Cannabis exerts bidirectional effects on the cardiovascular system – it can increase or decrease both heart rate and blood pressure.  Typical doses of cannabis slightly decrease blood pressure and increase heart rate.  Cannabinoids can dilate blood vessels, improving blood flow, and animal studies suggest that some cannabinoids could prevent or reduce atherosclerosis (hardening of the arteries).  Ultra-low doses of THC have been shown to limit the damage of heart attack while preserving cardiac function and promoting faster healing.

In general, therapeutic doses of cannabis have a cardioprotective effect, while very high doses of cannabis and synthetic cannabinoids could be dangerous to the heart, especially in patients with pre-existing heart conditions.

Abstracts: Medical Studies 

‘Cannabinoid receptor type 2 activation in atherosclerosis and acute cardiovascular diseases’

Carbone F, Mach F, Vuilleumier N, Montecucco

Current medicinal chemistry 21.35 (2014): 4046-4058

In the last decades, the cannabinoid system (comprising synthetic and endogenous cannabinoid agonists and antagonists, their receptors and degrading enzymes) has been shown to induce potent immunomodulatory activities in atherogenesis and acute ischemic complications. Different from the other cannabinoid receptors in which controversial results are reported, the selective activation of the cannabinoid receptor type 2 (CB2) has been shown to play antiinflammatory and protective actions within atherosclerotic vessels and downstream ischemic peripheral organs. CB2 is a transmembrane receptor that triggers protective intracellular pathways in cardiac, immune and vascular cells in both human and animal models of atherosclerosis. Considering basic research data, medications activating CB2 function in the circulation or peripheral target organs might be a promising approach against atherogenesis. This review updates evidence from preclinical studies on different CB2-triggered pathways in atherosclerosis and acute ischemic events.

‘An ultra-low dose of tetrahydrocannabinol provides cardioprotection’

Waldman M¹, Hochhauser E, Fishbein M, Aravot D, Shainberg A, Sarne Y

Biochemical pharmacology 85.11 (2013): 1626-1633

‘Cardiovascular pharmacology of cannabinoids’

P. Pacher, S. Bátkai, and G. Kunos

Cannabinoids and their synthetic and endogenous analogs affect a broad range of physiological functions, including cardiovascular variables, the most important component of their effect being profound hypotension. The mechanisms of the cardiovascular effects of cannabinoids in vivo are complex and may involve modulation of autonomic outflow in both the central and peripheral nervous systems as well as direct effects on the myocardium and vasculature. Although several lines of evidence indicate that the cardiovascular depressive effects of cannabinoids are mediated by peripherally localized CB₁ receptors, recent studies provide strong support for the existence of as-yet-undefined endothelial and cardiac receptor(s) that mediate certain endocannabinoid-induced cardiovascular effects. The endogenous cannabinoid system has been recently implicated in the mechanism of hypotension associated with hemorrhagic, endotoxic, and cardiogenic shock, and advanced liver cirrhosis. Furthermore, cannabinoids have been considered as novel antihypertensive agents. A protective role of endocannabinoids in myocardial ischemia has also been documented. In this chapter, we summarize current information on the cardiovascular effects of cannabinoids and highlight the importance of these effects in a variety of pathophysiological conditions.

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

Pacher, Steffens, Haskó, Schindler, Kunos

Dysregulation of the endogenous lipid mediators endocannabinoids and their G-protein-coupled cannabinoid receptors 1 and 2 (CB₁R and CB₂R) has been implicated in a variety of cardiovascular pathologies. Activation of CB₁R facilitates the development of cardiometabolic disease, whereas activation of CB₂R (expressed primarily in immune cells) exerts anti-inflammatory effects. The psychoactive constituent of marijuana, Δ⁹-tetrahydrocannabinol (THC), is an agonist of both CB₁R and CB₂R, and exerts its psychoactive and adverse cardiovascular effects through the activation of CB₁R in the central nervous and cardiovascular systems. The past decade has seen a nearly tenfold increase in the THC content of marijuana as well as the increased availability of highly potent synthetic cannabinoids for recreational use. These changes have been accompanied by the emergence of serious adverse cardiovascular events, including myocardial infarction, cardiomyopathy, arrhythmias, stroke, and cardiac arrest. In this Review, we summarize the role of the endocannabinoid system in cardiovascular disease, and critically discuss the cardiovascular consequences of marijuana and synthetic cannabinoid use. With the legalization of marijuana for medicinal purposes and/or recreational use in many countries, physicians should be alert to the possibility that the use of marijuana or its potent synthetic analogues might be the underlying cause of severe cardiovascular events and pathologies.

‘Synthetic and natural cannabinoids: the cardiovascular risk’

E.B.Russo

BrJCardiol22(2015):7-9.

Cannabis has been employed medicinally and recreationally for thousands of years,^1,2 but it was not until the 1960s that the structure and pharmacology of its primary phytocannabinoid components, cannabidiol (CBD)³ and tetrahydrocannabinol (THC)⁴ were identified, and another generation before the nature and function of the endocannabinoid system (ECS) were elucidated (see reference 5 for a comprehensive review). The ECS consists of endogenous cannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG), their biosynthetic and catabolic enzymes, and their receptors: CB₁, which is psychoactive, analgesic, neuromodulatory and the most abundant G-protein coupled receptor in the brain, and CB₂, which is non-psychoactive, immunomodulatory and anti-inflammatory. The ECS may be thought of as a grand homeostatic regulator of chordate physiological functions, whose roles have been summarised as: “relax, eat, sleep, forget and protect”.⁶ Those actions closely describe the effects of THC and AEA, which are both weak partial agonists at CB₁ and CB_2.