Background: Although cigarette smoking is a risk factor for heart failure (HF), smokers with HF have lower mortality rates during/following hospitalization compared to nonsmokers. We examined vascular endothelial function in chronic smokers and nonsmokers with HF as it relates to this smoker's paradox.
Hypothesis: Smokers with HF will have attenuated endothelial dysfunction compared to non-smokers with HF.
Methods: Brachial artery flow-mediated dilation (FMD), a measure of conduit vessel endothelial function, was measured in 33 smoking and nonsmoking patients with HF vs controls. In addition, soluble endoglin (sEng), a circulating mediator of endothelial function, was measured in a separate group of 36 smoking and nonsmoking patients with HF vs controls.
Results: FMD was significantly lower in smokers without HF compared to the nonsmokers without HF (P < 0.05). FMD was significantly higher in smokers with HF vs nonsmokers with HF (P < 0.05) and did not differ from values seen in nonsmokers without HF (P > 0.05). There were no differences in sEng between smokers and nonsmokers without HF (P > 0.05). sEng was lower in smokers with HF vs nonsmokers with HF (P < 0.05) and did not differ from values seen in nonsmokers without HF (P > 0.05).
Conclusions: Smokers with HF had higher brachial FMD and lower sEng than nonsmokers with HF, and values were comparable to nonsmokers without HF. These findings offer novel insight into the smoker's paradox and suggest that improved short-term outcome in patients hospitalized with HF may in part be mediated by preservation of vascular endothelial function in this setting.
© 2011 Wiley Periodicals, Inc.