Tobacco and Marijuana Induce Adverse Effects on Cardiac Function and Platelet Activity and Reduce Tissue Preservation Following Myocardial Infarction

Smoking disrupts cardiac autonomic regulation, vascular biology, and platelet function; however, the acute and longer-term cardiovascular effects of resurging and emerging tobacco and marijuana products remain incompletely characterized. We investigated the impact of exposure to smoke and aerosol from several tobacco and marijuana products on cardiac function, platelet activity, and myocardial susceptibility to ischemia/reperfusion myocardial infarction (MI). Male/female Sprague-Dawley rats underwent single or daily 5-min pulsatile exposure sessions to emissions from tobacco cigarettes, e-cigarettes (JUUL), heated tobacco products (IQOS), marijuana cigarettes, or cannabinoid-depleted (“placebo”) marijuana cigarettes; with an air negative control. Cardiac function was assessed immediately after single exposure using echocardiography and intraventricular hemodynamics. Platelet aggregation was measured immediately after single exposure and one day after repeated (2-week) exposure. Myocardial infarct size, normalized to area-at-risk, was assessed following MI after repeated (4-week) exposure. Single exposure to tobacco smoke or JUUL aerosol reduced left ventricular ejection fraction relative to pre-exposure. Acute marijuana smoke exposure similarly impaired left ventricular function assessed by hemodynamics. Single exposure to tobacco, marijuana, and placebo marijuana smoke increased collagen-induced platelet aggregation, with more pronounced responses in females, whereas repeated (2-week) exposure to smoke/aerosol from tobacco cigarettes, JUUL, IQOS, and placebo marijuana increased platelet aggregation across groups. Notably, repeated (4-week) exposure to tobacco smoke/aerosol or marijuana smoke prior to MI reduced myocardial tissue preservation, resulting in greater infarct size post-MI. These findings indicate that individual tobacco and marijuana smoking and vaping similarly impair cardiac function, enhance platelet reactivity, and reduce myocardial tolerance to ischemia/reperfusion injury.