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Combined effects of brachial pulse pressure and sialic acid for risk of cardiovascular events during 40 years of follow-up in 37 843 individuals

Khalili, Payam, 1977- (författare)
Örebro universitet,Institutionen för hälsovetenskap och medicin,Department of Cardiology and Acute Internal Medicine, Central Hospital, Karlstad, Sweden
Sundström, Johan (författare)
Uppsala universitet,Kardiovaskulär epidemiologi
Franklin, Stanley S. (författare)
Department of Medicine, Medical Sciences, University of California, Irvine, USA
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Jendle, Johan, 1963- (författare)
Örebro universitet,Institutionen för hälsovetenskap och medicin,Department of Cardiology and Acute Internal Medicine, Central Hospital, Karlstad, Sweden
Lundin, Fredrik (författare)
Statistical Unit, Värmland County Council, Karlstad, Sweden
Jungner, Ingmar (författare)
Karolinska Institutet
Nilsson, Peter (författare)
Lund University,Lunds universitet,Internmedicin - epidemiologi,Forskargrupper vid Lunds universitet,Internal Medicine - Epidemiology,Lund University Research Groups
Sundström, Johannes (författare)
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 (creator_code:org_t)
Philadelphia, USA : Lippincott Williams & Wilkins, 2012
2012
Engelska.
Ingår i: Journal of Hypertension. - Philadelphia, USA : Lippincott Williams & Wilkins. - 0263-6352 .- 1473-5598. ; 30:9, s. 1718-1724
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Objective: Pulse pressure (PP) is a risk marker for cardiovascular disease (CVD) in individuals 50 years and older. Inflammation is suggested to influence atherosclerosis, but could also increase PP. We aimed to examine the combined effects of PP and the inflammatory marker sialic acid, and their independent roles on CVD risk. Methods: From a population-based study in Sweden between 1962 and 1965, 18 429 men and 19 414 women at the age of 50 or older were selected and followed for first CVD event until 2005. We investigated the biological interactions between sialic acid and PP. The associations of PP and sialic acid with risk of CVD were calculated by using Cox proportional hazards model. Adjustments were made for conventional risk factors, mean arterial pressure (MAP) and socioeconomic status. Results: The mean age was 59.5 (SD 6.5) years and the number of incident CVD events in men and women were 3641 and 3227, respectively. No biological interaction was seen between PP and sialic acid. In men, the adjusted hazard ratio for PP was 0.92 [95% confidence interval (CI) 0.88-0.96, P < 0.0001) for 1 SD of PP, and 1.09 (95% CI 1.05-1.13, P < 0.0001) for 1 SD of sialic acid. In women, the corresponding figures were 1.02 (95% CI 0.97-1.07, P = 0.48) and 1.09 (95% CI 1.05-1.13, P < 0.0001). Conclusions: Sialic acid but not PP was an independent risk factor for CVD. The risk induced by PP is highly affected by MAP. This suggests that both estimated arterial stiffness and inflammation contribute through different pathways to risk of CVD.

Ämnesord

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

Nyckelord

Blood pressure
cardiovascular
epidemiology
population
pulse pressure
risk
screening
Medicin
Medicine

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