Ten serwis zostanie wyłączony 2025-02-11.
Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl

PL EN


Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników
2011 | 20 | 6 |
Tytuł artykułu

Common genetic polymorphisms and environmental risk factors in polish patients with angiographically documented coronary artery disease

Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
It has been suggested that the G894T NOS3, C677T MTHFR, A(-455)G FBB, and C(-1562)T MMP-9genetic polymorphisms were implicated in the pathogenesis of CAD. We assessed their prevalence among CAD and controls. A total of 180 individuals with angiographically documented CAD (138 males and 42 females, age range 37-84 years) were recruited into the study. 133 patients with ≥50% occlusion of the coronary artery lumen in angiography comprised the CAD group, a subgroup of 45 patients with one vessel occlusion as CAD1, 88 patients with multivessel occlusion as CAD2+3 and the control group consisted of 47 subjects without changes in coronary arteries. Risk factors (gender, BMI, smoking, diabetes mellitus, hypertension, lipid profile) were considered for all participants. Genotype analysis was assessed by PCR-RFLP. A logistic regression analysis with CAD and CAD severity (CAD2+3 vs. CAD1) as dependent variables was performed to estimate the age, gender, and cardiovascular risk factors (age, gender, BMI, smoking, hypertension) adjusting odds ratios for the genotypes. None of the polymorphisms studied were shown to be independently associated with an increased risk of CAD or multivessel CAD disease, in any mode of inheritance. A highly increased risk (OR 9.59) of the predisposition to advanced CAD, although only marginally significant, was observed in TT MMP-9 homozygotes. Our results suggest a lack of association between G894T NOS3, A(-455)G FBB, C677T MTHFR, or C(-1562)T MMP-9 genetic variants and CAD in Polish patients. Although a higher prevalence of classical risk factor was observed in our CAD patients.
Słowa kluczowe
Wydawca
-
Rocznik
Tom
20
Numer
6
Opis fizyczny
p.1491-1499,ref.
Twórcy
autor
  • Department of Cardiology, Pomeranian Medical University
autor
  • Department of Clinical and Molecular Biochemistry, Pomeranian Medical University,
  • Department of Clinical and Molecular Biochemistry, Pomeranian Medical University,
  • Department of Cardiosurgery, Pomeranian Medical University, Powstańców Wlkp. 72, 70-111 Szczecin, Poland
  • Department of Cardiology, Pomeranian Medical University
autor
  • Department of Clinical and Molecular Biochemistry, Pomeranian Medical University,
  • Department of Clinical and Molecular Biochemistry, Pomeranian Medical University,
Bibliografia
  • 1. DILLLON G.A., VITA J.A. Nitric oxide and endothelial function. In: Losxalzo J., Vita J.A., Eds. Nitric oxide and the cardiovascular system. Totowa, NJ: Human Press, pp. 207-26, 2000.
  • 2. NATHAN C., XIE Q-W. Nitric oxide syntheses: roles, tolls and controls. Cell, 78, 915, 1994.
  • 3. LLOYD-JONE D.M., BLOCH K.D. The vascular biology of nitric oxide and its role in atherogenesis. Annu. Rev. Med. 47, 365, 1996.
  • 4. WEVER R.M.F., LUSCHER T.F., COSENTINO F., RABELINK T.J. Atherosclerosis and the two faces of endothelial nitric oxide synthase. Circulation, 97, 108, 1998.
  • 5. IGNARRO L.J. Biosythesis and metabolism of endothelium-derived nitric oxide. Annu. Rev. Pharmacol. Toxicol., 30, 535, 1990.
  • 6. HIGNORANI A.D., LIANG C.F., FATIBENE J., LYON A., MONTHEITH S., PARSONS A., HAYDOC S., HOPPER R.V., STEPHENS N.G., O'SHAUGHNESSY K.M., BROWN M.J. A common variant of the endothelial nitric oxide synthase (Glu298→Asp) is a major risk factor for coronary artery disease in the UK. Circulation, 100, 1515, 1999.
  • 7. YOSHIMURA M., YASUE H., NAKAYAMA M., SHIMASAKI Y.,SUMIDA H., SUGIJAMA S., KUGIJAMA K., OGAWA H., OGAWA Y., SAITO Y., MIYAMOTO Y., NAKAO K. A missens Glu 298Asp wariant In the endothelial nitric oxide synthase genes associated with coronary spasm In the Japanes. Hum. Genet. 103, 65, 1998.
  • 8. TSUJITA Y., BABA S., YAMAUCHI R., MANNAMI T., KINOSHITA M., YAMAMOTO R., KATSUYA T., HIGAKI J., OGIHARA T., OGATA J., IWAI N. Assotiation analysed between genetic polymorphism of endothelial nitric oxide synthase gene and hypertension In Japanese: The Suita Study. J. Hypertens., 19, 1941, 2001.
  • 9. WALD D.S., LAW M., MORRIS J.K. Homocysteine and cardiovascular disease: evidence on causality from a meta–analysis. BMJ 325, 1202, 2002.
  • 10. DUNN J., TITLE L.M., BATA I., JOHNSTONE D.E., KIRKLAND S.A., O'NEIILL B.J., ZAYED E., MAC DONALD M.C., DEMPSY G., NASSAR B. Realtion of a common mutation in methylene hydrofolate reductase to plasma homocysteine and early onset coronary artery disease. Clin Biochem; 31, 95, 1998.
  • 11. GARDEMANN A., WEIDEMANN H., PHILLIPP M., KATZ N., TILLMANS H., HEHREILN F.W., HABERBOSCH W. The TT genotype of the methylenetetrahydrofolate reductase C677T gene polymorphism is associated with the extent of coronary atherosclerosis in patients at high risk for coronary artery disease. Eur. Heart J., 8, 584, 1999.
  • 12. MUKHERJEE M., JOSH S., BAGADI S., DALVI M., RAO A., SHETTY K.R. A low prelevelans of the C677T mutation in the methylenetetrahydrofolate reductase gene in Asian Indians. Clin. Genet. 61, 155, 2002.
  • 13. BRUGADA R., MARIAN A.J. A common mutation in methylenetetrahydrofolate reductase gene is not major risk of coronary disease or myocardial infarction. Atherosclerosis, 128, 107, 1997.
  • 14. DUPPERAY A., LANGUINO L.R., PLESCIA J., MCcDOWALL A., HOOG N., CRAIG AG., BERENDT A.R., ALTIERI D.C. Molecular identification of a novel fibrinogen binding site on the first domain of ICAM-1 regulating leukocyte-endothelium bridging. J. Biol. Chem., 272, (1), 435, 1997.
  • 15. HARLEY S.L., STURGE J., POWELL J.T. Regulation by fibrinogen and its products of intercellular adhesion molecule-1 expresion in human saphenous vein endothelial cells. Arterioscl. Thromb. Vasc. Biol., 20, (3), 652, 2000.
  • 16. THOMPSON S.G., KIENAST J., PYKE S.D., HAVERKATE F., VAN DE LOO JC. Hemostatic factors and the role of myocardial infarction or sudden death in patients with angina pectoris: European Concerted Action on Trombosis and Disabilites Angina Pectoris study group. N. Engl. J. Med., 332, 635, 1995.
  • 17. RESCH K.L., ERNST E., MATRAI A., PAULSEN H.F. Fibrinogen and viscosity as risk factors for subsequent cardiovascular events in strok survivors. Ann. Intern. Med., 19, 634, 1988.
  • 18. KOSTER T., ROSENDAAL F.R., REITSMA P.H., VAN DER VELDEN P.A., BRIET E., VANDBROUCKE J.P. Factor VII and fibrinogen levels as risk factors for venous thrombosis. Thromb. Haemost, 71, 719, 1994.
  • 19. HUMPHRIES S.E., COOK M., DDUBOWITZ M., STIRLING Y., MEADE TW. Role of genetic variation at the fibrinogen locus in determination of plasma fibrinogen concentration. Lancet, 1, 1452, 1987.
  • 20. BAUMAN R.E., HENSCHEN A.H. Human fibrinogen polymorphic site analysis by restriction endonuclease digestion and allele-specific polymerase chain reaction amplification: identification of polymorphism at positon Aα312 and Bβ. Blood, 7, 2117, 1993.
  • 21. GREEN F., HAMSTEN A., BLOMBAK M., HUMPHRIS S. The role of β-fibrinogen genotype in determining plasma fibrinogen levels in young survivirs of myocardial infarction and healthy controls from Sweden. Thromb. Haemost, 70, 915, 1993.
  • 22. BEHAGUE I., POIREIR O., NICAUD V., EVANS A., ARVEILER D., LUC G., CAMBOU J., SCARABIN P., BARA L., GREEN F., CAMBIEN F. β-fibrinogen gene polymorphism are associated with plasma fibrinogen and coronary artery disease in patients with myocardial infarction: the ECTIM study. Circulation, 93, 440, 1996.
  • 23. OPDENAKKER G., VAN DEN STEEN P.E., DUBOIS B., NELISSEN I., VAN COILLIE E., MASURE S., PROOST P., VAN DAMME J. Gelatinase B functions as regulator and effector in leukocyte biology. J. Leukoc. Biol., 69, 851, 2001.
  • 24. CREEMERS E.E., ClEUTIENS J.P., SMITS J.F., DAEMEN M.J. Matrix metalloproteinase inhibition after myocardial infarction: a new approach to prevent heart failure? Circ. Res., 89, 201, 2001.
  • 25. GALIS Z.S., KHATRI J.J. Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bed, and the ugly. Circ. Res., 90, 251, 2002.
  • 26. ZHANG B., YE S., HERMAN S.M., ERIKSSON P., DE MAAT M., EVANS A., ARVEILER D., LUC G., CAMBIEN F., HHAMSTEN A., WATKINS H., HENNEY A.M. Functional polymorphism in the regulatory region of gelatinase B gene in the reletion to severity of coronary atherosclerosis. Circulation, 99, 1788, 1999.
  • 27. CHO H.J., CHAE I.H., PARK K.W., JU J.R., OH S., LEE M.M., PARK Y.B. Functional polymorphism in the promoter region of the gelatinase B gene in relation to coronary disease and restenosis after percutaneus coronary intervention. J. Hum. Genet. 47, 88, 2002.
  • 28. GHADERIAN S.M., NAJAR R.A., TABATABAEI PANAH A.S., REZAIE G., REZAEI FARIMANI A., BEIGI HARCHEGANI A., AZARGASHB E. Matrix metalloproteinase: investigation from gene to protein as effrctive factor in myocardial infarction. J. Thromb. Thrombolysis, 30, 404, 2010.
  • 29. ABILLEIRA S., BEVAN S., MARKUS H.S. The role of genetic variants of matrix metalloproteinases in coronary and carotid atherosclerosis. J. Med. Genet., 43, 897, 2006.
  • 30. ALPERT J.S., THYGESEN K. Myocardial infarction redefined – a consensus document of The Joint European Society of Cardiology/American of Cardiology Committee for the Redefinition of Myocardial Infarction. Eur. Heat J., 21, 1502, 2000.
  • 31. ZHI H., WANG H., REN L., SHI Z., PENG H., CUI L., MA G.,YE X., FENG Y., SHEN C., ZHAI X., ZHANG C., ZEN K., LIU N. Functional polymorphism of matrix metallopeptidase-9 and risk of coronary artery disease I a Chinese population. Mol. Biol. Rep., 37, 13, 2010.
  • 32. VINUKONDA G., MOHAMMAD N.S., JAIN J.M.N., CHINTAKINDI K.P., AKELLA R.R.D. Genetic environmental influences on total plasma homocysteine and coronary artery disease (CAD) risk among South Indians. Clin. Chim. Acta, 405, 127, 2009.
  • 33. ALKHARFY K.M., AL-DAGHARI N., AL-ATTAS O., ALOKAIL M.S., DRAZ H.M., HUSSAIN T. Endothelial nitric oxide synthase gene polymorphism (894G>T and 786T>C) and risk of coronary artery disease in Saudi Population. Archives of Medical Research, 41, 134, 2010.
  • 34. MAAT MONIEK P.M., KASTELEIN J.P., JUKEMA J. W., ZWINDERMAN A. H., JANSEN H., GROENEMEIER B., BRUSHKE A.V.G., KLUFT C. On behalf of the REGRESS Group. -455 G/A polymorphism of the β-fibrinogen Gene is Associated With the Progression of Coronary Atherosclerosis in Symptomatic Men. Arterioscler Thromb. Vasc. Biol., 18, 265, 1998.
  • 35. FATTINI C., SOFI F., STICCHI E., GENSINI F., GORI A.M., FEDI S., LAPINI I., ROSTAGNO C., COMEGLIO M., BROGI D., GENSINI G., ABBATE R. Influence of endothelial nitric oxide synthase gene polymorphism (G894T, 4a4b, T-786C) and hyperhomocysteinemia on the predisposition to acute coronary syndromes. Am. Heart J. 147, 516, 2004.
  • 36. KIM I.J., BAE J., LIM S.W., CHA D.H., CHO H.J., KIM S., YANG D.H., HWANG S.G., OH D., KIM N.K. Influence of endothelial nitric oxide synthase gene polymorphism (-786>C, 4a4b, 894G>T) in Korean patients with coronary artery disease. Thromb. Res., 119, 579, 2007.
  • 37. CAM S.F., SEKURI C., TENGIZ I., ERKAN E., SAGCAN A., AKIN M., BERDELI A. The G894T polymorphism on endothelial nitric oxide synthase gene is associated with premature coronary artery disease in the Turkish population. Thromb. Res., 116, 287, 2005.
  • 38. LI J., WU X., LI X., FENG G., HE L., SHI Y. The endothelial nitric oxide synthase gene is associated with coronary artery disease: a meta-analysis. Cardiology, 116, 271, 2010.
  • 39. WANG S.L., SIM A.S., BADENHOP R.F., MCCREDIE R.M., WILCKEN D.E. A smoking-dependent risk of coronary artery disease associated with a polymorphism of the endothelial nitric oxide synthase gene. Nat. Med. 2, 41, 1996.
  • 40. RAGIA G., NIKOLAIDIS E., TAVIRDOU A., ARVANITIDIS K.L., KANONI S., DEDOUSSIS G.V., BOUGIOUKAS G., MANAOLOPOULOS V.G. Endothelial nitric oxide synthase gene polymorphism -786T>C and 894 G>T in coronary artery bypass graft surgery patients. Hum. Genomics 4, 375, 2010.
  • 41. MORA S., COOK N., BURING J.E., RIDKER P.M., LEE I.M. Physical activity and reduced risk of cardiovascular events: potential mediating mechanisms. Circulation 116, 2110, 2007.
  • 42. ANTONIADES Ch., SHIRODARIA Ch., LEESON P., BAARHOLM O.A., VAN-ASSCHE T., CUNNINGTON C., PILLAI R., RATNANUNGA Ch., TOUSOULIS D., STEFANADIS C., REFSUM H., CHANNON KM. MTHFR 677C>T polymorphism reveals functional importance for 5-Methyltetrahydrofolate, not homocysteine in regulation of vascular redox state and endothelial function in human atherosclerosis. Circulation, 119, 2507, 2009.
  • 43. SHIRIDARIA C., ANTHONIADES C., LEE J., JACKSON C.E., ROBSON M.D., FRANCIS J.M., MOAT S.J., RATNANUNGA C., PILLAI R., REFSUM H., NEUBAUER S., CHANNON KM. Global improvement of vascular function and redox state with low-dose folic acid: implication for folate therapy in patients with coronary artery disease. Circulation, 115, 2262, 2007.
  • 44. BRUNNER S., KIM J.O., METHE H. Relation of matrix metalloproteinase -9/tissue inhibitor of metalloproteinase-1 ratio in peripherial circulating CD14+ monocytes to progression of coronary artery disease. Am. J. Cardiol. 105, 429, 2010.
  • 45. GHADERIAN S.M., AKBARZADEH NAJAR R., TABATABAEI PANAH A.S. Genetic polymorphism and plasma levels of matrix metalloproteinases and their relationships with developing acute myocardial infarction. Coron. Artery Dis. 21, 330, 2010.
  • 46. HUNTER D.J. Gene-enviroment interactions in human disease. Nat. Rev. Genet., 6, 287, 2005.
  • 47. SYME S.L., MARMOT M.G., KAGAN A., KATO H., RHOADS G. Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: introduction. Am. J. Epidemiol. 102, 477, 1975.
  • 48. MENOTTI A., LANTI A., PUDDU P.E., KROHOUT D. Coronary heart disease incidence in northern and southern European populations: a reanalysis of the seven countries study for a European coronary risk chart. Heart, 84, 238, 2000.
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.agro-94a3375d-6744-4a6c-a3c0-f2307a6b185e
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.