Cannabis and Surgery: Heart Attack Risk, DVT, and USMLE Review

A study presented at the ANESTHESIOLOGY 2026 annual meeting found that surgical patients who use cannabis had a 46% higher risk of myocardial infarction (MI) during or shortly after surgery than nonusers. The same analysis found a 22% lower risk of venous thromboembolism (VTE). The authors stress that this is an association, and that the lower clot risk does not show cannabis is protective.

What happened

The researchers, led by Nader D. Nader of the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo, reviewed five studies covering data from 44,312 surgical patients. They compared perioperative outcomes in patients who used cannabis with outcomes in nonusers.

The main results:

• Myocardial infarction: cannabis use was associated with a 46% increased risk during or shortly after surgery.
• Venous thromboembolism: cannabis use was associated with a 22% lower risk.
• No significant associations were found with stroke, respiratory failure, acute kidney injury, or death.

The authors called the VTE finding surprising. They said it reflects the complex effects of cannabis on the heart and blood vessels and needs further study. They also said cannabis acts on receptors that may influence inflammation and clotting in different ways.

Why it matters

Cannabis is increasingly common and legal in most U.S. states, so anesthesiologists and surgeons will see more patients who use it. The authors argue that patients should not assume marijuana is harmless because it is legal or plant-derived. They also note that today's products are far more potent than those of decades ago, and higher THC levels can have serious cardiovascular effects (co-author Rose Berkun).

The study authors say that clinicians who know about a patient's cannabis use can adjust cardiovascular monitoring, the anesthetic plan, decisions about blood-thinning medications, and sometimes the timing of an elective procedure. They want patients to disclose how often they use cannabis, in what form, and when they last used it. This is a point about the clinical conversation, not advice for any individual.

The pairing of more MI with fewer VTE is the notable part. The two outcomes rest on different mechanisms, which makes the result a useful pathophysiology exercise for exam prep.

What to know for the USMLE — high-yield review

The news report only briefly describes mechanisms. The points below are standard textbook knowledge that you can connect to it.

• THC and CB1 receptors: THC is a partial agonist at CB1 receptors, which are G(i/o)-protein-coupled and are densest in the CNS (hippocampus, cerebellum, basal ganglia). CB1 is also found in vascular tissue and the myocardium. CB2 is found mainly on immune cells, which is why it is linked to inflammation and immune modulation.
• Hemodynamic effects: acute THC exposure causes tachycardia and increased blood pressure, according to the researchers. In textbook terms, this comes from sympathetic activation with reduced vagal tone. Higher heart rate shortens diastole, which reduces coronary perfusion time.
• Supply–demand mismatch: faster heart rate and higher blood pressure raise myocardial oxygen demand. Add the stress of surgery (catecholamine surge, anemia, hypotension, pain), and a patient with fixed coronary stenosis can develop a type 2 MI. This is the most common mechanism of perioperative MI.
• Coronary vasospasm: the researchers note that THC may trigger spasm of the coronary arteries. Vasospasm can cause ischemia without a ruptured plaque, as in Prinzmetal (variant) angina.
• Type 1 vs type 2 MI: type 1 is plaque rupture with thrombosis. Type 2 is a supply–demand imbalance without acute plaque rupture. On Step 2 CK, expect perioperative troponin rises in patients with tachycardia, hypotension, or anemia, and know that management targets the underlying trigger.
• Perioperative MI presentation: it is often silent because of anesthesia, sedation, and analgesics. Think of it with unexplained hypotension, arrhythmia, new ECG changes, or a troponin rise postoperatively.
• VTE and Virchow triad: postoperative DVT and PE arise from stasis, endothelial injury, and hypercoagulability. Surgery affects all three. Standard prevention includes early ambulation, pneumatic compression, and pharmacologic prophylaxis (heparin or LMWH) in appropriate patients.
• Why a lower VTE signal is not proof of protection: an observed association can arise from confounding (differences in age, comorbidities, surgery type, or prophylaxis use between groups). The source authors say the finding does not establish a protective effect. Know the difference between association and causation for exam questions on study interpretation.
• Pharmacology reminder: the source authors say cannabis can alter how the body responds to anesthesia. For Step 1, link this to CNS effects of CB1 activation and to the general principle that many substances interact with anesthetic agents. The source does not give specific drug interactions, so do not invent any.

Limitations

Read this study with caution.

• Conference presentation: the work was presented at a meeting. The source material does not describe peer-reviewed publication or provide full methods.
• Association, not causation: the study reports links between cannabis use and outcomes. The authors themselves caution about interpreting the VTE result.
• Pooled data from five studies: the source does not detail the designs of the included studies, how cannabis use was defined or measured (frequency, route, potency, timing of last use), or which surgeries were covered. Results may therefore not apply equally across settings.
• Possible confounding: patients who use cannabis may differ from nonusers in other ways, such as tobacco use, other substances, age, or baseline cardiovascular risk. The source does not say how these were handled.
• No significant link with other outcomes: the lack of an association with stroke, respiratory failure, acute kidney injury, or death does not prove no risk exists. It may also reflect limited statistical power.
• Absolute risks not provided: the source gives only relative changes (46% higher, 22% lower), so you cannot judge how many events this represents.

FAQ

Does cannabis use increase the risk of heart attack during surgery?

In this study of five studies and 44,312 surgical patients, cannabis use was associated with a 46% higher risk of MI during or shortly after surgery. It is an observational association, so it does not prove cannabis caused the heart attacks.

Does cannabis protect against blood clots after surgery?

No, that cannot be concluded. Cannabis use was associated with a 22% lower risk of venous thromboembolism. The authors emphasize that this does not establish a protective effect and that more research is needed.

Why can THC raise the risk of myocardial infarction?

According to the researchers, THC can increase heart rate, blood pressure, and the heart's oxygen demand, and may trigger spasm of the coronary arteries. During anesthesia and surgery, these effects can add to physiological stress and raise the risk of a heart attack.

Key takeaways

• A review of five studies (44,312 surgical patients) linked cannabis use to a 46% higher risk of perioperative MI and a 22% lower risk of VTE, with no significant links to stroke, respiratory failure, acute kidney injury, or death.
• The likely mechanisms for MI are THC-driven tachycardia, higher blood pressure, increased myocardial O2 demand, and possible coronary vasospasm. The VTE finding is unexplained and does not prove protection.
• For the USMLE, connect CB1 pharmacology, type 2 MI, and the Virchow triad, and remember that these data are observational and were presented at a conference.