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Lung function and cardiovascular risk: relationship with inflammation-sensitive plasma proteins.

Engström, Gunnar (författare)
Lund University,Lunds universitet,Institutionen för kliniska vetenskaper, Malmö,Medicinska fakulteten,Department of Clinical Sciences, Malmö,Faculty of Medicine
Lind, P (författare)
Hedblad, Bo (författare)
Lund University,Lunds universitet,Institutionen för kliniska vetenskaper, Malmö,Medicinska fakulteten,Department of Clinical Sciences, Malmö,Faculty of Medicine
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Wollmer, Per (författare)
Lund University,Lunds universitet,Klinisk fysiologi och nuklearmedicin, Malmö,Forskargrupper vid Lunds universitet,Clinical Physiology and Nuclear Medicine, Malmö,Lund University Research Groups
Stavenow, L (författare)
Janzon, Lars (författare)
Lund University,Lunds universitet,Institutionen för kliniska vetenskaper, Malmö,Medicinska fakulteten,Department of Clinical Sciences, Malmö,Faculty of Medicine
Lindgärde, Folke (författare)
Lund University,Lunds universitet,Institutionen för kliniska vetenskaper, Malmö,Medicinska fakulteten,Department of Clinical Sciences, Malmö,Faculty of Medicine
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 (creator_code:org_t)
2002
2002
Engelska.
Ingår i: Circulation. - 1524-4539. ; 106:20, s. 2555-2560
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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. Methods and 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 {approx}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 {approx}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 (>=2 proteins in top quartile) and 1.7 (95% CI 1.1 to 2.4) for those with low protein levels (<=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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kardiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)

Nyckelord

Human
Adult
Blood Proteins: analysis
Cardiovascular Diseases: epidemiology
Cardiovascular Diseases: mortality
Cohort Studies
Follow-Up Studies
Inflammation: blood
Male
Myocardial Infarction: epidemiology
Middle Age
Incidence
Vital Capacity
Survival Analysis
Prospective Studies
Risk Factors
Support
Non-U.S. Gov't

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