title: Lung function and cardiovascular risk: relationship with inflammation-sensitive plasma proteins.
abstract: BACKGROUND
  The inverse relationship between pulmonary function and incidence of cardiovascular disease remains largely unexplained. This prospective study explored the hypothesis of a relationship with inflammation-sensitive plasma proteins.
  
  
  RESULTS
  Forced vital capacity (FVC) and plasma levels of fibrinogen, alpha(1)-antitrypsin, haptoglobin, ceruloplasmin, and orosomucoid were determined in 5064 healthy men aged 28 to 61 years. All-cause mortality, cardiovascular mortality, and incidence of myocardial infarction were monitored over a mean follow-up period of 18.4 years. Low FVC (fourth quartile) was associated with higher protein levels and with increased incidences of myocardial infarction and cardiovascular death. Adjustments for protein levels reduced the age-adjusted relative risks (RRs) for myocardial infarction (from 1.99, 95% CI 1.5 to 2.6, to 1.70, 95% CI 1.3 to 2.2) and cardiovascular death (from 2.71, 95% CI 1.9 to 3.9, to 2.28, 95% CI 1.6 to 3.3) among men with low FVC, corresponding to approximately 25% of the excess risk. The risk factor-adjusted RRs were reduced from 1.45 (95% CI 1.1 to 1.9) to 1.38 (95% CI 1.1 to 1.8) and from 1.96 (95% CI 1.4 to 2.8) to 1.85 (95% CI 1.3 to 2.7) for myocardial infarction and cardiovascular death, respectively, corresponding to approximately 10% to 15% of the excess risk. Among men with low FVC, the risk factor-adjusted RR for myocardial infarction was 2.5 (95% CI 1.7 to 3.6) for those with high protein levels (> or =2 proteins in top quartile) and 1.7 (95% CI 1.1 to 2.4) for those with low protein levels (< or =1 protein in top quartile; reference, top quartile of FVC and low protein levels).
  
  
  CONCLUSIONS
  FVC is significantly and inversely associated with plasma levels of inflammation-sensitive plasma proteins. This relationship contributes to but cannot fully explain the increased cardiovascular risk among men with low FVC.
authors.affiliation: Department of Community Medicine, Malmö University Hospital, Malmö, Sweden. Gunnar.Engstrom@smi.mas.lu.se
authors.forename: G
authors.initials: G
authors.lastname: Engström
authors.forename: P
authors.initials: P
authors.lastname: Lind
authors.forename: B
authors.initials: B
authors.lastname: Hedblad
authors.forename: P
authors.initials: P
authors.lastname: Wollmer
authors.forename: L
authors.initials: L
authors.lastname: Stavenow
authors.forename: L
authors.initials: L
authors.lastname: Janzon
authors.forename: F
authors.initials: F
authors.lastname: Lindgärde
mesh_terms: D000328:Adult; D001798:Blood Proteins / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000401:mortality; D015331:Cohort Studies; D005500:Follow-Up Studies; D006801:Humans; D015994:Incidence; D007249:Inflammation / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology; D011446:Prospective Studies; D012307:Risk Factors; D016019:Survival Analysis; D014797:Vital Capacity
chemical_list: D001798:Blood Proteins