Association entre les paramètres du stress oxydatif et les marqueurs de l’inflammation selon la gravité du syndrome coronaire aigu
Mots-clés :
ox-LDL, omocysteine, CRPus, MDA, Syndrome coronaire aigu, gravitéRésumé
Prérequis : La maladie cardiovasculaire est la conséquence de l’apparition et du développement des lésions d’athérosclérose accompagnée d’une participation inflammatoire.
But : Rechercher une association entre les marqueurs de l’inflammation et du stress oxydant et l’incidence de la maladie coronaire.
Méthodes : Etude ayant concerné 93 sujets coronariens répartis en angor instable (AI ; n=42) ; angor stable (AS ; n=15) et infarctus de myocarde (IDM ; n=36) et 140 sujets témoins chez qui les paramètres lipidiques, oxydatifs et inflammatoires ont été déterminés.
Résultats : Une hyperhomocystéinemie modérée a été observée chez les coronariens, ainsi qu’une augmentation significative de la concentration plasmatique des LDL oxydées (ox-LDL) a (p<0.001).
Une corrélation positive a été trouvée entre les marqueurs de l’inflammation et la gravité du syndrome coronaire aigu. On note une augmentation significative du taux des ox-LDL et de la CRP ultra sensibles chez les IDM par rapports aux groupes AI et AS (p=0.00, et p=0.001 respectivement), qui est associée à une élévation de l’homocystéinemie.
Conclusion : Cette étude suggère une association entre les marqueurs de l’inflammation et les paramètres oxydatifs dans le syndrome coronaire aigu.
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Références
Braunwald E. Cardiovascular medicine at the turn of the millenium: triumphs, concerns, and opportunities. N Eng J Med 1997; 337 :1360-9.
Quilici J, Gallo R. Physiopathologie des syndromes coronariens aigus. Ann Cardiol Angéiol 1999; 48 :611-23.
Steinberg D. lipoprotein and the pathogenesis of atherosclerosis. Circulation 1987; 76 :508-14.
Young I. S, McEneny J. Lipoprotein oxidation and atherosclerosis. Biochemical Society Transactions 2001; 29 :358- 62.
P. Duriez. Mécanismes de formation de la plaque d'athérome. Rev Med Interne 2004; 25 :S3-S6.
Brattström L, Wilcken D.E.L. Homocysteine and cardiovascular disease: cause or effect? Am J Clin Nutr 2000; 72:315-23.
Li H, Cybulsky MI, Gimbrone MA Jr, Libby P. An atherogenic diet rapidly induces VCAM-1, a cytokine-regulatable mononuclear leukocyte adhesion molecule, in rabbit aortic endothelium. Arterioscler Thromb 1993; 13 :197-204.
Hansson GK. Immune mechanisms in atherosclerosis. Arterioscler Thromb Vasc Biol 2001; 21: 1876-90.
Engler R. Protéine de la réaction inflammatoire. Ann Biol Clin 1988; 46 :336-42.
Smaoui M, Hammami S, Chaaba R et al. Lipids and lipoprotein (a) concentration in Tunisian Type 2 diabetic patients relationship to glycaemic control and coronary heart disease. J Diabetes Complications 2004; 18 : 258-63.
Koubaa N, Nakbi A, Smaoui M, et al. Hyperhomocysteinemia and elevated ox-LDL in Tunisian type 2 diabetic patients: role of genetic and dietary factors. Clin Biochem. 2007; 40: 1007-14.
Ehara S, Ueda M, Naruko T, et al. Elevated levels of low-density lipoprotein show a positive relationship with the severity of acute coronary syndromes. Circulation 2001; 103 :1955-60
Bassuk SS, Rifai N, Ridker PM. High-sensitivity C-reactive protein: Clinical importance. Curr Probl Cardiol 2004; 29: 439- 93.
Ben Romthane H, Bougatef S, Skiri H, et al. The first tunisian cardiovascular diseases register: process and results. Rev Epidemiol Sante publique 2004; 52: 558-64.
Uusitupa MI, Niskanen LK, Siitonen O, Voutilainen E, Pyorala K. 5-year incidence of atherosclerotic vasculmar disease in relation to general risk factors, insulin level, and abnormalities in lipoprotein composition in non insulin-dependant diabetic and non diabetic subjects. Circulation 1990; 82: 27-36.
Ginon I, André-Fouet X. Hyperlipidémies et risque cardiovasculaire. Encycl Med Chir. Endocrinologie -Nutrition 2000; 10-368-H10 :1-9.
Stamler J, Wentworth DN, Neaton JD, for the MRFIT group. Is relationship between serum cholesterol and risk of premature death from coroary heart disease continous and graded? Findings in 356 222 primary screenees of the MRFIT. JAMA 1986; 256: 2823-28.
Castelli WP, Garrison RJ, Wilson PW, Abbott RD, Kalousdian S, Kannel WB. Incidenceof coronary heart disease and lipoprotein cholesterol levels. The Framingham study. Jama 1986; 256 :2835-38.
Castelli WP. The new pathophysiology of coronary artery disease .Am j Cardiol 1998; 82 :60T-65T.
Hoogeveen EK, Kostense PJ, Beks PJ, et al. Hyperhomocysteinaemia is associated with an increased risk of cardiovascular disease, especially in non-insulin-dependent diabetes mellitus: a population-based study. Arterioscler Thromb Vasc Biol 1998; 18 :133-8
Baydas G, Reiter RJ, Akbulut M, Tuzcu M, Tamer S. Melatonin inhbits neural apoptosis induced by homocysteine in hippocampus of rats via inhibition of cytochrome c translocation and caspase-3 activation and by regulating pro- ad anti-apoptotic protein levels. Neuroscience 2005; 135: 879-86.
Tyagi N, Moshal KS, Ovechkin AV, et al. Mitochondrial mechanism of oxidative stresss and systemic hypertension in hyperhomocystéinemie. J Cell Biochem 2005; 96:665-71.
Stamler J.S., Osborne J.A., Jaraki O, et al. Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen. J Clin Invest 1993; 91:308-18.
Shoichi Ehara, Makiko Ueda, Takahiko Naruko, et al. Elevated Levels of Oxidized Low Density Lipoprotein Show a Positive Relationship With the Severity of Acute Coronary Syndromes. Circulation 2001; 103:1955-60.
Koubaa N., Nakbi A., Smaoui M. Impact des habitudes de type2 originaires du Sud et du Sahel. RMEDR 2007; 12 :161-259.
Kasdallah-Grissa A., Nakbi A, Koubaa N., et al. Supplementation of virgin olive oil reduces oxidative damage in the livers of rats treated with ethanol. Nutr Res 2008; 28 : 472- 79.
Lecarpentier Y, Coirault C, Chenk D. Régulation cellulaire et moléculaire de la contraction cardiaque. Médecine thérapeutique 1996; 2 :301-10.
Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002; 105 :1135-43.
Ridker PM. High sensitivity C reactiv protein: potentiel adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 2001; 103:1813-18.
Sirol M., Bouzamondo A., Sanchez P, Lechat P. Les satines préviennent-elles le risque d'accident vasculaire cérébral? Ann Med Interne 2001; 152 :188-93.
Ridker PM, Rifai N, Clearfield M, et al., Measurement of Creactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. N Engl J M 2001; 344: 2016-2018.
Kwak B., Mulhaupt F., Mytt S.and Mach F. Statins as a newly recognized type of immunomodulator. Nat M 2000; 6:1399-1402.
Biasucci LM, Liuzzo G, Grillo RL, et al. Elevated levels of Creactive protein of discharge in patients with unstable angina predict recurrent instability.Circulation 1999; 99: 855-60.
Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med 1994; 331 :417-24.
Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. JAMA 2001; 285: 2481-5.