Effects of Electronic Cigarette Exposure on Myocardial Infarction and No-Reflow, and Cardiac Function in a Rat Model.

Introduction:
This manuscript reports a study investigating the effects of electronic cigarette (E-cig) exposure on myocardial infarction and no-reflow, and cardiac function in a rat model. The study compares E-cig exposure to purified air and standard cigarette smoke exposure.

Key Points:

* Rats were exposed to filtered air, E-cig with nicotine, E-cig without nicotine, or standard cigarette smoke for 8 hours/day, 4 days/week for a total of 8 weeks.
* Following exposure, rats underwent 30 minutes of left coronary artery occlusion followed by 3 hours of reperfusion.
* Exposure to E-cig vapor with or without nicotine or exposure to standard cigarettes did not increase myocardial infarct size or worsen the no-reflow phenomenon.
* E-cig exposure led to cardiovascular dysfunction, such as reductions in cardiac output, LV positive and negative dp/dt, suggesting a reduction in contractility and relaxation, and increased systemic arterial resistance after coronary artery occlusion and reperfusion in rats compared to air or cigarette exposure.
* E-cig exposure with nicotine reduced body weight gain and increased LV wall thickness and enhanced the collagen deposition within the LV wall.
* No significant differences in ischemic risk area, infarct size, or no-reflow size were seen among the 4 exposure groups.
* The study suggests that E-cig exposure does not increase myocardial infarct size or worsen the no-reflow phenomenon, but induces deleterious changes in LV structure leading to cardiovascular dysfunction and increased systemic arterial resistance after coronary artery occlusion followed by reperfusion.

Main Message:
This study provides evidence that long-term E-cig exposure does not alter the substrate of the heart to increase myocardial infarct size or worsen the no-reflow phenomenon compared to exposure to purified air; but induced deleterious changes to LV structure and cardiovascular function. While E-cig effects are less harmful than those of smoking, they should not be considered a no-risk, harm-reduction alternative to traditional tobacco cigarettes. More investigations are needed to determine the potential time-course effects of varying exposure/usage levels in both males and females. The contribution of specific components of the E-cig, such as carbonyl compounds, nicotine, and flavorings, for mediating these cardiovascular effects remains unknown and needs to be addressed in the future. Studies are also needed to determine the molecular mechanisms and the principal pathways of E-cig exposure-induced cardiovascular impairment.

Dai W, Shi J, Siddarth P, et al. Effects of Electronic Cigarette Exposure on Myocardial Infarction and No-Reflow, and Cardiac Function in a Rat Model. Journal of cardiovascular pharmacology and therapeutics. 2023;28:10742484231155992. doi:10.1177/10742484231155992