Chronic exposure to nicotine via E-cigarettes or standard cigarettes significantly impaired LV-arterial coupling following induced myocardial infarction in rats compared to controls (P<0.05).
Does chronic exposure to nicotine via E-cigarettes or standard cigarettes impair LV-arterial coupling in a rat model of myocardial infarction?
Chronic exposure to nicotine via e-cigarettes or standard cigarettes impairs LV-arterial coupling following myocardial infarction in a rat model, suggesting vaping may not be a safe cardiovascular alternative to smoking.
p-value: p=<0.05
Abstract Introduction Previous studies have shown that nicotine delivered by either electronic cigarette (E-cigarette) vapor or standard cigarette smoke can impair cardiovascular function. However, their underlying effects on left ventricular (LV)-arterial coupling in the context of myocardial infarction (MI) have not been fully elucidated. Purpose In this study, we measure the impact of chronic exposure to E-cigarettes (with and without nicotine) and standard cigarette smoke on LV-arterial coupling in a rat model of MI. Methods We exposed healthy adult Sprague Dawley rats (49% female, 6 weeks old, body weight ~260-370 g) to one of four conditions: purified air (control, n=28), E-cigarette vapor without nicotine (EC NIC(-), n=24), E-cigarette vapor with nicotine (EC NIC(+), n=26), or standard cigarette smoke (n=31). Exposures were for 5 hours per day, 4 days per week, over a period of 8 weeks (puff frequency=1 puff/min, puff duration=2 seconds, flow rate= 1.67 Lit/min, Fig1). After the 8 weeks exposure, MI was induced using the standard occlusion/reperfusion MI model (Fig1), where the proximal left coronary artery was mechanically occluded for 30 minutes, followed by 3 hours of reperfusion. Post-surgery, MI occurrence was confirmed via the triphenyl tetrazolium chloride (TTC) staining technique. Hemodynamics were measured invasively throughout the MI surgeries, and intrinsic frequency (IF) metrics were computed from carotid pressure waveforms. LV-arterial coupling was assessed using changes in intrinsic frequency variation (∆ω) from baseline to 3 hours post-reperfusion. Results Intrinsic frequency variation (∆ω) was measured over the period of progression of MI from baseline to 3 hours post-reperfusion. Rats exposed to E-cigarette vapor with nicotine (EC NIC(+)) and standard cigarette smoke exhibited a significant increase (P0.05) in ∆ω during MI compared to the control and EC NIC(-) groups (Fig2). Conclusions Chronic exposure to nicotine, whether delivered via E-cigarettes or standard cigarettes, leads to impaired LV-arterial coupling following myocardial infarction. Our findings highlight a previously unappreciated danger of nicotine inhalation delivery via either E-cigarette or traditional cigarette use in the setting of myocardial infarction, and calls into question the benefit of vaping as a substitute for smoking in individuals at risk of MI.Study Flowchart Changes of LV-Artereial Coupling
Alavi et al. (Sat,) conducted a other in Myocardial infarction (n=109). E-cigarette vapor with nicotine or standard cigarette smoke vs. Purified air (control) or E-cigarette vapor without nicotine was evaluated on LV-arterial coupling assessed using changes in intrinsic frequency variation (∆ω) from baseline to 3 hours post-reperfusion (p=<0.05). Chronic exposure to nicotine via E-cigarettes or standard cigarettes significantly impaired LV-arterial coupling following induced myocardial infarction in rats compared to controls (P<0.05).