Clinical Chemistry
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Clinical Chemistry 55: 322-335, 2009. First published December 18, 2008; 10.1373/clinchem.2008.112334
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(Clinical Chemistry. 2009;55:322-335.)
© 2009 American Association for Clinical Chemistry, Inc.


Lipids, Lipoproteins, and Cardiovascular Risk Factors

Determinants of the Acute-Phase Protein C-Reactive Protein in Myocardial Infarction Survivors: The Role of Comorbidities and Environmental Factors

Regina Rückerl1, Annette Peters1,2, Natalie Khuseyinova3, Mariarita Andreani4, Wolfgang Koenig3,a, Christa Meisinger1,5, Konstantina Dimakopoulou6, Jordi Sunyer7,8,9,10, Timo Lanki11, Fredrik Nyberg12,13 and Alexandra Schneider1

1 Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Epidemiology, Munich, Germany; 2 Helmholtz Zentrum München, German Research Center for Environmental Health, Focus-Network Nanoparticles and Health (NanoHealth), Munich, Germany; 3 Department of Internal Medicine II, Cardiology, University of Ulm Medical Center, Ulm, Germany; 4 Local Health Authority RM E, Department of Epidemiology ASL RME, Rome, Italy; 5 Central Hospital of Augsburg, MONICA/KORA Myocardial Infarction Registry, Augsburg, Germany; 6 Department of Hygiene and Epidemiology, University of Athens Medical School, Athens, Greece; 7 Center for Research in Environmental Epidemiology (CREAL), 8 Municipal Institute of Medical Research (IMIM-Hospital del Mar), 9 CIBER Epidemiologìa y Salud Pública (CIBERESP), and 10 Universitat Pompeu Fabra (UPF), Barcelona, Spain; 11 Environmental Epidemiology Unit, National Public Health Institute (KTL), Kuopio, Finland; 12 Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden; 13 AstraZeneca R&D, Mölndal, Sweden.

aAddress correspondence to this author at: Department of Internal Medicine II—Cardiology, University of Ulm Medical Center, Robert-Koch Str. 8, D-89081 Ulm, Germany. Fax 49-731-500-45021; e-mail wolfgang.koenig{at}uniklinik-ulm.de.

Background: C-reactive protein (CRP), a sensitive marker of the acute-phase response, has been associated with future cardiovascular endpoints independently of other risk factors. A joint analysis of the role of risk factors in predicting mean concentrations and variation of high-sensitivity CRP (hsCRP) in serum has not been carried out previously.

Methods: We used data from 1003 myocardial infarction (MI) survivors who had hsCRP measured monthly up to 8 times and multivariate mixed effects statistical models to study the role of time-variant and -invariant factors on the geometric mean of and the intraindividual variation in hsCRP concentrations.

Results: Patients with ≥6.5% glycosylated hemoglobin (HbA1c) had 26.2% higher hsCRP concentrations (95% CI, 7.2%–48.6%) and 20.7% greater variation in hsCRP values (P = 0.0034) than patients with lower baseline Hb A1c values (<6.5%). Similar but less pronounced differences were seen in patients with a self-reported diagnosis of type 2 diabetes. hsCRP concentrations showed less variation in patients who reported angina pectoris, congestive heart failure, or emphysema (–11.0%, –24.9%, and –41.6%, respectively, vs patients without these conditions) but greater variation in males and smokers (+24.8% and +27.3%, respectively, vs females and nonsmokers). Exposures in the 24 h before blood sampling, including exposure to environmental tobacco smoke, alcohol consumption, and extreme stress, did not have a major impact.

Conclusions: One or 2 hsCRP measurements may not be sufficient to adequately characterize different patient groups after MI with similar precisions. We found hsCRP concentrations to be especially variable in males, smokers, and patients with increased Hb A1c values.







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Copyright © 2009 by the American Association for Clinical Chemistry.