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Home » Marijuana use may be linked to temporarily weakened heart muscle

Marijuana use may be linked to temporarily weakened heart muscle

American Heart Association Meeting Report – Poster: S4054 – Session: HF.APS.P14
American Heart Association

NEW ORLEANS, Nov. 13, 2016 — Active marijuana use may double the risk of stress cardiomyopathy, an uncommon heart muscle malfunction that can mimic heart attack symptoms, according to research presented at the American Heart Association’s Scientific Sessions 2016.

The researchers found that marijuana users were almost twice as likely to develop stress cardiomyopathy compared to non-users, even after taking other cardiovascular risk factors into consideration. Active marijuana use was identified either by information provided by the patient in their medical history, or by a marker in the patient’s urine.

“The effects of marijuana, especially on the cardiovascular system, are not well known yet. With its increasing availability and legalization in some states, people need to know that marijuana may be harmful to the heart and blood vessels in some people,” said Amitoj Singh, M.D. study co-author and chief cardiology fellow at St. Luke’s University Health Network in Bethlehem, Pennsylvania.

Stress cardiomyopathy is a sudden, usually temporary, weakening of the heart muscle that reduces the heart’s ability to pump, leading to chest pain, shortness of breath, dizziness and sometimes fainting.

Data from the Nationwide Inpatient Sample identified 33,343 people who were hospitalized with stress cardiomyopathy between 2003-2011 in the United States. Of those, 210 (less than one percent) were also identified as marijuana users.
Compared with non-users, researchers found that marijuana users were more likely to be younger, male with fewer cardiovascular risk factors, including less high blood pressure, diabetes and high cholesterol.

However, despite being younger and with fewer cardiovascular risk factors than non-users, during stress cardiomyopathy the marijuana users were significantly more likely to go into cardiac arrest (2.4 percent vs. 0.8 percent) and to require an implanted defibrillator to detect and correct dangerously abnormal heart rhythms (2.4 percent vs. 0.6 percent).

“This development of stress cardiomyopathy in younger patients who used marijuana suggests a possible link that needs to be further investigated,” said Sahil Agrawal, M.D., co-author of the paper and also a chief cardiology fellow at St. Luke’s.

Marijuana users were more likely than non-users to have a history of depression (32.9 percent vs. 14.5 percent), psychosis (11.9 percent vs. 3.8 percent), anxiety disorder (28.4 percent vs. 16.2 percent), alcoholism (13.3 percent vs. 2.8 percent), tobacco use (73.3 percent vs. 28.6 percent) and multiple substance abuse (11.4 percent vs. 0.3 percent). Because some of these can increase the risk of stress cardiomyopathy, the researchers adjusted for known risk factors to investigate the association between marijuana use and stress cardiomyopathy.

“If you are using marijuana and develop symptoms such as chest pain and shortness of breath, you should be evaluated by a healthcare provider to make sure you aren’t having stress cardiomyopathy or another heart problem,” Singh said.

The study has some limitations. Because this was a retrospective study, the researchers could not determine how frequently the marijuana users were using marijuana, or what the timeframe was between the use of marijuana and occurrence of stress cardiomyopathy. Observational studies are not designed to prove cause and effect; therefore, it cannot be said that marijuana is or is not a direct cause of stress cardiomyopathy. In addition, because the database the researchers used reports regional but not state-by-state statistics, the researchers could not analyze whether possibly marijuana-related heart problems are increasing where use is legal.

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Co-authors are Mark Fegley, M.D.; Yugandhar Manda, M.D.; Sudip Nanda, M.D.; and Jamshid Shirani, M.D. Author disclosures are on the abstract.

This study did not receive outside funding.

Note: Scientific presentation is at 2 p.m. CT, Sunday, Nov. 13 in the Science and Technology Hall, Clinical Science Section.

Additional Resources:
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Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www.heart.org/corporatefunding.