scholarly journals Serum caeruloplasmin as a coronary risk factor in the elderly: the Rotterdam Study

1999 ◽  
Vol 81 (2) ◽  
pp. 139-144 ◽  
Author(s):  
Kerstin Klipstein-Grobusch ◽  
Diederick E. Grobbee ◽  
J. F. Koster ◽  
J. Lindemans ◽  
Heiner Boeing ◽  
...  

Serum Cu and caeruloplasmin levels have been suggested to be independent risk factors for CHD operating through oxidative modification of LDL. However, given its function as an acute-phase protein, the question has been raised whether an elevated caeruloplasmin level is not merely an indicator of inflammation. In the current study, we investigated whether serum caeruloplasmin was associated with subsequent myocardial infarction, taking into account indices of inflammation. The study population consisted of 210 cases of first myocardial infarction and controls, frequency-matched on age (5-year categories) and sex, selected from the population-based cohort of the Rotterdam Study. Serum caeruloplasmin levels were significantly elevated in cases of myocardial infarction compared with controls (510 (sd 110) v. 470 (sd 100) mg/1; P = 0·007). Risk of myocardial infarction for the highest compared with the lowest quartile of caeruloplasmin was 2·46 (95 % CI 1·04, 6·00; Ptrend = 0·043) after adjustment for age, sex, BMI, pack-years smoked, serum cholesterol, systolic blood pressure, and income. The relative risk was most evident in current smokers. Adjustment for C-reactive protein and leucocyte count reduced the excess risk by 33 %. This suggests that a substantial part of the observed association between serum caeruloplasmin and CHD may be attributed to inflammation processes rather than to the pro-oxidant activity of caeruloplasmin.

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Johannes Beller ◽  
Johann Bauersachs ◽  
Andreas Schäfer ◽  
Lars Schwettmann ◽  
Margit Heier ◽  
...  

1999 ◽  
Vol 69 (2) ◽  
pp. 261-266 ◽  
Author(s):  
Kerstin Klipstein-Grobusch ◽  
Johanna M Geleijnse ◽  
Johanna H den Breeijen ◽  
Heiner Boeing ◽  
Albert Hofman ◽  
...  

2018 ◽  
Vol 25 (12) ◽  
pp. 1316-1323 ◽  
Author(s):  
Marijn Albrecht ◽  
Chantal M Koolhaas ◽  
Josje D Schoufour ◽  
Frank JA van Rooij ◽  
M Kavousi ◽  
...  

Background The association between physical activity and atrial fibrillation remains controversial. Physical activity has been associated with a higher and lower atrial fibrillation risk. These inconsistent results might be related to the type of physical activity. We aimed to investigate the association of total and types of physical activity, including walking, cycling, domestic work, gardening and sports, with atrial fibrillation. Design Prospective cohort study. Methods Our study was performed in the Rotterdam Study, a prospective population-based cohort. We included 7018 participants aged 55 years and older with information on physical activity between 1997–2001. Cox proportional hazards models were used to examine the association of physical activity with atrial fibrillation risk. Models were adjusted for biological and behavioural risk factors and the remaining physical activity types. Physical activity was categorised in tertiles and the low group was used as reference. Results During 16.8 years of follow-up (median: 12.3 years, interquartile range: 8.7–15.9 years), 800 atrial fibrillation events occurred (11.4% of the study population). We observed no association between total physical activity and atrial fibrillation risk in any model. After adjustment for confounders, the hazard ratio and 95% confidence interval for the high physical activity category compared to the low physical activity category was: 0.71 (0.80–1.14) for total physical activity. We did not observe a significant association between any of the physical activity types with atrial fibrillation risk. Conclusion Our results suggest that physical activity is not associated with higher or lower risk of atrial fibrillation in older adults. Neither total physical activity nor any of the included physical activity types was associated with atrial fibrillation risk.


2002 ◽  
Vol 87 (01) ◽  
pp. 105-109 ◽  
Author(s):  
Jan-Håkan Jansson ◽  
Sverker Jern ◽  
Torbjörn Nilsson ◽  
Anna Tjärnlund ◽  
Kurt Boman ◽  
...  

SummaryWe recently identified a polymorphic Sp1 binding site in an enhancer at the tissue-type plasminogen activator (tPA) locus (tPA –7,351C/T), which was associated with vascular tPA release. Subjects homozygous for the –7,351C allele had twice the tPA release rate compared to subjects carrying the –7,351T allele. In this study we tested the hypothesis that the tPA –7,351C/T polymorphism is associated with myocardial infarction (MI). In a population-based prospective nested case-control study within northern Sweden, genotypes were determined among 61 MI cases and 120 controls. In a multivariate model, the tPA –7,351C/T polymorphism (OR 2.68 for T allele carriers; 95% CI 1.31– 5.50), tPA antigen (OR 1.16; 95% CI 1.07–1.25) and apo A-I (OR, 0.997; 95% CI 0.995–0.999) were independently associated with a first MI. These findings suggest that genetic markers of local tPA release and circulating steady-state tPA levels carry independent prognostic information.


1999 ◽  
Vol 69 (6) ◽  
pp. 1231-1236 ◽  
Author(s):  
Kerstin Klipstein-Grobusch ◽  
Johan F Koster ◽  
Diederick E Grobbee ◽  
Jan Lindemans ◽  
Heiner Boeing ◽  
...  

2001 ◽  
Vol 1 (S2) ◽  
Author(s):  
IM der Meer ◽  
MPM Maat ◽  
JG der Bom ◽  
A Hofman ◽  
JCM Witteman

Heart ◽  
2010 ◽  
Vol 96 (18) ◽  
pp. 1458-1462 ◽  
Author(s):  
M. J. G. Leening ◽  
S. E. Elias-Smale ◽  
J. F. Felix ◽  
J. A. Kors ◽  
J. W. Deckers ◽  
...  

2019 ◽  
Vol 75 (6) ◽  
pp. 1089-1094 ◽  
Author(s):  
Laura M Pérez ◽  
Babak Hooshmand ◽  
Francesca Mangialasche ◽  
Patrizia Mecocci ◽  
A David Smith ◽  
...  

Abstract We aimed to investigate the association between baseline levels of total serum glutathione (tGSH) and rate of chronic disease accumulation over time. The study population (n = 2,596) was derived from a population-based longitudinal study on ≥60-year-olds living in Stockholm. Participants were clinically assessed at baseline, 3- and 6-year follow-ups. Multimorbidity was measured as the number of chronic conditions from a previously built list of 60 diseases. Linear mixed models were applied to analyze the association between baseline tGSH levels and the rate of multimorbidity development over 6 years. We found that at baseline, participants with ≥4 diseases had lower tGSH levels than participants with no chronic conditions (3.3 vs 3.6 µmol/L; p < .001). At follow-up, baseline levels of tGSH were inversely associated with the rate of multimorbidity development (β * time: −0.044, p < .001) after adjusting for age, sex, education, levels of serum creatinine, C-reactive protein, albumin, body mass index, smoking, and time of dropout or death. In conclusion, serum levels of tGSH are inversely associated with multimorbidity development; the association exists above and beyond the link between tGSH and specific chronic conditions. Our findings support the hypothesis that tGSH is a biomarker of multisystem dysregulation that eventually leads to multimorbidity.


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