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Published on: May 24, 2017
The effects of cigarette smoking and smoking cessation on high-density lipoprotein functions: implications for
Hong-Ying Chen1, Shi-Cheng Li1, Lian-Feng Chen1
1Department of Cardiology, Peking Union Medical College Hospital (PUMCH), Beijing, P. R. China.
Insights
Smoking cessation improves high-density lipoprotein (HDL) function in coronary artery disease patients, enhancing its antioxidant and anti-inflammatory properties. This highlights the importance of quitting smoking for cardiovascular health.
Area of Science:
- Cardiovascular Disease Research
- Lipid Metabolism and Function
- Smoking Cessation Science
Background:
- Smoking cessation improves coronary artery disease (CAD) prognosis.
- Investigating the impact of smoking cessation on high-density lipoprotein (HDL) functionality in CAD patients.
Purpose of the Study:
- To evaluate the effect of smoking cessation on HDL antioxidative and antichemotactic properties.
- To assess HDL-induced cellular cholesterol efflux after smoking cessation in CAD patients.
Main Methods:
- Prospective, randomized controlled study comparing CAD smokers, healthy smokers, and non-smokers.
- Assessed HDL antioxidative and antichemotactic abilities, and cholesterol efflux before and after a 3-month cessation period.
- In vitro experiments investigated effects of carbon monoxide and nicotine on HDL function.
Main Results:
- HDL antioxidative and antichemotactic abilities were significantly reduced in CAD smokers compared to non-smokers.
- Smoking cessation significantly improved HDL antioxidative and antichemotactic abilities in CAD patients.
- HDL-induced cellular cholesterol efflux was not significantly increased by smoking cessation.
Conclusions:
- Smoking cessation effectively enhances HDL function in CAD smokers.
- This study reinforces the critical role of smoking cessation in the secondary prevention of CAD.
Background:
Smoking cessation was associated with improved prognosis of coronary artery disease. This study was designed to investigate the effect of smoking cessation on high-density lipoprotein functionality in coronary artery disease patients.
Methods:
In this prospective, randomized and parallel controlled study, coronary artery disease smokers ( n = 28) and healthy smokers ( n = 30) were divided into smoking cessation group and continuous smoking group, respectively. Blood samples were collected before and after three-month smoking cessation. Plasma high-density lipoprotein was isolated by density gradient centrifugation. The ability of high-density lipoprotein against copper-induced oxidation of lipoprotein was determined to evaluate the antioxidative property of high-density lipoprotein, and the macrophage migration inhibited by high-density lipoprotein was tested to identify the antichemotactic property of high-density lipoprotein. High-density lipoprotein-induced macrophage cholesterol efflux was measured by fluorescence spectrometry using NBD cholesterol analogue. Healthy non-smoking volunteers were enrolled as the baseline control.
Results:
The baseline antioxidative, antichemotactic ability of high-density lipoprotein and high-density lipoprotein-induced cellular cholesterol efflux in coronary artery disease smokers and healthy smokers were significantly attenuated when compared with those in healthy non-smokers. After three-month smoking cessation, both the antioxidative ability and antichemotactic ability of high-density lipoprotein were improved significantly in coronary artery disease smokers. However, high-density lipoprotein-induced cellular cholesterol efflux was not increased by smoking cessation. In in vitro experiments, carbon monoxide reduced the antioxidative ability and nicotine enhanced the antichemotactic ability of high-density lipoprotein.
Conclusions:
Smoking cessation is an effective measure to improve high-density lipoprotein functions in coronary artery disease smokers. Our study re-emphasizes the importance of smoking cessation in the secondary prevention of coronary artery disease.
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