Physicians' Academy for Cardiovascular Education

Smoking heaviness associated with CVD risk-associated inflammatory markers

King CC, Arterioscler Thromb Vasc Biol, 2017

Longitudinal Impact of Smoking and Smoking Cessation on Inflammatory Markers of Cardiovascular Disease Risk

King CC, Piper ME, Gepner AD, et al.
Arterioscler Thromb Vasc Biol 2017;37:published online ahead of print


Tobacco smoking increases the CVD risk by activating inflammatory pathways, lipid oxidation, hypercoagulability, and vascular dysfunction [1,2]. There are data showing that smokers have higher levels of CVD risk-associated inflammatory markers, however, the effects of smoking cessation on such inflammatory markers have not been evaluated [3,4].
In this study, the cross-sectional and longitudinal relationships between smoking burden, smoking cessation and six inflammatory markers were assessed, in a large cohort of smokers.
The inflammatory markers, which are predictive of CVD events, included: c-reactive protein (CRP), D-dimer, fibrinogen, urinary F2 isoprostane:creatinine [F2:Cr] ratio, myeloperoxidase, and WBC count. These were compared with smoking heaviness markers exhaled carbon monoxide (CO), cigarettes per day, and packyears.

Main results



In a large cohort, smoking heaviness was independently associated with urinary F2:Cr ratio, myeloperoxidase and WBC count, which are three inflammatory markers related to CVD risk. However, no association was observed with CRP, fibrinogen or D-dimer. In addition, cessation reduced urinary F2:Cr ratios and WBC counts. As F2:CR ratio and myeloperoxidase reflect oxidative stress, these results suggest that oxidant stress may mediate increased inflammation and CVD risk in smokers.
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