Монголын Анагаахын Сэтгүүлүүдийн Холбоо (МАСХ)
Mongolian Journal of Health Sciences, 2006, 2(3)
Coronary artery disease risk factors and their relationship with the endothelial dysfunction among mongols
( Судалгааны өгүүлэл )

N.Erdenekhuu1, Ch.Gansukh1, H.Mungun-Ubi3, Z.Lkhagvasuren2, E.Saranzaya1, M.Undram1, P.Altantsetseg2,B.Anarhuu1, D.Tsegeenjav2, G.Batbaatar1 and Ts.Lkhagvasuren1

1School of Biomedicine, Health Sciences University, Mongolia

2 Shastin Memorial Hospital,Mongolia

3National Yang-Min University, Taiwan

 
Абстракт

The inflammatory process plays a key role in coronary artery disease initiation, progression, and complication. The inflammatory response in large vessels involves the up-regulation of vascular adhesion molecules such as vascular cell adhesion molecule (VCAM)-l and E-selectinand inflammatory cytokines such as TNF, IL-1, or IL-6. A healthy endothelium plays a core role in cardiovascular control. Besides its regulatory functions on vasomotor tone and blood flow, endothelial NO is known to inhibit the platelet activation and modulate migration and growth of the vascular smooth muscle. Unfortunately, none of related studies has been done in Mongolia at the molecular level. Thus, the main goal of this study was to determine the prevalence and means of risk factors for CAD in Mongolia. 60 patients with macroangiopathy and 60 healthy controls were enrolled in the study. Serum mean NO values were (17.2±9.8) uM in the CAD patients and (19.6± 12) |.iM in the healthy controls without any statistical significance. In addition, serum NOx levels was not associated with presence of plaques (r=^-0.111), but significantly correlated with soluble VCAM-1 (r=-0.384) and triglyceride level (r=0.544). Levels of sVCAM-1 showed a strong correlation with IL-1. In summary, among Mongols, pathogenesis of atherosclerosis is might be mostly explained by inflammation mechanisms in addition to traditional risk factors such as age, family history of CAD, gender and dyslipidemia.

Ном зүй

1. World Health Organization, 2002. The world Health Report.: 2002. Retrieved from Web. January 15,h, 2006
2. World Health Organization, 2002. Strategic priorities of the WHO Cardiovascular Disease program. Retrieved from Web. June 1 st, 2006. htlp:/
/www.who.Int/cardiovascular _ diseases / priorities/en/
3. Mackay J, Mensah A.G, 2004. The atlas of heart disease and stroke. Retrieved from web. June 1st, 2006. http://www.who. in t/ cardiovascular
diseases/resources/at las/en/ index.html
4. Mongolian Steps Survey on non-communicable Disease Risk Factor-2006. www.moh.mn
5. Libby P, 2005. The pathogenesis of atherosclerosis. Harrison\'s (16lh ed.) Internal Medicine, pp.1425-1430
6. Libby P, Ridker PM, Maseri A, 2002. Inflammation and atherosclerosis. Circulation. 105: pp. 1135-1143
7. Brevetti G, Silvestro A., Di Giacomo S., et al., 2003. Endothelial dysfunction in peripheral arterial disease is related to increase in plasma markers of
inflammation and severity of peripheral circulatory impairment but not to classic risk factors and atherosclerotic burden. J Vase Surg 38:374-379
8. Holmlund A, Hulthe J, Millgard J. et al.: 2002. Soluble intercellular adhesion molecule-1 is related to endothelial vasodilatory function in healthy
individuals. Atherosclerosis 165:271-276
9. Sinisalo J, Paronen J. Mattila KJ, et al.: 2000. Relation of inflammation to vascular function in patients with coronary heart disease. Atherosclerosis
149:403-411
10. Lale A and Guler O, 2004. NO Level and Endothelial NO Synthase Gene Polymorphism (Glu298Asp) in the Patients with Coronary Artery Disease from
the Turkish Population. Acta Biochimica et Biophysica Sinica 36:661-666
11. Hoffmann J, Haendeler J, Aicher A, Rossig L, Vasa M, Andreas M. Zeiher, Dimmeler S, 2001. Aging Enhances the Sensitivity of Endothelial Cells Toward
Apoptotic Stimuli Important Role of Nitric Oxide. CircRes 89:709-715
12. Brevetti G Martone VD, De Cristofaro T, et al., 2001. High levels of adhesion molecules are associated with impaired endothelium-dependent
vasodilatation in patients with peripheral arterial disease. Thromb Haemost 85:63-66
13. Stocker R, Keaney JF, 2004. The role of oxidative modifications in atherosclerosis. Physiol Rev 84:1381-1478
14. Nistri S, Mazzetti L, Failli P and Bani D, 2002. High-Yield Method for Isolation and Culture of Endothelial Cells from Rat Coronary Blood Vessels
26 Erdenekhuu et al. Coronarv artery disease risk Suitable for Analysis of Intracellular Calcium and Nitric Oxide Biosynthetic Pathways. Biol. Proced.
4:32-37
15. Zouridakis E, Avanzas P, Arroyo-Espliguero R, Fredericks S, Juan Carlos K, 2004. Markers of Inflammation and Rapid Coronary Artery Disease
Progression in Patients with Stable Angina Pectoris. Circulation 110:1747-1753
16. Anderson JL: 2005. Infection, antibiotics, and atherothrombosis: End ofthe road or new beginnings NEnglJMed 352:1706-1709
17. VallanceP, Collier J, BhagatK, 1997. Infection, inflammation, and infarction: Does acute endothelial dysfunction provide a link Lancet 349:1391-1392
18. Hingorani AD, Cross J, Kharbanda RK, et al, 2000. Acute systemic inflammation impairs endothelium-dependent dilatation in humans. Circulation 102:994-
999
19. Yang R, Lee M, Hu H, Pollin T, Alice S. Ryan, Barbara J. Nicklas, Snitker S, Richard B. Horenstein, Hull K, Nelson H. Goldberg, Andrew P. Goldberg, Alan R.
Shuldiner, Susan K. Fried, Da-Wei Gong, 2006. Acute-Phase Serum Amyloid A: An Inflammatory Adipokine and Potential Link between Obesity and Its
Metabolic Complications. Journal Plos Medicine. 3;287 : 0001-0011
 


Зохиогчийн оруулсан түлхүүр үгс


Нийтлэлийн нээгдсэн тоо: 581
Зохиогчийн эрх хуулиар хамгаалагдсан. Дэлхийн Эрүүл Мэндийн Байгууллага, ©  2012.
Вебийг бүтээсэн Слайд ХХК