What do we tell patients with coronary artery disease about marijuana use?
A relative paucity of research exists that establishes links between marijuana use and total mortality for those affected by CHD. One study showed that over a median follow-up of 3.8 years, there was a three-fold increased risk of mortality following acute myocardial infarction (MI) in patients with CHD after marijuana use, after adjusting for smoking status and socioeconomic status, with a graded increase in risk (i.e. a dose–response) with more frequent use 3. This study analyzed self-reported use of marijuana in the preceding year. Furthermore, smoking marijuana has been implicated as a trigger for inducing MI with the risk of MI onset being elevated almost five-fold in the hour after smoking 4. However, long-term results for marijuana use are somewhat mixed as one study in patients with CHD with a follow-up of 18 years found no statistically significant association between marijuana use and total mortality, although mortality rate was 29% higher (P=0.28) among those reporting any marijuana use 5. Though the long-term effects of marijuana use are less clear, all three of these studies paint a negative picture for marijuana use in coronary artery disease patients by indicating an elevated risk of increase in MI and/or mortality. With rates of marijuana use in the USA clearly increasing, this area is ripe for further research.
From a physiologic point of view, tetrahydrocannabinol (THC) is the major active component of marijuana that acts on cannabinoid receptors CB1 and CB2 6. The proatherogenic CB1 found in the heart, liver, brain, and smooth muscles increases blood pressure, induces tachycardia and coronary ischemia, increases myocardial oxygen demand because of a rise in norepinephrine, lowers angina threshold, and can decrease vascular resistance leading to orthostatic hypotension 3,7,8. A marijuana dose-related increase in blood pressure, greater for systolic than diastolic, has been found to occur, along with an increase in heart rate 9. Furthermore, marijuana use may increase the risk for hypertension-related mortality 10. The antiatherogenic CB2 is mostly present in immune cells and may have anti-inflammatory and plaque-reducing properties 11. The relative effects of CB1 and CB2 receptors on the triggering of MI and on the progression of CHD needs to be more clearly studied as they undoubtedly have significant and potentially interactive cardiovascular effects.
It should be noted that the method of delivering marijuana to the body has an impact upon its physiologic effects. Pulmonary assimilation of inhaled THC causes a maximum plasma concentration within minutes whereas oral ingestion takes 2–3 h for it to peak 12. The primary constituent of marijuana is rapidly transferred from lungs to blood during smoking 13. In addition, smoking marijuana clearly increases expired carbon monoxide (CO) levels, whereas an oral or vaporized route of administration has no such effect and this difference would almost certainly affect the angina threshold 14.