title: Smoking interacts with sleep apnea to increase cardiovascular risk.
abstract: BACKGROUND
  Sleep apnea syndrome is an important risk factor for atherosclerosis and cardiovascular morbidity and so is cigarette smoking. In both atherosclerosis and cardiovascular disease, oxidative stress and inflammation have been implicated as underlying pathophysiologic mechanisms. We investigated oxidative stress and inflammatory markers in 70 non-smoking and smoking patients with sleep apnea.
  
  
  METHODS
  Thirty-five sleep apnea patients aged 20-60 years who smoke 20 or more cigarettes/day and for at least 5 years were individually matched by gender, age (+/-5 years), body mass index (BMI; categorized as, 'normal weight', 'overweight', and 'obese'), sleep apnea severity (categorized as 'mild', 'moderate', and 'severe'), and presence of cardiovascular diseases, with 35 patients who never smoked. Blood samples were drawn after an overnight fasting for determination of lipids profile, oxidative stress markers thiobarbituric acid reactive substances, peroxides and paraoxonase-1 and inflammatory markers C-reactive protein, ceruloplasmin, and haptoglobin.
  
  
  RESULTS
  Smokers showed significantly higher levels of C-reactive protein, ceruloplasmin, and haptoglobin and triglycerides and lower levels of high-density lipoprotein (HDL) cholesterol than non-smokers. There was a significant interaction effect between smoking and apnea severity on ceruloplasmin and HDL levels. Smokers with severe sleep apnea had the highest level of ceruloplasmin and the lowest level of HDL.
  
  
  CONCLUSIONS
  There is a synergistic effect between cigarette smoking and sleep apnea on some of the biochemical cardiovascular risk markers. Patients with severe sleep apnea who smoke are at a greater cardiovascular risk than smokers with mild-moderate sleep apnea and patients who do not smoke.
authors.affiliation: Lloyd Rigler Sleep Apnea Research Laboratory Ruth and Bruce Rappaport, Faculty of Medicine, Technion-Israel Institute of Technology, Efron Street 7, Bat Galim, Haifa, Israel.
authors.forename: Lena
authors.initials: L
authors.lastname: Lavie
authors.forename: Peretz
authors.initials: P
authors.lastname: Lavie
mesh_terms: D000328:Adult; D043303:Aryldialkylphosphatase / Q000097:blood; D050197:Atherosclerosis / Q000097:blood / Q000453:epidemiology / Q000209:etiology; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D016022:Case-Control Studies; D002570:Ceruloplasmin / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D015897:Comorbidity; D003404:Creatinine / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D006242:Haptoglobins / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D010100:Oxygen / Q000097:blood; D017286:Polysomnography; D012016:Reference Values; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000097:blood / Q000150:complications* / Q000453:epidemiology; D012907:Smoking / Q000009:adverse effects* / Q000097:blood / Q000453:epidemiology; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D006242:Haptoglobins; D018836:Inflammation Mediators; D008055:Lipids; D017392:Thiobarbituric Acid Reactive Substances; D002097:C-Reactive Protein; D003404:Creatinine; D002570:Ceruloplasmin; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human; D010100:Oxygen