Abstract 9869: Adverse Effects of Smoking/Vaping of Several Types of Tobacco Products and Marijuana on Cardiac Function and Platelet Aggregation

Abstract

Tobacco and marijuana smoke contains ~7,000 chemicals that cause disorders in cardiac autonomic function, vascular biology, and platelet function. Along with marijuana, e-cigarettes (e-cigs) and heat-not-burn tobacco products (e.g., IQOS) are often viewed as being less harmful than smoking tobacco. However, there are many unknowns about how marijuana, e-cigs, and IQOS impact cardiovascular physiology and platelet function over the long term. To explore cardiovascular effects of smoking/vaping, we exposed conscious rats to single (one time) and multiple (one time daily for 10 days) pulsatile mainstream smoking/vaping of e-cigs (JUUL), IQOS (American and Russian HeatSticks), marijuana (~10% THC), and cannabinoid-depleted (“placebo”) marijuana, relative to regular tobacco (Marlboro Red) smoking and air controls. Cardiac function was assessed by echocardiography pre- and post- single exposure. Platelet aggregation was measured to determine changes in platelet response immediately post-single exposure and one day after the last of multiple exposures. Single exposure induced acute effects on echocardiographic function with reduced ventricular end-diastolic volume (EDV) in IQOS and marijuana groups of both genders (Fig. A), potentially indicating incomplete ventricular relaxation between heart beats after exposure. However, marijuana caused adjustments of end-systolic volume (ESV) and EDV without changes in ejection fraction (EF) in females, with smaller ESV and reduced EDV. Tobacco, marijuana, and placebo marijuana smoking immediately increased collagen-induced platelet aggregation post-single exposure in female rats. Tobacco smoking, JUUL, IQOS, and both kinds of marijuana significantly increased platelet aggregation post-multiple exposure as compared to air controls in mixed genders (Fig. B). P values ≤ 0.1 are shown. Conclusion: smoking/vaping causes clinically relevant adverse effects on cardiac function and platelet aggregation.