Abstract 16718: Electronic Cigarette Aerosols Alter Cardiac Expression of Genes Key to Electrical and Structural Remodeling in Mice

Abstract

Background: Electronic cigarette (e-cig) use has mounted. Some health authorities have even proclaimed e-cigs are profoundly safer than conventional cigarettes. However, e-cigs generate several potentially cardiotoxic constituents by heating their solvent vehicles propylene glycol (PG) and vegetable glycerin (VG) into aerosols to deliver nicotine and flavors. Objectives: To investigate the effects of chronic E-cig exposures, with or without nicotine, on cardiac gene expression compared to mainstream cigarette smoke (MCS). Methods: Healthy C57BL/6J male mice were exposed chronically (12 weeks, 3 hours/day) to e-cig aerosols from an equal-ratio mixture of PG and VG (PG:VG) with nicotine (36 mg/mL) or without nicotine, or to MCS, and compared to filtered air control group (Air). Hearts (n=8/group) were assayed by quantitative PCR for expression of genes associated with electrical and structural remodeling. Results: PG:VG exposure increased gene expression for a gap junction protein (connexin 43, 1.8-fold), voltage-gated potassium and sodium channels (K v 4.3, 2.5-fold; Na v 1.5, 1.6-fold), calcium sequestration protein (sarco/endoplasmic reticulum calcium ATP-ase, 1.4-fold), cytokines (TGFβ1, 1.8-fold; TNF-α, 3.8-fold), and collagen III (3.8-fold) relative to Air (all P < 0.05). Nicotine did not enhance PG:VG’s effects on gene expression relative to PG:VG-alone (all P > 0.05), and cigarette smoke did not significantly affect any of the transcripts assayed (all P > 0.05 vs. Air). Conclusions: E-cigs may induce cardiac electrical and structural remodeling via their primary vehicle ingredients and irrespective of nicotine or flavors. Such effects could precipitate fatal arrhythmia, stroke, and/or heart failure. Electronic nicotine delivery systems may pose cardiac risks distinct from conventional cigarettes.