pubmed-article:16046222 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16046222 | lifeskim:mentions | umls-concept:C0032105 | lld:lifeskim |
pubmed-article:16046222 | lifeskim:mentions | umls-concept:C0010068 | lld:lifeskim |
pubmed-article:16046222 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:16046222 | lifeskim:mentions | umls-concept:C0071973 | lld:lifeskim |
pubmed-article:16046222 | lifeskim:mentions | umls-concept:C2603343 | lld:lifeskim |
pubmed-article:16046222 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:16046222 | pubmed:dateCreated | 2006-3-6 | lld:pubmed |
pubmed-article:16046222 | pubmed:abstractText | The pathogenesis of ischemic coronary events involves degradation of the extracellular matrix in atherosclerotic lesions. The cysteine protease inhibitor cystatin-C may be involved in this phenomenon. The association of plasma cystatin-C with the incidence of myocardial infarction-coronary death and angina, was examined in a nested case-control (two controls per case) design within the prospective cohort study (Prospective Epidemiological Study of Myocardial Infarction (PRIME Study)) which included 9,758 men aged 50-59 years who were free of coronary heart disease (CHD) on entry and followed for a 5-year period. Three hundred and thirteen participants suffered myocardial infarction or coronary death (n = 159) or angina pectoris (n = 154) during follow-up. Cystatin-C was positively correlated with body mass index (BMI), low-density lipoprotein (LDL)-cholesterol, triglycerides and several inflammatory markers such as fibrinogen (r = 0.18), C-reactive protein (CRP) (r = 0.24), interleukin-6 (= 0.20), tumor necrosis factor-alpha (TNFalpha) (r = 0.27) and two TNFalpha receptors: TNFR1A (r = 0.43) and TNFR1B (r = 0.41); and negatively with high-density lipoprotein (HDL)-cholesterol (r = -0.25). After adjustment for traditional risk factors (age, diabetes, smoking, hypertension, BMI, triglycerides, LDL- and HDL-cholesterol), cystatin-C was significantly associated with the occurrence of the first ischemic coronary event. However, this association was no longer significant when CRP was included in the analysis. A decrease in glomerular filtration rate did not explain higher cystatin-C in cases than in controls. Cystatin-C appears to participate in the inflammatory phenomenon observed in the atherosclerotic process. Cystatin-C is not a more predictive risk marker of CHD than CRP or interleukin-6, but could be useful in detecting moderate chronic renal disease. | lld:pubmed |
pubmed-article:16046222 | pubmed:language | eng | lld:pubmed |
pubmed-article:16046222 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16046222 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16046222 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16046222 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16046222 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16046222 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:16046222 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16046222 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16046222 | pubmed:month | Apr | lld:pubmed |
pubmed-article:16046222 | pubmed:issn | 0021-9150 | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:PRIME Study... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:Juhan-VagueIr... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:EvansAlunA | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:ArveilerDomin... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:LucGéraldG | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:AmouyelPhilip... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:FruchartJean-... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:FerrieresJean... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:BardJean-Mari... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:DucimetierePi... | lld:pubmed |
pubmed-article:16046222 | pubmed:author | pubmed-author:LesueurCéline... | lld:pubmed |
pubmed-article:16046222 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16046222 | pubmed:volume | 185 | lld:pubmed |
pubmed-article:16046222 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16046222 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16046222 | pubmed:pagination | 375-80 | lld:pubmed |
pubmed-article:16046222 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:16046222 | pubmed:meshHeading | pubmed-meshheading:16046222... | lld:pubmed |
pubmed-article:16046222 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16046222 | pubmed:articleTitle | Plasma cystatin-C and development of coronary heart disease: The PRIME Study. | lld:pubmed |
pubmed-article:16046222 | pubmed:affiliation | Department of Atherosclerosis, SERLIA-INSERM UR545, Institut Pasteur de Lille, 1, rue du Professeur Calmette, 59019 Lille Cedex, France and University Lille II, France. Gerald.Luc@pasteur-lille.fr | lld:pubmed |
pubmed-article:16046222 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16046222 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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