Effects of Smoking and Smoking Cessation on Endothelial Function 1-Year Outcomes From a Randomized Clinical Trial

University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53792, USA.
Journal of the American College of Cardiology (Impact Factor: 16.5). 03/2010; 55(18):1988-95. DOI: 10.1016/j.jacc.2010.03.002
Source: PubMed


The purpose of this study was to determine whether smoking cessation improves flow-mediated dilation (FMD) of the brachial artery.
The long-term effects of continued smoking and smoking cessation on endothelial function have not been described previously.
This was a 1-year, prospective, double-blind, randomized, placebo-controlled clinical trial of the effects of 5 smoking cessation pharmacotherapies. FMD was measured by B-mode ultrasonography before and 1 year after the target smoking cessation date. Cessation was verified by exhaled carbon monoxide levels. DeltaFMD was compared among study arms and between subjects who successfully quit smoking and those who continued to smoke. Predictors of baseline FMD and DeltaFMD were identified by multivariable regression.
The 1,504 current smokers (58% female, 84% white) were 44.7 +/- 11.1 years of age and smoked 21.4 +/- 8.9 cigarettes/day. Baseline FMD was similar in each treatment arm (p = 0.499) and was predicted by BA diameter (p < 0.001), reactive hyperemia blood flow (p < 0.001), high-density lipoprotein cholesterol (p = 0.001), and carbon monoxide (p = 0.012) levels. After 1 year, 36.2% quit smoking. FMD increased by 1% (6.2 +/- 4.4% to 7.2 +/- 4.2%) after 1 year (p = 0.005) in those who quit, but did not change (p = 0.643) in those who continued to smoke. Improved FMD among quitters remained significant (p = 0.010) after controlling for changes in brachial artery diameter, reactive hyperemia, low-density lipoprotein cholesterol, and the presence of a home smoking ban.
Despite weight gain, smoking cessation leads to prolonged improvements in endothelial function, which may mediate part of the reduced cardiovascular disease risk observed after smoking cessation. (Smoking Cessation Medications: Efficacy, Mechanisms and Algorithms; NCT00332644).

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    • "and others [9] have previously shown that active cigarette smoking and even exposure to secondhand smoke [6] leads to acute impairment of endothelial function and might also have a longer-lasting effects by negatively impacting vascular repair mechanisms, including the migratory function of endothelial cells. Endothelial dysfunction is a major mechanism by which cigarette smoking promotes atherosclerosis [10] [11]. "
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