You are here

Home » Content

İzole koroner arter ektazisi olan hastalarda plazma asimetrik dimetil arginin düzeyleri

Journal Name:

  • Süleyman Demirel Üniversitesi Tıp Fakültesi Dergisi

Publication Year:

  • 2010

Key Words:

Keywords (Original Language):

Author NameUniversity of AuthorFaculty of Author
Abstract (2. Language): 
Objective: The main objective of this study was to compare the plasma asymmetric dimethylarginine (ADMA) levels between the patients with isolated coronary artery ectasia (CAE) and individuals with normal coronary arteries or patients with coronary artery disease (CAD) (diameter loss>50%). Methods Eighty-eight consecutive patients meeting study inclusion criteria who have undergone coronary angiography between August 2007 and pebruary 2008, were participated in this study. All patients were separated into three groups: CAE, CAD and normal coronary artery. Serum levels of ADMA were measured by using ELISA method and nitric oxide metabolites levels were measured by using photometric method. Results: Although statistically insignificant, serum levels of ADMA was lower in patients with CAE than CAD (pl: 0.058) or normal coronary arteries (p2: 0.08). There was no statistically significantly difference between CAE, normal coronary arteries or CAD with regard to nitric oxide levels. Conclusion: There was no statistically significant difference between CAE, normal coronary arteries and CAD with regard to plasma ADMA levels but there was a trend of lower plasma ADMA levels in patients with CAE compared to normal coronary arteries or CAD.
Bookmark/Search this post with
Abstract (Original Language): 
Amaç: Bu çalışmanın temel amacı, koroner anjiyografide koroner arter ektazisi (KAE) saptanan olgularda asimetrik dimetil arginin (ADMA) düzeylerinin koroner arterleri normal olan ve koroner arter hastalığı (KAH) (çap daralması >%50) olan olgular ile karşılaştırılmasıdır. Metod: Çalışmaya, Ağustos 2007-Şubat 2008 tarihleri arasında koroner anjiyografi yapılan ve çalışmaya alınma kriterlerini karşılayan ardışık 88 hasta dahil edildi. Hastalar, KAE, KAH ve normal koroner arter gruplarından birine alındılar. Çalışmaya alınan hastaların serum örnekleri oda sıcaklığında eritildikten sonra Hasta serum ADMA düzeyleri ELISA yöntemiyle ve nitrik oksid (NO) metabolitleri fotometrik yöntem ile çalışıldı. Bulgular: KAE olan hastalarda istatistiksel olarak anlamlı olmamakla birlikte ADMA düzeyleri KAH (pl: 0.058) ve normal koroner gruplarına göre (p2: 0.08) daha düşük bulundu. Ortalama NO düzeyleri açısından KAE ile KAH arasında ve KAE ile normal koronerler arasında anlamlı fark tespit edilmedi. Sonuç: KAE, KAH ve normal koroner arterleri bulunan hastalar arasında ADMA düzeyleri açısından istatiksel olarak anlamlı fark bulunamadı ancak KAE grubunda KAH ve normal koroner arter gruplarına göre daha düşük olma eğiliminde idi.
FULL TEXT (PDF): 
PDF icon arastirmax-izole-koroner-arter-ektazisi-olan-hastalarda-plazma-asimetrik-dimetil-arginin-duzeyleri.pdf
  • 1
19-25
  • Turkish

REFERENCES

References: 

1. Swanton RH Lea, Thomas M, Coltart DJ, Jenkins BS, Webb-Peploe MM, Williams BT. Coronary artery ectasia, a variant ofocclusive coronary arteriosclerosis. Br HeartJ 1978;40:393-400.
2. Falsetti HL, Carroll RJ. Coronary artery aneurysm. Chest 1976; 69:630-36.
3. Befeler B, Aranda JM, Embi A, Mullin FL, El-Sherif N, Lazzara R. Coronary artery aneurysms: Study of their etiology, clinical course and effect on left ventricular function and prognosis. Am J Med 1977;62:597-607.
4. Krüger D, Stierle U, Herrmann G, Simon R, Sheikhzadeh A. Exercise-Induced myocardial ischemia in isolated coronary artery ectasias and aneurysms ("Dilate coronaropathy"). Am J Cardiol 1999; 34:461¬70.
5. Jian-Jun L, Zheng L, Jie L. Is any link between inflammation and coronary artery ectasia?. Medical Hypotheses 2007;69;678-683.
6. Böger RH. The emerging role ofasymmetric dimethylarginine as a novel cardiovascular risk factor. Cardıovascular Research 2003;59:824-833.
7. Hori T, Matsubara T, Ishibashi T et al. Significance ofasymmetric dimethylarginine(ADMA) concentrations during coronary circulation in patients with vasospastic angina. Circ J 2003;67:305-311.
8. Williams MJA, Stewart RAH. Coronary artery ectasia, local pathology or diffüse disease. Cathet Cardiovasc Diagn 1994;33: 116-119.
9. Demopoulus VP, Olympios CD, Fakiolas CN, Pissimissis BG, Economides NM, Adamapoulou E, Foussas SG. The natural history ofaneurysmal coronary arterydisease. Heart 1997;78: 136-41.
10. MarkisJE, JoffeCD, CohnPF,FeenDJ,Herman MV, Gorlin R. Clinical significance ofcoronary artery ectasia. Am J Cardiol 1976; 37:217-22.
11. Sorrel VL, Davis MJ, Bove AA. Origins of coronary artery ectasia. Lancet 1996; 347:136-37.
12.
Özaydı
n M, Kahraman H, Varol E, Aslan SM, Doğan A, Altınbaş A. Herbisidlere maruz kalma ile koroner arter ektazisi arasındaki ilişki. S.D.Ü. Tıp Fak. Derg. 2007:14(3): 13-16.
13. Sudhir K,Ports TA, Amidon TM, Goldgerger JJ, Brushan V, Kane JP, Yock P, Malloy MJ. Increased prevalence ofcoronary ectasia in heterozygous familial hypercholesterolemia. Circulation 1995;91:1375-80.
14. Lu T-M, Ding Y-A, Leu H-B et all. Effect ofrosuvastatin on plasma levels ofasymmetric dimethylarginine in patients with hypercholesterolemia. The American Journal ofCardiology. 2004;94;:157-161.
15. Oguz A, Uzunlulu M. Short term fluvastatin treatment lowers serum asymmetric dimethylarginine levels in patients with metabolic syndrome. Int Heart J.
2008;49:303-311.
S.D.Ü. Tıp pak.
Derg
. 2010:17(1)/ 19-25
Küçüktepe, koroner arter ektazide asimetrik dimetil arginin 25
16. Böger RH, Bode-Böger SM, Szuba A et al. Asymmetric dimethylarginine (ADMA): a novel risk factor for endothelial dysfunction: its role in hypercholesterolemia. Circulation. 1998;98:1842-1847.
17. Cooke JP. Does ADMA cause endothelial dysfunction? Arteriocler Thromb Vasc Biol 2000;20:2032-2037.
18. Böger RH. Asymmetric dimethylarginine (ADMA): A novel risk marker in cardiovascular medicine and beyond. Annals ofmedicine 2006;38:126-136.
19. Wang D, Strandgaard S, Iversen JS, Wilcox CS. Asymmetric Dimethylarginine, Oxidative Stress and Vascular Nitric Oxide Synthase in Essential Hypertension. Am J Physiol Regul Integr Comp Physiol 2009;296: R195-R200.
20. Yada T, Kaji S, Akasaka T et all. Changes ofasymmetric dimethylarginine, nitric oxide, tetrahydrobiopterin, and oxidative stress in patients with acute myocardial infarction by medical treatments. Clin Hemorheol Microcirc. 2007;37;269-76.
21. Böger RH, Schwedhelm E, Maas R, Quispe-Bravo S, Skamira C. ADMA and oxidative stress may relate to the progression ofrenal disease: rationale and design ofthe VIVALDI study. Vasc Med. 2005;10:97-102.
22. Sydow K, Münzel T. ADMA and oxidative stress. Atheroscler Suppl. 2003;4:41-51.
23. Lentz AR, Rodionov RN, Dayal S. Hyperhomocysteinemia, endothelial dysfunction, and cardiovascular risk:the potential role ofADMA. Atheroscler Suppl 2003;4:61-65.

Thank you for copying data from http://www.arastirmax.com