Why Do Marijuana and Synthetic Cannabimimetics Induce Acute Myocardial Infarction in Healthy Young People?

Cells. 2022 Mar 28;11(7):1142. doi: 10.3390/cells11071142.

Abstract

The use of cannabis preparations has steadily increased. Although cannabis was traditionally assumed to only have mild vegetative side effects, it has become evident in recent years that severe cardiovascular complications can occur. Cannabis use has recently even been added to the risk factors for myocardial infarction. This review is dedicated to pathogenetic factors contributing to cannabis-related myocardial infarction. Tachycardia is highly important in this respect, and we provide evidence that activation of CB1 receptors in brain regions important for cardiovascular regulation and of presynaptic CB1 receptors on sympathetic and/or parasympathetic nerve fibers are involved. The prototypical factors for myocardial infarction, i.e., thrombus formation and coronary constriction, have also been considered, but there is little evidence that they play a decisive role. On the other hand, an increase in the formation of carboxyhemoglobin, impaired mitochondrial respiration, cardiotoxic reactions and tachyarrhythmias associated with the increased sympathetic tone are factors possibly intensifying myocardial infarction. A particularly important factor is that cannabis use is frequently accompanied by tobacco smoking. In conclusion, additional research is warranted to decipher the mechanisms involved, since cannabis use is being legalized increasingly and Δ9-tetrahydrocannabinol and its synthetic analogue nabilone are indicated for the treatment of various disease states.

Keywords: THC; cannabinoid receptor; cannabinoids; heart; marijuana; myocardial infarction; oxygen consumption; sympathetic system; tachycardia; thrombus.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Analgesics
  • Cannabinoid Receptor Agonists
  • Cannabinoids* / adverse effects
  • Cannabis* / adverse effects
  • Heart
  • Humans
  • Myocardial Infarction* / chemically induced
  • Myocardial Infarction* / drug therapy

Substances

  • Analgesics
  • Cannabinoid Receptor Agonists
  • Cannabinoids