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      C-Reactive Protein and Coronary Heart Disease: All Said—Is Not It?

      1 , * , 2

      Mediators of Inflammation

      Hindawi Publishing Corporation

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          Abstract

          C-reactive protein (CRP) and coronary heart disease (CHD) have been the subject of intensive investigations over the last decades. Epidemiological studies have shown an association between moderately elevated CRP levels and incident CHD whereas genetic studies have shown that polymorphisms associated with elevated CRP levels do not increase the risk of ischemic vascular disease, suggesting that CRP might be a bystander rather than a causal factor in the progress of atherosclerosis. Beside all those epidemiological and genetic studies, the experimental investigations also try to reveal the role of CRP in the progress of atherosclerosis. This review will highlight the complex results of genomic, epidemiological, and experimental studies on CRP and will show why further studies investigating the relationship between CRP and atherosclerosis might be needed.

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          Most cited references 75

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          'Mendelian randomization': can genetic epidemiology contribute to understanding environmental determinants of disease?

          Associations between modifiable exposures and disease seen in observational epidemiology are sometimes confounded and thus misleading, despite our best efforts to improve the design and analysis of studies. Mendelian randomization-the random assortment of genes from parents to offspring that occurs during gamete formation and conception-provides one method for assessing the causal nature of some environmental exposures. The association between a disease and a polymorphism that mimics the biological link between a proposed exposure and disease is not generally susceptible to the reverse causation or confounding that may distort interpretations of conventional observational studies. Several examples where the phenotypic effects of polymorphisms are well documented provide encouraging evidence of the explanatory power of Mendelian randomization and are described. The limitations of the approach include confounding by polymorphisms in linkage disequilibrium with the polymorphism under study, that polymorphisms may have several phenotypic effects associated with disease, the lack of suitable polymorphisms for studying modifiable exposures of interest, and canalization-the buffering of the effects of genetic variation during development. Nevertheless, Mendelian randomization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to understanding and preventing the adverse effects on human health of modifiable exposures.
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            C-reactive protein: a critical update.

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              Development and validation of improved algorithms for the assessment of global cardiovascular risk in women: the Reynolds Risk Score.

              Despite improved understanding of atherothrombosis, cardiovascular prediction algorithms for women have largely relied on traditional risk factors. To develop and validate cardiovascular risk algorithms for women based on a large panel of traditional and novel risk factors. Thirty-five factors were assessed among 24 558 initially healthy US women 45 years or older who were followed up for a median of 10.2 years (through March 2004) for incident cardiovascular events (an adjudicated composite of myocardial infarction, ischemic stroke, coronary revascularization, and cardiovascular death). We used data among a random two thirds (derivation cohort, n = 16 400) to develop new risk algorithms that were then tested to compare observed and predicted outcomes in the remaining one third of women (validation cohort, n = 8158). Minimization of the Bayes Information Criterion was used in the derivation cohort to develop the best-fitting parsimonious prediction models. In the validation cohort, we compared predicted vs actual 10-year cardiovascular event rates when the new algorithms were compared with models based on covariates included in the Adult Treatment Panel III risk score. In the derivation cohort, a best-fitting model (model A) and a clinically simplified model (model B, the Reynolds Risk Score) had lower Bayes Information Criterion scores than models based on covariates used in Adult Treatment Panel III. In the validation cohort, all measures of fit, discrimination, and calibration were improved when either model A or B was used. For example, among participants without diabetes with estimated 10-year risks according to the Adult Treatment Panel III of 5% to less than 10% (n = 603) or 10% to less than 20% (n = 156), model A reclassified 379 (50%) into higher- or lower-risk categories that in each instance more accurately matched actual event rates. Similar effects were achieved for clinically simplified model B limited to age, systolic blood pressure, hemoglobin A(1c) if diabetic, smoking, total and high-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and parental history of myocardial infarction before age 60 years. Neither new algorithm provided substantive information about women at very low risk based on the published Adult Treatment Panel III score. We developed, validated, and demonstrated highly improved accuracy of 2 clinical algorithms for global cardiovascular risk prediction that reclassified 40% to 50% of women at intermediate risk into higher- or lower-risk categories.
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                Author and article information

                Journal
                Mediators Inflamm
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi Publishing Corporation
                0962-9351
                1466-1861
                2014
                7 April 2014
                : 2014
                Affiliations
                1Medizinische Klinik II, Universitätsklinikum Schleswig-Holstein, UKSH Campus Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany
                2Klinik für Herz- und Kreislauferkrankungen, Deutsches Herzzentrum München, Technische Universität München, Lazarettstraße 36, 80636 München, Germany
                Author notes

                Academic Editor: Jan Torzewski

                Article
                10.1155/2014/757123
                3997990
                24808639
                Copyright © 2014 F. Strang and H. Schunkert.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Review Article

                Immunology

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