Among other things, inflammation of the heart can cause cardiovascular cells to become damaged or even die. This can be brought on by certain diseases, viruses, medications, or even an autoimmune attack. If inflammation isn’t treated, it could result in death.
In this article, we take a look at the possible therapeutic range of CBD for heart disease, as well as some of the latest medical research on the topic.
CBD for Heart Disease: Reducing Inflammation
One of the latest studies on CBD for heart disease was carried out by researchers from Fudan University in Shanghai and published in Science Direct. It found that cannabis could be useful in the management of both stroke and cardiac arrest. The study focused on the effects that CBD has on a condition known as cerebral ischemia. This disease is a deficiency of blood flow to the brain and is associated with several health problems such as cardiac arrest, brain damage, and stroke.
Some doctors believe it to be just as effective, if not more effective than pharmaceuticals. Others have a hard time acknowledging the various reports that claim CBD to be a powerful alternative for the treatment of heart disease. Hopefully, with continued research, CBD will be recognized for its therapeutic value on a larger scale.
Another study found that in addition to its ability to lower blood pressure, CBD could also be useful in the prevention and treatment of myocardial ischemia-reperfusion injury. In this study, the authors discovered that CBD produces a substantial cardioprotective effect from ischemia, which reduces infarction size.
An excerpt from The Essential Guide to CBD by the editors of Reader’s Digest & Project CBD .
CBD may also protect against cardiac arrhythmias, or irregular heartbeats, where the heart beats too fast, too slowly, or with an irregular pattern. Arrhythmias can be brought on by long-term stress, as high cortisol levels can raise blood pressure, blood cholesterol, blood sugar, triglycerides, and other risk factors for heart disease in general. CBD ’s anti-anxiety properties can help combat stress, lower cortisol, and protect against arrhythmias related to those causes.
THC and CBD are both vasodilators, meaning they widen your blood vessels, a process regulated by the endocannabinoid system. This can have a pronounced positive effect on blood pressure. In a 2017 study, British researchers gave a group of men either 600 mg of CBD or a dummy supplement and monitored their blood pressure at rest and again after stress tests that normally increased blood pressure. Just that single dose of CBD reduced the participants’ resting systolic blood pressure by 6 mmHg. Plus, they had less of a spike in blood pressure in response to stress than those taking a single dose of a placebo pill.
Inside Your Arteries
“The reduction of arterial stiffness, and improvements in internal carotid artery blood flow and endothelial function after chronic CBD treatment, indicate a positive effect in vascular function that warrants further investigation in relevant patient populations,” lead researcher Saoirse E. O’Sullivan, PhD, reported.
In a follow-up study, where the researchers gave 26 men 600 mg of CBD or a placebo for seven days, the results were mixed. Measurements of resting blood pressure revealed that the participants had developed a tolerance to the CBD over time, but CBD ’s ability to lower blood pressure during stress persisted. (Of course, if you are already dealing with low blood pressure, the blood pressure–reducing effects of CBD are something to be aware of, and you may need to avoid high doses.)
Similarly, a stroke, which is sometimes called “ brain attack,” occurs when blood flow to the brain is blocked or reduced. So the same precautions that protect against heart attacks and other cardiovascular disease (like diet, exercise, and a healthy lifestyle that can include CBD supplementation) can help prevent stroke. CBD can also play a key role in protecting the brain after a stroke.
CBD may protect against cardiac arrhythmias or irregular heartbeat.
A variety of mechanisms of protection from cardiac ischemia-reperfusion injury implicate endocannabinoids. Ischemic preconditioning is well known for its potent cardioprotective effects, resulting in smaller infarct sizes, reduced risk of I-R arrhythmias, and improved recovery of ventricular function. Joyeux et al.  reported that isolated hearts preconditioned with heat stress reduced the infarct size significantly after an I-R sequence. This protection was abolished when treating isolated hearts with a CB2 receptor antagonist, SR144528, implicating the CB2 receptor in the observed cardioprotection.
Of the proposed mechanisms of CBD cardioprotection, vasorelaxation undoubtedly plays a major role in limiting damage to the cardiac tissue over time in the presence of hypertension, heart failure, and chronic vascular diseases. CBD stimulates the production of endothelial nitric oxide synthase (eNOS)  and hence, vasorelaxation via nitric oxide (NO) synthesis [36, 37].
Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide . They have a set of characteristic molecular components, such as a proinflammatory profile present in heart failure (HF) , diabetic cardiomyopathy , and autoimmune myocarditis . In addition, alterations to oxidative phosphorylation and mitochondrial reactive oxygen species (ROS) are linked to hypoxia  and ischemia/reperfusion injury [13, 14], where excess ROS and alterations to the renin-angiotensin-aldosterone system are linked to hypertension [15, 16]. Similarly, the handling of intracellular Ca 2+ is paramount in HF as well as arrhythmias . All these molecular components, associated with diverse CVDs, can be modulated with CBD administration. The objective of this study is to review the current evidence related to CBD and other nonpsychoactive cannabinoids, including their use in CVDs, especially HF and cardiomyopathies. From this evidence, we finalize with a proposed roadmap of the pathways of CBD’s effects on CVDs.
2.6.2. Cardioprotective Effect of Cannabinoids against Arrhythmias
The role of mitochondria in cellular redox reactions is one of the most important contributions to electron transfer balance. Hao et al.  observed the cardiotoxicity derived from the use of doxorubicin which can be attenuated by CBD therapy, as it can activate mitochondrial complex 1 providing additional oxidative protection accompanied by an increase in the number of mitochondria and biogenesis stimulation. The mechanism that involves mitochondrial ROS production and biogenesis possibly depends on the mitochondrial Ca 2+ uptake promoting the dephosphorylation of transcription factor A (TFAM), which consequently induces mitochondrial biogenesis .
Under ischemia/reperfusion injury, CBD attenuates the RhoA activation  and its pathways ROCK/p38 and MAPK/MAPKAPK2 [11, 23], which are activated in response to inflammatory and proliferative stimuli. CBD plays a significant antiapoptotic role by protecting the cell from oxidative damage and Ca 2+ overload, preventing the activation of caspase 3 cleavage, PARP activity, FasL expression, and chromatin fragmentation [11, 36, 37]. Both the antiproliferative and the antiapoptotic effects are naturally modulated by the action of endocannabinoids. CBD is known to inhibit the enzyme fatty acid amide hydrolase (FAAH), resulting in increased levels of available systemic endocannabinoids , which is an indirect mechanism of cellular protection.
This work was partially supported by the Cardiovascular Medicine Research Group-Tecnológico de Monterrey 0020CAT131 as well as CONACYT-México grants 151136 and 256577 (G. García-Rivas).
Gorbunov et al.  reported the use of the CB1 and CB2 agonist HU-210 to reduce the infarction effect of reperfusion after local ischemia in the heart by mimicking the postconditioning phenomenon. In the study, HU-210 decreased the infarction size in the area at the risk ratio significantly, preventing reperfusion injury after ischemia. HU-210 decreased the pumping function of the heart, leading to a reduction of its work and oxygen demand during reperfusion, probably promoting cardiomyocyte survival during reperfusion. Moreover, HU-210 decreased end-diastolic pressure values during the reperfusion period, suggesting a reduction in the Ca 2+ overload of cardiomyocytes.