Effects of Electronic Cigarette Vaping on Cardiac and Vascular Function, and Post-myocardial Infarction Remodeling in Rats

Abstract

The effect of electronic cigarette (E-cig) vaping on cardiac and vascular function during the healing phase of myocardial infarction (MI), and post-MI remodeling was investigated. Sprague Dawley rats were subjected to left coronary artery ligation to induce MI. One week later, rats were randomized to receive either 12 weeks of exposure to purified air (n = 37) or E-cig vapor (15 mg/ml of nicotine) (n = 32). At 12 weeks, cardiac and vascular function, and post-MI remodeling were assessed. Baseline blood flow in the femoral artery did not differ between groups, but peak reperfusion blood flow was blunted in the E-cig group (1.59 ± 0.15 ml/min) vs. the air group (2.11 ± 0.18 ml/min; p = 0.034). Femoral artery diameter after reperfusion was narrower in the E-cig group (0.54 ± 0.02 mm) compared to the air group (0.60 ± 0.02 mm; p = 0.023). Postmortem left ventricular (LV) volumes were similar in the E-cig (0.69 ± 0.04 ml) and air groups (0.73 ± 0.04 ml; p = NS); and myocardial infarct expansion index did not differ between groups (1.4 ± 0.1 in E-cig group versus 1.3 ± 0.1 in air group; p = NS). LV fractional shortening by echo did not differ between groups at 12 weeks (E-cig at 29 ± 2% and air at 27 ± 1%; p = NS). Exposure to E-cig during the healing phase of MI was associated with altered vascular function with reduced femoral artery blood flow and diameter at reperfusion, but not with worsened LV dilation or worsened cardiac function.

Myocardial infarction injury is exacerbated by nicotine in vape aerosol exposure

“…64,65 Clinical case reports document the impact of chronic heavy vape aerosol exposure leading to cardiopulmonary damage 66 , but whether vaping predisposes the heart to impaired recovery from acute injury remains poorly understood. A recent study found that exposure to ecigarettes during the recovery phase after infarction injury did not correlate with worsened left ventricular dilation or cardiac function 52 , a finding that contrasts sharply with similarly conceived studies assessing the effect of traditional cigarette smoking. 49 The experimental design of these studies examine impact of exposure after myocardial infarction, but effects of cigarette smoking prior to myocardial injury are much more controversial.…”

“…45 The immunomodulatory action of nicotine may impair healing following tissue injury 46,47 with concomitant pro-fibrotic action [33][34][35] . Indeed, there is evidence supporting worsened outcomes in cardiac structure and function resulting from smoking or nicotine exposure prior to infarction 26,[48][49][50][51][52] , but specific contribution of nicotine in exacerbating myocardial injury is poorly defined. This issue is particularly germane to vape aerosol exposure where bioavailability of nicotine can far exceed that of traditional smoking.…”