I021 Impact du polymorphisme génétique C(-260)T du CD14 sur la pression pulsée en fonction d’autres facteurs de risque cardiovasculaires : etude populationnelle transversale à partir du registre monica

Objectif de l’étudeLe CD14 est à l’intersection entre l’inflammation, les maladies infectieuses et le syndrome métabolique. Une corrélation positive entre la concentration plasmatique du CD14 soluble (sCD14) et la rigidité aortique a été décrite dans une étude transversale. Mais différents résultats ont été retrouvés sur l’incidence des évènements cardiovasculaires en fonction du polymorphisme C(-260)T du gène du CD14.L’objectif de cette étude est d’étudier l’influence du polymorphisme C(-260)T du CD14 sur la pression pulsée et indirectement sur le risque cardiovasculaire à partir de l’étude populationnelle transversale MONICA.Déroulement de l’étude1 155 sujets âgés entre 35 et 64 ans, en prévention primaire, ont été recrutés à partir des listes électorales de la Haute Garonne entre 1995 et 1997.MéthodesLa pression pulsée brachiale était mesurée au repos à 2 reprises puis moyennée. La concentration plasmatique du sCD14 a été mesurée par méthode immunoenzymatique. La randomisation est de type mendélienne. Les sujets ont été répartis en fonction du polymorphisme C(-260)T du CD14 après génotypage : homozygotes CC, homozygotes TT ou hétérozygotes CT.RésultatsLes sujets homozygotes TT ont une pression pulsée (PP) significativement plus basse et une concentration en sCD14 significativement plus élevée. Après ajustement avec les principaux facteurs confondants (âge, sexe, facteurs de risque cardiovasculaires traités), seul le génotype du CD14 reste corrélé à la PP. Cette corrélation n’intervient qu’en présence de facteurs de risque traités. Les diabétiques traités homozygotes TT sont ceux qui bénéficient de la plus importante baisse de PP par rapport aux homozygotes diabétiques CC (− 19,4mmHg, p=0,006).ConclusionCette étude suggère que les facteurs de risque ont un impact différent sur la pression pulsée en fonction du polymorphisme C(-260)T du CD14. Cette observation pourrait contribuer à affiner le risque cardiovasculaire absolu individuel, les sujets homozygotes TT ayant un risque cardiovasculaire moindre

Depression and mortality: Artifact of measurement and analysis?

Background Previous research demonstrates various associations between depression, cardiovascular disease (CVD) incidence and mortality, possibly as a result of the different methodologies used to measure depression and analyse relationships. This analysis investigated the association between depression, CVD incidence (CVDI) and mortality from CVD (MCVD), smoking related conditions (MSRC), and all causes (MALL), in a sample data set, where depression was measured using items from a validated questionnaire and using items derived from the factor analysis of a larger questionnaire, and analyses were conducted based on continuous data and grouped data. Methods Data from the PRIME Study (N=9798 men) on depression and 10-year CVD incidence and mortality were analysed using Cox proportional hazards models. Results Using continuous data, both measures of depression resulted in the emergence of positive associations between depression and mortality (MCVD, MSRC, MALL). Using grouped data, however, associations between a validated measure of depression and MCVD, and between a measure of depression derived from factor analysis and all measures of mortality were lost. Limitations Low levels of depression, low numbers of individuals with high depression and low numbers of outcome events may limit these analyses, but levels are usual for the population studied. Conclusions These data demonstrate a possible association between depression and mortality but detecting this association is dependent on the measurement used and method of analysis. Different findings based on methodology present clear problems for the elucidation and determination of relationships. The differences here argue for the use of validated scales where possible and suggest against over-reduction via factor analysis and grouping. CrownCopyright © 2013PublishedbyElsevierB.V.Allrightsreserved

Clinical research Are the Framingham and PROCAM coronary heart disease risk functions applicable to different European populations? The PRIME StudyM

Aims To assess whether the Framingham and PROCAM risk functions were applicable to men in Belfast and France. Methods and results We performed an external validation study within the PRIME (Prospective Epidemiological Study of Myocardial Infarction) cohort study. It comprised men recruited in Belfast (2399) and France (7359) who were aged 50 to 59 years, free of CHD at baseline (1991 to 1993) and followed over 5 years for CHD events (coronary death, myocardial infarction, angina pectoris). We compared the relative risks of CHD associated with the classic risk factors in PRIME with those in Framingham and PROCAM cohorts. We then compared the number of predicted and observed 5-year CHD events (calibration). Finally, we estimated the ability of the risk functions to separate high risk from low risk subjects (discrimination). The relative risk of CHD calculated for the various factors in the PRIME population were not statistically different from those published in the Framingham and PROCAM risk functions. The number of CHD events predicted by these risk functions however clearly overestimated those observed in Belfast and France. The two risk functions had a similar ability to separate high risk from low risk subjects in Belfast and France (c-statistic range: 0.61-0.68). Conclusion The Framingham and PROCAM risk functions should not be used to estimate the absolute CHD risk of middle-aged men in Belfast and France without any CHD history because of a clear overestimation. Specific population risk functions are needed

Systemic chemokine levels, coronary heart disease, and ischemic stroke events: The PRIME Study

OBJECTIVES: To quantify the association between systemic levels of the chemokine regulated on activation normal T-cell expressed and secreted (RANTES/CCL5), interferon-γ-inducible protein-10 (IP-10/CXCL10), monocyte chemoattractant protein-1 (MCP-1/CCL2), and eotaxin-1 (CCL11) with future coronary heart disease (CHD) and ischemic stroke events and to assess their usefulness for CHD and ischemic stroke risk prediction in the PRIME Study. METHODS: After 10 years of follow-up of 9,771 men, 2 nested case-control studies were built including 621 first CHD events and 1,242 matched controls and 95 first ischemic stroke events and 190 matched controls. Standardized hazard ratios (HRs) for each log-transformed chemokine were estimated by conditional logistic regression. RESULTS: None of the 4 chemokines were independent predictors of CHD, either with respect to stable angina or to acute coronary syndrome. Conversely, RANTES (HR = 1.70; 95% confidence interval [CI] 1.05–2.74), IP-10 (HR = 1.53; 95% CI 1.06–2.20), and eotaxin-1 (HR = 1.59; 95% CI 1.02–2.46), but not MCP-1 (HR = 0.99; 95% CI 0.68–1.46), were associated with ischemic stroke independently of traditional cardiovascular risk factors, hs-CRP, and fibrinogen. When the first 3 chemokines were included in the same multivariate model, RANTES and IP-10 remained predictive of ischemic stroke. Their addition to a traditional risk factor model predicting ischemic stroke substantially improved the C-statistic from 0.6756 to 0.7425 (p = 0.004). CONCLUSIONS: In asymptomatic men, higher systemic levels of RANTES and IP-10 are independent predictors of ischemic stroke but not of CHD events. RANTES and IP-10 may improve the accuracy of ischemic stroke risk prediction over traditional risk factors

An outbreak of cardiovascular syndromes requiring urgent medical treatment and its association with environmental factors: an ecological study

<p>Abstract</p> <p>Background</p> <p>In April 2005, syndromic surveillance based on statistical control chart methods in Sydney, Australia, signalled increasing incidence of urgent emergency department visits for cardiovascular and chest pain syndromes compared to the preceding twelve months. This paper aimed to determine whether environmental factors could have been responsible for this 'outbreak'.</p> <p>Methods</p> <p>The outcome studied was daily counts of emergency department visits for cardiovascular or chest pain syndromes that were considered immediately or imminently life threatening on arrival at hospital. The outbreak had a mean daily count of 5.7 visits sustained for eight weeks, compared with 4.0 in the same months in previous years. Poisson regression was used to systematically assess the emergency department visits in relation to available daily weather and pollution variables by first finding the best model that explained short-term variation in the outcome over the period 25 January 2002 to 31 May 2005, and then assessing interactions of all available variables with the 'outbreak' period, April-May 2005. Rate ratios were estimated for an interquartile increase in each variable meaning that the ratio measures the relative increase (or decrease) in the emergency department visits for an interquartile increase in the weather or pollution variable. The rate ratios for the outbreak period measure the relative increase (or decrease) in the emergency department visits for an interquartile increase in the weather or pollution variable during the outbreak period only.</p> <p>Results</p> <p>The best fitting model over the whole study period included minimum temperature with a rate ratio (RR) of 0.86 (95% confidence interval (CI), 0.77–0.96), maximum relative humidity of 1.09 (95% CI 1.05–1.14) and minimum daily particulate matter less than 10 microns (PM₁₀) of 1.05 (95% CI, 1.01–1.09). During the outbreak period, maximum temperature (RR 1.27, 95% CI 1.03–1.57), solar radiation (RR 1.44, 95% CI, 1.00–2.07) and ozone (RR 1.13, 95% CI 1.01–1.26) were associated with the outcome.</p> <p>Conclusion</p> <p>The increase may have been associated with photochemical pollution. Syndromic surveillance can identify outbreaks of non-communicable diseases associated with environmental factors.</p