2008, Number 09-10
<< Back Next >>
Medicina & Laboratorio 2008; 14 (09-10)
Proteína C reactiva ultrasensible (PCR-us) como marcador de riesgo de enfermedad cardiovascular
Domínguez-Amorocho O, Patiño-Cuervo D
Language: Spanish
References: 58
Page: 457-478
PDF size: 789.01 Kb.
ABSTRACT
The importance of classical risk factors for cardiovascular disease has been demonstrated; however, new risk factors, called emergent risk factors, that optimize the management and detection of cardiovascular risks and as a consequence benefit the population with more efficient preventive programs, have been identified. In order to improve the prediction of cardiovascular risk, the scientific community has centered its interest in the determination of high sensitivity C-reactive protein (hs-CRP) as an inflammation marker, since different epidemiologic prospective studies have demonstrated its usefulness in the prediction of some cardiovascular diseases such as myocardial infarct, stroke and peripheral vascular disease. Additionally, during the past few years, many researchers have showed the participation of different cells and molecules of the immune response as mediators of vascular lesion related to atherosclerosis. The C-reactive protein is an acute phase protein that has classically been considered as an inflammation marker. Under normal conditions, its hepatic synthesis is less than 1 mg/L which is increased if the person undergoes any infectious or inflammation process. This elevation can be as high as 100 times the normal level during the first 24 to 48 hours and remains for a few days. It has been demonstrated that the hs-CRP can provide information on each of the cardiovascular risk levels according to Framingham scale; hs-CRP levels lower than 1 mg/L, between 1 and 3 mg/L and higher than 3 mg/L, correspond to low, medium and high cardiovascular risk, respectively. The predictive value of hs-CRP is increased when it is evaluated in association with the lipid profile and the appropriated correlation is done.
REFERENCES
Rifai N, Ridker PM. High-sensitivity C-reactive protein: a novel and promising marker of coronary heart disease. Clin Chem 2001; 47: 403-411.
Vane JR, Anggard EE, Botting RM. Regulatory functions of the vascular endothelium. N Engl J Med 1990; 323: 27-36.
Prasad K. C-reactive protein and cardiovascular diseases. Int J Angiol 2003; 12: 1-12.
Wilson PW, D‘Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation 1998; 97: 1837-1847.
Lopez EP, Rice C, Weddle DO, Rahill GJ. The relationship among cardiovascular risk factors, diet patterns, alcohol consumption, and ethnicity among women aged 50 years and older. J Am Diet Assoc 2008; 108: 248-256.
Jarvis CM, Hayman LL, Braun LT, Schwertz DW, Ferrans CE, Piano MR. Cardiovascular risk factors and metabolic syndrome in alcohol- and nicotinedependent men and women. J Cardiovasc Nurs 2007; 22: 429-435.
McCluskey S, Baker D, Percy D, Lewis P, Middleton E. Reductions in cardiovascular risk in association with population screening: a 10-year longitudinal study. J Public Health (Oxf) 2007; 29: 379-387.
Ferns GA. New and emerging risk factors for CVD. Proc Nutr Soc 2008; 67: 223-231.
Stanner S. Cardiovascular disease: Diet, nutrition and emerging risk factors. British Nutrition Foundation 2005; 1 edición, 380 págs.
Murray C, López A. Quantifying the burden of disease and injury attributable to ten major risk factors. In The global burden of disease, eds. CJL Murray & AD López, Vol I. Cambridge: Harvard University Press.1996; 295-324
Poulter N. Global risk of cardiovascular disease. Heart 2003; 89 Suppl 2: ii2-5; discussion ii35-37.
Fernández-Mora T, Patiño-Cuervo D. La inflamación como factor causal emergente de la ECV. Universitas Scientiarium 2007; 12: 15-33.
Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO, 3rd, Criqui M, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499-511.
O’Brien KD, Chait A. Serum amyloid A: the “other” inflammatory protein. Curr Atheroscler Rep 2006; 8: 62-68.
Davidson MH, Corson MA, Alberts MJ, Anderson JL, Gorelick PB, Jones PH, et al. Consensus panel recommendation for incorporating lipoprotein- associated phospholipase A2 testing into cardiovascular disease risk assessment guidelines. Am J Cardiol 2008; 101: 51F-57F.
Bonn D. Plaque detection: the key to tackling atherosclerosis? Lancet 1999; 354: 656.
Baumgart D, Schmermund A, Goerge G, Haude M, Ge J, Adamzik M, et al. Comparison of electron beam computed tomography with intracoronary ultrasound and coronary angiography for detection of coronary atherosclerosis. J Am Coll Cardiol 1997; 30: 57-64.
Tillett W, Francis T. Serological reactions in pneumonia with non-protein somatic fraction of pneumococcus. J Exp Med 1930; 52: 561-571.
Hurlimann J, Thorbecke GJ, Hochwald GM. The liver as the site of C-reactive protein formation. J Exp Med 1966; 123: 365-378.
Pepys MB, Hirschfield GM. C-reactive protein: a critical update. J Clin Invest 2003; 111: 1805-1812.
Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. Jama 2001; 286: 327-334.
Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336: 973-979.
Rifai N, Tracy RP, Ridker PM. Clinical efficacy of an automated high-sensitivity C-reactive protein assay. Clin Chem 1999; 45: 2136-2141.
Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 2001; 103: 1813-1818.
Du Clos TW. Function of C-reactive protein. Ann Med 2000; 32: 274-278.
Bhakdi S, Torzewski M, Klouche M, Hemmes M. Complement and atherogenesis: binding of CRP to degraded, nonoxidized LDL enhances complement activation. Arterioscler Thromb Vasc Biol 1999; 19: 2348-2354.
Kindmark CO. Stimulating effect of C-reactive protein on phagocytosis of various species of pathogenic bacteria. Clin Exp Immunol 1971; 8: 941-948.
Frazier L. Novel predictors of acute coronary syndrome outcomes. Biol Res Nurs 2003; 5: 30-36.
Postadzhiyan AS, Tzontcheva AV, Kehayov I, Finkov B. Circulating soluble adhesion molecules ICAM-1 and VCAM-1 and their association with clinical outcome, troponin T and C-reactive protein in patients with acute coronary syndromes. Clin Biochem 2008; 41: 126-133.
Boguslawski G, Labarrere C. The rol of C-reactive protein as a cardiovascular risk predictor. Kardiochirurgia i Torakochirurgia Polska 2006; 3: 16-28.
Ferri C, Croce G, Cofini V, De Berardinis G, Grassi D, Casale R, et al. C-reactive protein: interaction with the vascular endothelium and possible role in human atherosclerosis. Curr Pharm Des 2007; 13: 1631-1645.
Wang J, Zhang S, Jin Y, Qin G, Yu L, Zhang J. Elevated levels of platelet-monocyte aggregates and related circulating biomarkers in patients with acute coronary syndrome. Int J Cardiol 2007; 115: 361-365.
Jialal I, Devaraj S, Venugopal SK. C-reactive protein: risk marker or mediator in atherothrombosis? Hypertension 2004; 44: 6-11.
Pinon P, Kaski JC. [Inflammation, atherosclerosis and cardiovascular disease risk: PAPP-A, Lp-PLA2 and cystatin C. New insights or redundant information?]. Rev Esp Cardiol 2006; 59: 247-258.
Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation 2000; 102: 2165-2168.
Venugopal SK, Devaraj S, Yuhanna I, Shaul P, Jialal I. Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation 2002; 106: 1439-1441.
Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002; 105: 1135- 1143.
Ramzy D, Rao V, Tumiati LC, Xu N, Sheshgiri R, Jackman J, et al. Endothelin-1 accentuates the proatherosclerotic effects associated with C-reactive protein. J Thorac Cardiovasc Surg 2007; 133: 1137-1146.
Labarrere CA, Lee JB, Nelson DR, Al-Hassani M, Miller SJ, Pitts DE. C-reactive protein, arterial endothelial activation, and development of transplant coronary artery disease: a prospective study. Lancet 2002; 360: 1462-1467.
Calabro P, Willerson JT, Yeh ET. Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation 2003; 108: 1930-1932.
Singh U, Devaraj S, Vasquez-Vivar J, Jialal I. Creactive protein decreases endothelial nitric oxide synthase activity via uncoupling. J Mol Cell Cardiol 2007; 43: 780-791.
Di Napoli M, Papa F. Inflammation, blood pressure, and stroke: an opportunity to target primary prevention? Curr Hypertens Rep 2005; 7: 44-51.
Ballou SP, Lozanski G. Induction of inflammatory cytokine release from cultured human monocytes by C-reactive protein. Cytokine 1992; 4: 361- 368.
Woollard KJ, Phillips DC, Griffiths HR. Direct modulatory effect of C-reactive protein on primary human monocyte adhesion to human endothelial cells. Clin Exp Immunol 2002; 130: 256-262.
Williams TN, Zhang CX, Game BA, He L, Huang Y. C-reactive protein stimulates MMP-1 expression in U937 histiocytes through Fc[gamma]RII and extracellular signal-regulated kinase pathway:: an implication of CRP involvement in plaque destabilization. Arterioscler Thromb Vasc Biol 2004; 24: 61-66.
Chang MK, Binder CJ, Torzewski M, Witztum JL. C-reactive protein binds to both oxidized LDL and apoptotic cells through recognition of a common ligand: Phosphorylcholine of oxidized phospholipids. Proc Natl Acad Sci U S A 2002; 99: 13043-13048.
Zwaka TP, Hombach V, Torzewski J. C-reactive protein-mediated low density lipoprotein uptake by macrophages: implications for atherosclerosis. Circulation 2001; 103: 1194-1197.
Kobayashi S, Inoue N, Ohashi Y, Terashima M, Matsui K, Mori T, et al. Interaction of oxidative stress and inflammatory response in coronary plaque instability: important role of C-reactive protein. Arterioscler Thromb Vasc Biol 2003; 23: 1398-1404.
Ji SR, Wu Y, Zhu L, Potempa LA, Sheng FL, Lu W, et al. Cell membranes and liposomes dissociate Creactive protein (CRP) to form a new, biologically active structural intermediate: mCRP(m). Faseb J 2007; 21: 284-294.
Biasucci LM, Colizzi C, Rizzello V, Vitrella G, Crea F, Liuzzo G. Role of inflammation in the pathogenesis of unstable coronary artery diseases. Scand J Clin Lab Invest Suppl 1999; 230: 12-22.
Haverkate F, Thompson SG, Pyke SD, Gallimore JR, Pepys MB. Production of C-reactive protein and risk of coronary events in stable and unstable angina. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Lancet 1997; 349: 462-466.
Ridker PM, Rifai N, Pfeffer MA, Sacks FM, Moye LA, Goldman S, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation 1998; 98: 839-844.
Kuller LH, Tracy RP, Shaten J, Meilahn EN. Relation of C-reactive protein and coronary heart disease in the MRFIT nested case-control study. Multiple Risk Factor Intervention Trial. Am J Epidemiol 1996; 144: 537-547.
Tracy RP, Lemaitre RN, Psaty BM, Ives DG, Evans RW, Cushman M, et al. Relationship of C-reactive protein to risk of cardiovascular disease in the elderly. Results from the Cardiovascular Health Study and the Rural Health Promotion Project. Arterioscler Thromb Vasc Biol 1997; 17: 1121-1127.
Eda S, Kaufmann J, Roos W, Pohl S. Development of a new microparticle-enhanced turbidimetric assay for C-reactive protein with superior features in analytical sensitivity and dynamic range. J Clin Lab Anal 1998; 12: 137-144.
Wood WG, Ludemann J, Mitusch R, Heinrich J, Maass R, Frick U. Evaluation of a sensitive immunoluminometric assay for the determination of Creactive protein (CRP) in serum and plasma and the establishment of reference ranges for different groups of subjects. Clin Lab 2000; 46: 131-140.
Albert MA, Glynn RJ, Ridker PM. Plasma concentration of C-reactive protein and the calculated Framingham Coronary Heart Disease Risk Score. Circulation 2003; 108: 161-165.