the relationships between cannabinoid exposure and cardiovascular disease, summarizes acute and chronic outcomes, evaluates therapeutic potential of non-psychoactive cannabinoids, and identifies future research priorities. Cannabinoid type 1 receptors in cardiovascular tissues promote sympathetic activation, tachycardia, and endothelial dysfunction, while cannabinoid type 2 receptor activation exerts anti-inflammatory and athero-protective effects. Acute THC exposure in humans produces tachycardia, increased myocardial oxygen demand, vascular stiffness, and transient blood-pressure alterations. Recent large observational studies and meta-analyses suggest associations between cannabis/cannabinoid use and increased risk of major adverse cardiovascular events. While causality has not yet been definitively established, the accumulation of in vitro and in vivo evidence indicates potentially significant cardiovascular risks associated with frequent and/or heavy cannabinoid use, particularly in individuals with underlying cardiovascular disease or other risk factors. In the future, clinicians should screen for cannabinoid use, and standardized exposure metrics, longitudinal studies and randomized controlled trials are urgently needed.