SYNTHETIC CANNABINOIDS: A LESS UNDERSTOOD CAUSE OF ACUTE CORONARY SYNDROME

Abstract

SESSION TITLE: Monday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM PURPOSE: Current research suggests there is an association between natural cannabinoid use and acute coronary syndrome (ACS). Via an extensive literature review we will describe how synthetic marijuana can cause ACS in patients lacking typical cardiac risk factors. METHODS: Cardiology, critical care, and emergency medicine journals were searched for keywords including marijuana, tetrahydrocannabinol (THC), K2/spice in addition to ACS, myocardial infarction and sudden death. Inclusion criteria were topic relevance, peer review, and recent publication. RESULTS: A Norwegian study revealed THC as the only drug present in six postmortem patients with unexplained sudden death. Another larger study identified a 4.8-fold increase in acute myocardial infarction risk within an hour of marijuana use. Multiple case reports have linked synthetic derivatives, known as K2/spice, with ACS in young patients with no known health issues including three cases of myocardial infarction in teenage boys as well as several ACS events in healthy adults. CONCLUSIONS: An active component of both natural and synthetic marijuana is THC. It blocks parasympathetic pathways via norepinephrine release and is thought to be the cause of most cardiovascular effects. One study found a 6-53% increase in heart rate and a 4-9% rise in cardiac output after smoking marijuana, while another found a 30% increase in cardiac output and a dose-dependent increased heart rate of 20-100%. Both factors can lead to oxygen demand/delivery mismatch, which marijuana exacerbates further by increasing carboxyhemoglobin. THC can also disrupt oxygen delivery via vasospasm of the coronary vessels, increased shear stress of the arterial walls, and by forming a procoagulant state due to increased tissue factor expression in monocytic cells. Cannabinoid receptor type 1 (CB1R) is one of two receptors found abundantly in the central and peripheral nervous systems. When bound by THC, CB1R triggers autonomic responses which directly affect the vascular endothelial and smooth muscles, myocardium, and circulating erythrocytes. A recent study found CB1R leads to p38 and JNK mitogen-activated protein kinase (MAPK) activation. This increases reactive oxygen species (ROS) generation and contributes to endothelial and cardiomyocyte cell dysfunction or death. Synthetic cannabinoids are mixtures of several synthetic CB1R agonists. They can be up to 170-times more potent, leading to severe cardiac outcomes. CLINICAL IMPLICATIONS: More research is needed to fully understand effects of synthetic cannabinoids on the cardiovascular system, as synthetic marijuana may be much more dangerous than natural cannabis. It is paramount for both emergency and critical care physicians to be cognizant of the possible detrimental effects of synthetic marijuana in order to prevent ACS related events in the future. DISCLOSURES: No relevant relationships by Gary Esper, source=Web Response No relevant relationships by Peter Nesbitt, source=Web Response No relevant relationships by Ravi Patel, source=Web Response No relevant relationships by Heidi Storer, source=Web Response No relevant relationships by O'Rell Williams, source=Web Response No relevant relationships by Thijs Wolf, source=Web Response