The effect of electronic cigarettes on young versus old normal hearts and pathologic hearts

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Project Summary/Abstract E-cigarettes (E-C) continue to gain popularity, but the effects of E-C on the cardiovascular (CV) system of either normal individuals or those with heart disease are unknown. Cigarette smoke can increase heart rate, blood pressure, worsen endothelial dysfunction, and accelerate atherosclerosis. Some suggest that substituting E-C could be a safer approach to reduce cigarette smoking risks as they lack tar and some of the other noxious chemicals associated with cigarette smoke. However, E-C can still deliver nicotine and other potentially dangerous chemicals such as acrolein, propylene glycol, glycerol, aldehydes, and flavorings. In addition, the small particle size that may result from E-C vaping could result in increased toxicity to the lungs and cardiovascular system. There is a large knowledge gap in that there are no studies that have examined the effect of chronic exposure to E-C on the CV system in otherwise healthy young individuals where there has been a rapid increase in E-C use versus older individuals who may be turning to E-C as a way to quit standard cigarettes. In addition there is not data on the long-term effect of E-C on subjects with known CV disease. Thus, before suggesting that individuals can feel safe that their use of E-C is not going to cause or exacerbate CV disease, rigorous controlled studies are needed to assess the effect of E-C on CV phenotype and genotype. Our goal will be to determine the acute and chronic effects that E-C has in comparison to standard cigarette smoke on the young versus the old CV system and on the diseased CV system, including left ventricular (LV) dysfunction due to previous myocardial infarction (MI). We will determine whether E-C are safer, equally safe or less safe for subjects who have these underlying CV conditions versus standard cigarettes. We hypothesize that E-C, especially if they carry nicotine, will contribute to adverse LV remodeling post myocardial infarction, worsen heart failure, and endothelial dysfunction. We will determine whether these effects will be lessened if E-C does not contain nicotine, and whether certain therapies can reverse the effects. A well-established rodent model of MI will be used and there will be collaborative effort between a laboratory that has extensive experience subjecting rodents to exposure to smoke and pollution with a laboratory that has extensive experience with analyzing the pathophysiology of in vivo cardiac disease models including assessment by echocardiography, cardiac catheterization, detailed histologic and histochemical analyses, biochemical analyses, assessment of endothelial function, assessment of mitochondrial function, ultrastructural analysis, and assessment of gene expression.