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Air Temperature and Inflammatory Responses in Myocardial Infarction Survivors
Alexandra Schneider, Demosthenes Panagiotakos, Sally Picciotto, Klea Katsouyanni, Hannelore Löwel, Bénédicte Jacquemin, Timo Lanki, Massimo Stafoggia, Tom Bellander, Wolfgang Koenig and Annette Peters
Vol. 19, No. 3 (May, 2008), pp. 391-400
Published by: Lippincott Williams & Wilkins
Stable URL: http://www.jstor.org/stable/20485655
Page Count: 10
You can always find the topics here!Topics: Blood, Epidemiology, Relative humidity, Mortality, Disease risks, Myocardial infarction, Climate models, Cardiovascular diseases, Inflammation, Modeling
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Background: Temperature changes have been associated with increased cardiovascular risk, but the role of inflammatory markers in this relationship is not well understood. The objective of this study was to analyze the association between air temperature and C-reactive protein, interleukin-6 and fibrinogen in postmyocardial infarction patients. Methods: In a multicenter panel study, the 3 inflammatory blood markers were measured repeatedly. In total, 5813 blood samples in 1003 subjects were collected in 6 European cities representing different climates. Data on patient characteristics and disease history were gathered at the baseline visit. Meteorologic data were obtained from the city-specific network stations. The association was analyzed using a semiparametric model with random patient effects. Results: A 10°C decrease in the 5-day-average of air temperature before the blood withdrawal was associated with a 4% increase in C-reactive protein (4.3% [95% confidence interval = 0.2% to 8.1%]). Correspondingly, an increase of interleukin-6 was observed for the same time window (3.3% [0.1% to 6.3%]) whereas fibrinogen showed an increase of 1.3% (0.2% to 2.4%) with a lag of 3 days. Conclusion: A decrease in air temperature, particularly the average temperature of the last 5 days, was associated with an increase in both C-reactive protein and interleukin-6, whereas fibrinogen seemed to react to temperature changes after 3 days. In susceptible patients this might lead to an additional risk for cardiovascular events and suggests a biologic mechanism for the observed seasonal variation in death from ischemic heart disease and stroke in the elderly.
Epidemiology © 2008 Lippincott Williams & Wilkins