Cannabis and the Heart: A Clinical Interpretation of the Evidence

Cannabis and the Heart: A Clinical Interpretation of the Evidence

Authored by the SCC Media Response Committee

The relationship between cannabis and its impact on cardiovascular health has attracted growing attention. Recent headlines stating “Cannabis Doubles Risk for Cardiovascular Death” have raised questions within the clinical community and for patients as well. It is crucial to have a scientifically sound examination of the pros and cons of cannabis therapeutics in clinical practice and be able to examine risks objectively. However, as is common with many media narratives on cannabis, the evidence does not match the strength of the claims.

A closer examination of a recent review by Storck et al., published in BMJ Heart, revealed significant methodological concerns. The paper highlights associations suggesting negative effects of cannabis on cardiac health, but its conclusions should be interpreted with caution. The study also has design and interpretation flaws that limit its applicability in clinical practice. An analysis of the stated claims in the Storck et al. paper is outlined below.

Study Design and Bias

Storck et al. presented their study as a systematic review, which suggests a high level of evidence and the ability to draw robust conclusions. But the analysis primarily incorporated observational studies, where 17 of the 24 were cross-sectional. The study designs don’t establish cause and effect or clarify whether cannabis use preceded the outcome. Relying heavily on such studies limits the reliability of pooled results and makes strong clinical recommendations problematic.

In addition, the majority of the included studies were defined by the authors as having a high risk of bias. Only four were rated as having “some concern” regarding methodological quality (Storck et al., 2025). This significantly weakens confidence in the study’s conclusions. Furthermore, it remains unresolved whether cannabis use preceded cardiovascular events or whether pre-existing cardiovascular conditions influenced cannabis use patterns (Grimes & Schulz, 2002; Mann, 2003).

Additionally, there were no socio-demographic restrictions in the review. Their analysis reports baseline characteristics when available. The authors didn’t analyze results by key demographic factors such as sex, race, income, or education to see if risks differed across subgroups (Storck et al., 2025). This strongly limits the understanding of whether risks vary across different populations.

Ambiguity of “Cannabis Use” & Co-Exposures

Cannabis consumers often co-use tobacco, alcohol, or other psychoactive substances. These all have established risks for cardiovascular health (National Cancer Institute). The authors note in the paper’s abstract that exposure to other psychoactive substances was considered. But their methods were not strong enough to rule out confounding (Sidney, 2002). While Storck et al. acknowledged co-exposures, their analysis did not adequately adjust for their effects. This makes it difficult to isolate cannabis as the independent cause. Attributing cardiovascular risk to cannabis alone is speculative at best.

Another solid issue is that the concept of “cannabis use” was not standardized. The differences in frequency (daily vs. occasional), method (smoking, edibles, vaping), dose, and potency (THC/CBD ratio) were not stratified in their review. One study even focused on medical cannabis, which often has different compositions (higher CBD, lower THC) than adult use products. These factors are important to consider because they influence physiologic effects and safety profiles (Volkow et al., 2014).

Contemporary cannabis chemovars have been selectively bred to produce higher concentrations of THC than those available in the past. This alters both risk profiles and pharmacologic effects. Cannabinoids demonstrate biphasic properties—therapeutic benefits at lower doses may become problematic at higher ones. In addition, smoking cannabis exposes individuals to harmful byproducts of combustion (Sidney, 2002; Volkow et al., 2014). The long-term health effects of vaping and dabbing remain unknown. Current evidence is lacking on whether THC-induced tachycardia could play a role in major cardiovascular events (Qian & Zhou, 2025).

Cannabis products differ substantially in their composition and use context. For example, oral administration for chronic pain is different from vaporization for anxiety (NASEM). Lumping all types of cannabis use together introduces misclassification bias and makes it difficult to determine whether cannabis itself is the cause.

Small Effect Sizes with Wide Confidence Intervals

The reported relative risks (1.20–2.10) were modest, and several confidence intervals were close to 1.0. This suggests weak associations. Small effect sizes in observational studies are easily influenced by confounding and should be interpreted cautiously when generalizing to broader populations (Ioannidis, 2005). Other inconsistencies further weaken confidence in the findings. For example, when ACS and stroke were combined as a composite outcome in two studies, no significant association was observed (Ferreira-González et al., 2007). This inconsistency suggests the associations for each outcome may be unreliable.

Publication Bias and Selective Inclusion

Publication bias may limit the reliability of the review’s conclusions. The studies included in the Storck et al. paper were published between 2016 and 2023, meaning earlier research showing no association could have been overlooked. With research involving cannabis, studies suggesting harm are more likely to be published. This increases the risk of bias because negative or neutral studies are less likely to be published or included in systematic reviews (Dwan et al., 2013).

Clinical Recommendations

Clinicians should recognize that cannabis carries potential risks for cardiovascular health, as well as other systems. Cannabis is not a single, uniform therapy. The plant’s pharmacologic effects vary widely depending on formulation and route of administration. For instance, CBD-only products differ from those that mix several cannabinoids, terpenes, and delivery methods to provide therapeutic effects.

Assessing cannabis use in patients with cardiovascular disorders requires nuance, not blanket recommendations. The potential risks that cannabis may have are dependent on the person and their unique medical profile. The authors’ call to screen all cardiovascular patients employing cannabis overgeneralizes the evidence. This approach is unsupported by the limited, low-quality data outlined in the paper (Guyatt et al., 2011). Any potential risks that cannabis could pose must be contextualized relative to dose, delivery method, product composition, and patient-specific factors.

Conclusion

Continued investigation into the impact of cannabis on cardiovascular outcomes is warranted and necessary. However, the current evidence on this topic does not justify framing cannabis as an independent or major cardiovascular risk factor. Clinicians should interpret cannabis use carefully. They need to take into account pharmacology, the patient’s medical history, and the balance of risks and benefits.

The Society of Cannabis Clinicians advocates for evidence-informed, patient-centered care that adapts to ongoing advancements in the study of cannabinoid medicine. As emerging research evolves, clinicians should rely on careful judgment and foundational evidence rather than fear when guiding patient care and communicating with the public.

Article edited by Sarah Russo.

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