Acute smoke-induced endothelial dysfunction is more prolonged in smokers than in non-smokers

Karatzi, Kalliopi; Papamichael, Christos; Karatzis, Emmanouil; Papaioannou, Theodore G.; Stamatelopoulos, Kimon; Zampelas, Antonis; Lekakis, John

doi:10.1016/j.ijcard.2006.07.200

Cited by 35 publications

(25 citation statements)

References 8 publications

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“…Linear Regression of Plasma Cotinine (Independent, ng/ml) and Biological Parameters (Dependent) The immediate transient decrease in FMD, a measure of vascular endothelial NO activity, from normal values (15) (approximately 7% at baseline) approached chronic active smoker's values (4% at 0 h) (12,29,37) and is consistent with the results published previously. Kato et al (11) have shown a similar reduction of FMD in nonsmokers after SHS exposure.…”

Section: Discussionsupporting

confidence: 88%

Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function

Heiß

Amabile

Lee

et al. 2008

Journal of the American College of Cardiology

265

159

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Section: Discussionsupporting

confidence: 88%

Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function

Heiß

Amabile

Lee

et al. 2008

Journal of the American College of Cardiology

265

159

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“…24,27 These results are in line with those of previous studies measuring acute smoke-induced endothelial dysfunction measured by flow-mediated dilatation (FMD); endothelial dysfunction was more prolonged in smokers than in nonsmokers. 61 The effect of chronic smoking on endothelial dysfunction is also detrimental; studies comparing the FMD of habitual smokers and nonsmokers found smoking to be associated with greater endothelial dysfunction. 6,62 However, the effect of chronic smoking on arterial stiffness is slightly more controversial.…”

Section: Discussionmentioning

confidence: 99%

“…As discussed above, numerous previous studies have shown that smoking causes significant endothelial dysfunction as assessed by FMD. 5,6,61,62,64 However, it is important to note that FMD has been previously shown to be significantly associated with arterial stiffness under a number of conditions and disease states. [122][123][124][125][126] Wright et al 127 noted that this association was weak and suggested that measurements of arterial stiffness should not replace FMD.…”

Section: Mechanismsmentioning

confidence: 99%

The effect of smoking on arterial stiffness

et al. 2010

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A systematic literature review was conducted using PubMed, Embase and the Cochrane Library to determine the effect of acute, chronic and passive smoking on arterial stiffness and to determine whether these effects are reversible after smoking cessation. A total of 39 relevant studies were identified and included. Acute smoking was found to cause an acute increase in arterial stiffness. Similarly, passive smoking increased arterial stiffness acutely and chronically. The majority of studies identified chronic smoking as a risk factor for increasing arterial stiffness. However, some studies found no statistical difference in arterial stiffness between nonsmokers and long-term smokers, although chronic smoking seems to sensitize the arterial response to acute smoking. In addition, whether arterial stiffness is reversed after smoking cessation and the timeline in which this may occur could not be determined from the identified literature. The effect of smoking discontinuation on arterial stiffness remains to be established by prospective smoking cessation trials.

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“…The FMD technique has increasingly been applied in physiological studies to examine the mechanisms that underlie the acute or chronic impact of stimuli that alter vascular function and risk (e.g., exercise training, smoking, hypercholesterolemia, hypertension) (20,26,34,41,54,81,101,134) or to study hemodynamic effects on the vasculature in vivo (85,87,98,115,120,121,131). Consequently, the FMD test represents an important tool to improve our physiological insight and understanding of mechanisms that alter endothelial and vascular function.…”

mentioning

confidence: 99%

Assessment of flow-mediated dilation in humans: a methodological and physiological guideline

Thijssen

Black

Pyke

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

1,232

1,345

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Endothelial dysfunction is now considered an important early event in the development of atherosclerosis, which precedes gross morphological signs and clinical symptoms. The assessment of flow-mediated dilation (FMD) was introduced almost 20 years ago as a noninvasive approach to examine vasodilator function in vivo. FMD is widely believed to reflect endothelium-dependent and largely nitric oxide-mediated arterial function and has been used as a surrogate marker of vascular health. This noninvasive technique has been used to compare groups of subjects and to evaluate the impact of interventions within individuals. Despite its widespread adoption, there is considerable variability between studies with respect to the protocols applied, methods of analysis, and interpretation of results. Moreover, differences in methodological approaches have important impacts on the response magnitude, can result in spurious data interpretation, and limit the comparability of outcomes between studies. This review results from a collegial discussion between physiologists with the purpose of developing considered guidelines. The contributors represent several distinct research groups that have independently worked to advance the evidence base for improvement of the technical approaches to FMD measurement and analysis. The outcome is a series of recommendations on the basis of review and critical appraisal of recent physiological studies, pertaining to the most appropriate methods to assess FMD in humans.

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Acute smoke-induced endothelial dysfunction is more prolonged in smokers than in non-smokers

Cited by 35 publications

References 8 publications

Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function

Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function

The effect of smoking on arterial stiffness

Assessment of flow-mediated dilation in humans: a methodological and physiological guideline

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