Did Marijuana Save Kevin Smith's Life?

Christopher Labos, MD, CM, MSc


July 23, 2018

Christopher Labos, cardiologist and epidemiologist

Kevin Smith is a great storyteller. So naturally, when he was on the Late Show With Stephen Colbert in May, he used up the entire segment to deliver what was essentially a 9-minute monologue without giving Colbert a chance to ask a single question. The segment was funny and poignant, and it provided a glimpse into a vulnerable, self-conscious man who views the scariest night of his life as the best thing to have ever happened to him. His story, in a nutshell, was this: He had a heart attack. Marijuana saved his life.

The Widowmaker

After recording part 1 of his comedy special Silent but Deadly, Smith suddenly started feeling unwell. He began sweating and experienced shortness of breath and nausea. As he told Colbert, he thought he was just too high because he had smoked marijuana before going on stage. His team, ignoring his assurances that he was fine, canceled the second show of the evening and called an ambulance.

Kevin Smith

Smith was taken to the hospital, where he was found to have a 100% occluded left anterior descending artery. After his angioplasty, he asked his doctor whether the marijuana could have contributed to his infarct, and says he was told, "No, quite the opposite; that weed saved your life."

"The thing that I got out of his interview more than anything else," says Jean-Philippe Pelletier, an interventional cardiologist at the McGill University Health Centre, "[is that] there's a lot of misconceptions about what the symptoms of a STEMI [ST-segment elevation myocardial infarction] can be." He points out that one of the most important factors in determining survival after a myocardial infarction (MI) is the delay in calling 911. Many, like Smith, think their heart attack symptoms are caused by something else. "It's very common for us to get patients who present very late, sometimes with very dramatic deleterious results, not knowing they were having a heart attack."

Smith was told that marijuana had kept him calm during his heart attack. Pelletier acknowledges that staying calm may have had some impact and is probably a good thing, because a combative or uncooperative patient can prevent him from doing his job. However, he does add that someone having a heart attack will have an increased adrenergic drive even if they are not feeling particularly anxious. Still, he is uncertain about how much of a role the marijuana played. "I don't think it had any direct effect on survival, but the fact that it made him stay calmer during the whole thing may be a good thing."

Marijuana and Anxiety

In some people, however, marijuana can have paradoxical effects, with some studies suggesting that it may actually increase anxiety[1,2] and others suggesting no effect at all.[3,4] Presumably, staying calm and lowering your heart rate would help by decreasing myocardial oxygen demand, but the limited evidence that exists suggests that marijuana increases heart rate instead.

In 1972, Beaconsfield and colleagues[5] exposed volunteers to marijuana smoke and found that heart rate increased by a mean of > 20 beats/min and systolic blood pressure by 5-10 mm Hg. Another study involving healthy volunteers found that intravenous administration of delta-9-tetrahydrocannabinol (THC) increased heart rate but not blood pressure.[6] Of note, prior administration of a beta-blocker attenuated the effects of THC, suggesting that marijuana acts as a sympathomimetic.

In 1976, Gottschalk and colleagues[7] published one of the few randomized, double-blind, placebo-controlled, crossover trials with marijuana, albeit with only 10 people. Participants with angiographically documented coronary artery disease were given either a marijuana cigarette or a placebo cigarette that contained only trace amounts of THC. The researchers found that marijuana had no effect on anxiety, decreased myocardial oxygen delivery, and decreased the exercise threshold for angina in the study participants.

Marijuana and MI

Unfortunately, studies looking at hard clinical endpoints are less numerous and not entirely consistent. Some suggest an increased risk for incident MI. In the Determinants of MI Onset Study, Mittleman and colleagues[8] examined the role of marijuana in triggering an MI. In this case-crossover study, where patients serve as their own control, the risk for MI was elevated 4.8-fold in the hour after marijuana use, but no increased risk was observed after 2 hours.

This almost fivefold increase in relative risk may be misleading, however. The study included 3882 patients with MI; of these, 124 reported smoking marijuana in the year before their heart attack, including nine who smoked the hour before. A similarly designed case-crossover study reported a 50% increase in the risk for MI in the hour after drinking a cup of coffee.[9] In a somewhat satirical letter to the editor, Charles Poole demonstrated how this increase in risk could be translated into one extra heart attack for every 2 million cups of coffee consumed.[10]

Suffice to say, given that the baseline risk of having an MI in any 60-minute period is quite low, even large increases in relative risk translate into only small increases in absolute terms. Using Poole's calculations, a relative risk of 4.8 would translate into one extra MI for roughly every 230,000 uses of marijuana. Notwithstanding the low absolute risk, the data suggest that, mechanistically, marijuana does have adverse cardiovascular effects.

Two subsequent cohort studies offered conflicting evidence on the association between marijuana use and survival post-MI. In the first, from 2008, Mukamal and colleagues[11] reported that over a median of 3.8 years of follow-up, the hazard ratio (HR) for MI was 2.5 (95% confidence interval [CI], 0.9-7.3) for marijuana use less than once per week and 4.2 (95% CI, 1.2-14.3) for marijuana use once or more per week compared with nonusers. Only 52 of the 1913 patients reported marijuana use in the year before their heart attack. However, a subsequent publication from the Determinants of MI Onset Study that included 3886 patients followed for up to 18 years showed no association between marijuana use and mortality, contradicting the earlier findings (HR, 1.27; 95% CI, 0.63-2.56).[12]

Do I think it contributed to his surviving a large heart attack? It's possible, but it also may have contributed to him having one.

Lori Walker, PhD, from the University of Colorado Denver Anschutz Medical Campus, has studied the effects of marijuana on heart disease and presented findings at the American College of Cardiology 2016 Scientific Sessions[13] linking marijuana use to improved hospital survival after MI. However, she cautions that the data are far from definitive and insufficient to attribute Smith's recovery to marijuana use.

"Do I think it saved his life? Absolutely not," says Walker. "Do I think it contributed to his surviving a large heart attack? It's possible, but it also may have contributed to him having one." A potential survival benefit for marijuana was also observed in a 2017 study that compared 35,771 MI patients with a history of marijuana use and 2,416,162 patients without such a history from the National Inpatient Sample database. Desai and colleagues[14] showed a decrease in hospital mortality among marijuana users, but also an increased incidence of actually having an MI.

Significant baseline differences between users and nonusers may have confounded the results. In particular, marijuana users were younger, which could easily explain the improved outcomes even after statistical adjustment for age and other variables. Rupak Desai, MBBS, a research fellow at the Atlanta Veterans Affairs Medical Center, says that there were many factors they couldn't control for in their analysis. For example, they could only assess ever-use of marijuana and had no data on timing or frequency of use before the MI. "To be frank, we would require many more prospective studies [on this issue]," says Desai.

This potential marijuana "paradox"—at once increasing the incidence of MI and provoking MI at a younger age, but then also improving survival post-MI—is reminiscent of many prior paradoxes. The obesity paradox,[15] the aspirin paradox,[16] and other similar examples can generally be explained as consequences of index event bias,[17] a form of selection bias that can occur in observational research.[18] Teasing out the cardiovascular effects of marijuana is made difficult by the many confounding variables. For example, data from the CARDIA study showed that marijuana users had worse diets, were more likely to smoke cigarettes, and were more likely to use illicit drugs.[19] The influence of the type of marijuana used on cardiac risk also remains unclear. Although smoked marijuana may be more harmful than edible marijuana products because of its combustion by-products, data comparing different types of marijuana are lacking.

Walker points out that it is difficult to draw any firm conclusions. "The evidence base we have is very poor, and I think we definitely need more," she admits. "In the face of changing legislation, before we can even begin to look at whether there could possibly be a benefit [to marijuana use], we have to be able to show that there is no harm. I don't know that we've done that yet."

Editor's Note: Labos reached out to Smith's cardiologist for comment but received no response.

Follow Christopher Labos on Twitter: @drlabos

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