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Articles by A Peters
Total Records ( 5 ) for A Peters
  K Wolf , A Schneider , S Breitner , S von Klot , C Meisinger , J Cyrys , H Hymer , H. E Wichmann , A Peters and for the Cooperative Health Research in the Region of Augsburg (KORA) Study Group

Background— Air temperature changes have been associated with cardiovascular mortality and morbidity. The objective of this study was to examine in detail the registry-based myocardial infarction (MI) rates and coronary deaths in relation to air temperature in the area of Augsburg, Germany.

Methods and Results— Between 1995 and 2004, the Monitoring Trends and Determinants on Cardiovascular Diseases/Cooperative Health Research in the Region of Augsburg (MONICA/KORA) registry recorded 9801 cases of MI and coronary deaths. Over the same period, meteorological parameters and air pollutant concentrations were measured in the study region. Poisson regression analyses adjusting for time trend, relative humidity, season, and calendar effects were used to estimate immediate, delayed, and cumulative temperature effects on the occurrence of MIs. The daily rates of total MI, nonfatal and fatal events, and incident and recurrent events were analyzed. For the total MI cases, a 10°C decrease in 5-day average temperature was associated with a relative risk of 1.10 (95% confidence interval, 1.04 to 1.15). The effect of temperature on the occurrence of nonfatal events showed a delayed pattern, whereas the association with fatal MI was more immediate. No association could be observed for recurrent events. The effects of temperature decreases on total MI cases were more pronounced in years with higher average temperatures and were visible in summer.

Conclusions— We observed an inverse relationship between temperature and MI occurrence not only during winter but also during summer. Thus, our results suggest not a pure "cold effect" but an influence of unusual temperature decreases.

  N. L Smith , M. H Chen , A Dehghan , D. P Strachan , S Basu , N Soranzo , C Hayward , I Rudan , M Sabater Lleal , J. C Bis , M. P. M de Maat , A Rumley , X Kong , Q Yang , F. M. K Williams , V Vitart , H Campbell , A Malarstig , K. L Wiggins , C. M Van Duijn , W. L McArdle , J. S Pankow , A. D Johnson , A Silveira , B McKnight , A. G Uitterlinden , Aleksic Wellcome Trust Case Control Consortium; , J. B Meigs , A Peters , W Koenig , M Cushman , S Kathiresan , J. I Rotter , E. G Bovill , A Hofman , E Boerwinkle , G. H Tofler , J. F Peden , B. M Psaty , F Leebeek , A. R Folsom , M. G Larson , T. D Spector , A. F Wright , J. F Wilson , A Hamsten , T Lumley , J. C. M Witteman , W Tang and C. J. O'Donnell

Background— Plasma levels of coagulation factors VII (FVII), VIII (FVIII), and von Willebrand factor (vWF) influence risk of hemorrhage and thrombosis. We conducted genome-wide association studies to identify new loci associated with plasma levels.

Methods and Results— The setting of the study included 5 community-based studies for discovery comprising 23 608 European-ancestry participants: Atherosclerosis Risk In Communities Study, Cardiovascular Health Study, British 1958 Birth Cohort, Framingham Heart Study, and Rotterdam Study. All subjects had genome-wide single-nucleotide polymorphism (SNP) scans and at least 1 phenotype measured: FVII activity/antigen, FVIII activity, and vWF antigen. Each study used its genotype data to impute to HapMap SNPs and independently conducted association analyses of hemostasis measures using an additive genetic model. Study findings were combined by meta-analysis. Replication was conducted in 7604 participants not in the discovery cohort. For FVII, 305 SNPs exceeded the genome-wide significance threshold of 5.0x10–8 and comprised 5 loci on 5 chromosomes: 2p23 (smallest P value 6.2x10–24), 4q25 (3.6x10–12), 11q12 (2.0x10–10), 13q34 (9.0x10–259), and 20q11.2 (5.7x10–37). Loci were within or near genes, including 4 new candidate genes and F7 (13q34). For vWF, 400 SNPs exceeded the threshold and marked 8 loci on 6 chromosomes: 6q24 (1.2x10–22), 8p21 (1.3x10–16), 9q34 (<5.0x10–324), 12p13 (1.7x10–32), 12q23 (7.3x10–10), 12q24.3 (3.8x10–11), 14q32 (2.3x10–10), and 19p13.2 (1.3x10–9). All loci were within genes, including 6 new candidate genes, as well as ABO (9q34) and VWF (12p13). For FVIII, 5 loci were identified and overlapped vWF findings. Nine of the 10 new findings were replicated.

Conclusions— New genetic associations were discovered outside previously known biological pathways and may point to novel prevention and treatment targets of hemostasis disorders.

  A Dehghan , Q Yang , A Peters , S Basu , J. C Bis , A. R Rudnicka , M Kavousi , M. H Chen , J Baumert , G. D.O Lowe , B McKnight , W Tang , M de Maat , M. G Larson , S Eyhermendy , W. L McArdle , T Lumley , J. S Pankow , A Hofman , J. M Massaro , F Rivadeneira , M Kolz , K. D Taylor , C. M van Duijn , S Kathiresan , T Illig , Y. S Aulchenko , K. A Volcik , A. D Johnson , A. G Uitterlinden , G. H Tofler , C Gieger , Psaty Wellcome Trust Case Control Consortium , D. J Couper , E Boerwinkle , W Koenig , C. J O`Donnell , J. C Witteman , D. P Strachan , N. L Smith and A. R. Folsom

Background— Fibrinogen is both central to blood coagulation and an acute-phase reactant. We aimed to identify common variants influencing circulation fibrinogen levels.

Methods and Results— We conducted a genome-wide association analysis on 6 population-based studies, the Rotterdam Study, the Framingham Heart Study, the Cardiovascular Health Study, the Atherosclerosis Risk in Communities Study, the Monitoring of Trends and Determinants in Cardiovascular Disease/KORA Augsburg Study, and the British 1958 Birth Cohort Study, including 22 096 participants of European ancestry. Four loci were marked by 1 or more single-nucleotide polymorphisms that demonstrated genome-wide significance (P<5.0x10–8). These included a single-nucleotide polymorphism located in the fibrinogen β chain (FGB) gene and 3 single-nucleotide polymorphisms representing newly identified loci. The high-signal single-nucleotide polymorphisms were rs1800789 in exon 7 of FGB (P=1.8x10–30), rs2522056 downstream from the interferon regulatory factor 1 (IRF1) gene (P=1.3x10–15), rs511154 within intron 1 of the propionyl coenzyme A carboxylase (PCCB) gene (P=5.9x10–10), and rs1539019 on the NLR family pyrin domain containing 3 isoforms (NLRP3) gene (P=1.04x10–8).

Conclusions— Our findings highlight biological pathways that may be important in regulation of inflammation underlying cardiovascular disease.

  M Karakas , J Baumert , S Greven , R Ruckerl , A Peters and W. Koenig

Background: Among the numerous emerging biomarkers, high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6) have received widespread interest, and a large database has been accumulated on their potential role as predictors of cardiovascular risk. The concentrations of inflammatory biomarkers, however, are influenced, among other things, by physiological variation, which is the natural within-individual variation occurring over time. Implementation of hsCRP and IL-6 measurement into clinical practice requires data on the reliability of such measurements.

Methods: We serially measured hsCRP and IL-6 concentrations in up to 6 blood samples taken at monthly intervals from 200 post–myocardial infarction patients who participated in the AIRGENE study.

Results: The mean (SD) of the ln-transformed plasma concentrations (in milligrams per liter for hsCRP and nanograms per liter for IL-6) for all participants over all samples was 0.16 (1.04) for hsCRP and 0.76 (0.57) for IL-6, with no significant differences between men and women. The within-individual and analytical variance component for the ln-transformed hsCRP data was 0.37, and the between-individual variance component was 0.73. For the ln-transformed IL-6 data, these values were 0.11 and 0.22, respectively. A substantial part of the total variation in plasma hsCRP and IL-6 concentrations was explained by the between-individual variation (as a percentage of the total variance, 66.1% for the ln-transformed hsCRP data and 66.2% for the ln-transformed IL-6 data). For both markers, 2 measurements were needed to reach a sufficient reliability.

Conclusions: Our results demonstrate considerable stability and good reproducibility for serial hsCRP and IL-6 measurements. Thus, there should be no major concern about misclassification in clinical practice if at least 2 subsequent measurements are taken.

  D. B Panagiotakos , K Katsouyanni , T Bellander , M Grau , W Koenig , T Lanki , R Pistelli , A Schneider , A Peters and on behalf of the AIRGENE Study Group

Background Within the framework of the multi-centre AIRGENE project we studied the association of the Mediterranean diet on plasma levels of various inflammatory markers, in myocardial infarction (MI) survivors from six geographic areas in Europe.

Methods From 2003 to 2004, 1003 patients were repeatedly clinically examined. On every clinical visit (on average 5.8 times), blood EDTA-plasma samples were collected. High sensitivity C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen concentrations were measured based on standardized procedures. Dietary habits were evaluated through a semi-quantitative Food Frequency Questionnaire (FFQ), whereas adherence to the Mediterranean diet was assessed by a diet score.

Results A protective effect of adherence to the Mediterranean diet was found. For each unit of increasing adherence to the Mediterranean diet score there was a reduction of 3.1% in the average CRP levels (95% CI 0.5–5.7%) and of 1.9% in the average IL-6 levels (95% CI 0.5–3.4%) after adjusting for centre, age, sex, body mass index, physical activity, smoking status, diabetes and medication intake. No significant association was observed between the diet score and fibrinogen levels. Moderate intake of red wine (1–12 wine glasses per month) was associated with lower levels of CRP, IL-6 and fibrinogen.

Conclusions Adherence to the traditional Mediterranean diet was associated with a reduction of the concentrations of inflammatory markers in MI survivors. This may, in part, explain the beneficial effects of this diet on various chronic diseases such as atherosclerosis and cancer, and expands its role to secondary prevention level.

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