Review links cannabis to possible heart attack mechanisms, not proven risk

Myocardial infarction (MI) remains a major public health problem worldwide. The use of illicit substances is increasing. These substances may be associated with an increased incidence of MI through various mechanisms, regardless of the presence of pre-existing risk factors. Although data on this subject are limited, it is important to highlight this issue. The aim of this review is to establish the association between substance misuse and MI, particularly in young adults, and to evaluate the underlying mechanisms based on the current literature. This review was prepared using publications identified through searches of the PubMed/MEDLINE, Scopus, and Web of Science databases using the names of the relevant substances in combination with terms associated with MI. The most commonly misused substances are classified as stimulants, depressants, and performance-enhancing hormones. Stimulants (cocaine, amphetamines, etc.) cause an imbalance between myocardial oxygen supply and demand through effects such as tachycardia, coronary vasospasm, and thrombosis resulting from increased sympathetic activity. Opioids, which belong to the depressant class, cause an imbalance between myocardial oxygen supply and demand by altering coronary hemodynamics secondary to complications such as hypotension, hypoxemia due to respiratory depression, and infection. In the case of cannabis and synthetic cannabinoids, coronary vasospasm, thrombosis, and plaque rupture are important effects. Anabolic-androgenic steroids (AAS) adversely affect the lipid profile. Furthermore, effects associated with AAS use include atherosclerosis, thrombosis, and erythrocytosis. These effects resulting from substance use are recognized as mechanisms underlying the development of MI.