Journals / MN Kardiyoloji / 2010 / Cilt: 17 - Sayı: 1

Frequency of factor 13 Valin34Lösin gene polymorphism and relation between gene polymorphism and clinic results in coronary artery disease

Koroner arter hastalığında faktör 13 Valin 34 Lösin gen polimorfizmi sıklığı ve gen polimorfizmi ile klinik sonuçlar arasındaki ilişki

Pages
19–25
DOI
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Conclusion: It seems that polymorphism of F13 Valin34Leucine is associated factor with acute coronary syndrome and atherosclerotic process

📌 3 Key Takeaways

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Objective & Hypothesis:Aim: Factor 13 (F13) have important role in coagulation after rupture of atherosclerotic plaque.
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Key Findings & Data:Plasma level of F13 is associated with genetic polymorphism.
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Conclusion & Impact:Conclusion: It seems that polymorphism of F13 Valin34Leucine is associated factor with acute coronary syndrome and atherosclerotic process
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Aim: Factor 13 (F13) have important role in coagulation after rupture of atherosclerotic plaque. Plasma level of F13 is associated with genetic polymorphism. Although previous studies showed relationship between F13 Valin34Leucine and coronary artery disease, frequency of this polymorphism changes with ethnic difference. In our study, we investigated that frequency of F13 genetic poly-morphism and that relationship between genetic polymorphism and clinic and angiographic results of patients with coronary artery disease. Material and Method: We enrolled 68 patients [myocardial infarction (MI):23, unstable angina pectoris (USAP):22, stable angina pectoris (SAP):23]. Coronary angiography was performed to all patients. Gensini and Extent scores were used to evaluate the severity and intensity of coronary atherosclerosis. Morphologic properties of atherosclerotic lesions were evaluated according to ACC/AHH lesion classification Genetic polymorphism was detected with CVD StripAssay method. Results: The genotype frequencies in all patients for F13 were 85.2(Valin34Valin), 13.6% (Valin34Leucine) and 1.2% (Leucine34Leucine). The frequency of Valin34Valin genetic polymorphism was similar in patients with SAP, USAP and MI. Factor 13 Valin34Leu polymorphism was higher MI and USAP. The number of diseased vessel, Extent score and type C lesion were higher in patient who had F 13 Valin34Valin. Conclusion: It seems that polymorphism of F13 Valin34Leucine is associated factor with acute coronary syndrome and atherosclerotic process

Özet

Amaç: Faktör 13 (F13) aterosklerotik plağın rüptüründen sonraki koagülasyon aşamasında önemli rol oynayan hemostatik faktördür. Faktör 13 plazma düzeyi genetik polimorfizm ile ilişkilidir. Daha önceki çalışmalarda F13 Valin 34 Lösin polimorfizmi ile koroner arter hastalığı (KAH) arasında ilişki olabileceği göstermesine rağmen, bu polimorfizm sıklığı etnik faklılık göstermektedir. Çalışmamızda F13 polimorfizminin bölgemizdeki sıklığını ve bu polimorfizmin KAH’ lı hastaların klinik ve anjiyografik sonuçları ile olan ilişkisini araştırdık. Gereç ve Yöntem: Çalışmaya hastanemize başvuran miyokardiyal enfarktüslü (MI) 23, unstable angina pektorisli (USAP) 22 ve stabil angina pektorisli (SAP) 23 olmak üzere 68 hasta alındı. Çalışmaya alınan tüm hastalara koroner anjiyografi yapıldı. Koroner aterosklerozun şiddetinin ve yaygınlığının değerlendirilmesinde Gensini ve Extent skoru kullanıldı. Aterosklerotik lezyonların morfolojik özellikleri ACC/AHA lezyon klasifikasyonuna göre değerlendirildi. Genetik polimorfizm CVD StripAssay yöntemi ile belirlendi. Bulgular: Tüm hasta populasyonundaki hastalarda F13 için; % 85,2 Valin34Valin, % 13,6 Valin34Lösin ve % 1,2 Lösin34Lösin genetik yapısı vardı. Faktör 13 Valin34Valin genotip sıklığı SAP, USAP ve MI’ lı hastalarda benzerdi. Heterozigot genetik yapı ise Mİ ve USAP grubunda daha yüksek orandaydı. Faktör 13 genotipi Valin34Valin olan hastalarda hastalıklı damar sayısı, extent skoru ve Tip C lezyon oranı anlamlı olarak daha yüksek bulundu. Sonuç: Faktör 13 V34L polimorfizmi akut koroner sendrom ve aterosklerotik süreçle ile ilgili genetik bir faktör olarak görünmektedir.

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Cite This Article

KALAY, N., GÜL, İ., TOPSAKAL, R., ERYOL, N. K., ÖZDOĞRU, İ., DOĞAN, A., İNANÇ, M. T., ÇETİNKAYA, Y., ŞIVGIN, H., DÜNDAR, M., ÇAĞLAYAN, O., ÖZKUL, Y., OĞUZHAN, A., ERGİN, A. (2010). Frequency of factor 13 Valin34Lösin gene polymorphism and relation between gene polymorphism and clinic results in coronary artery disease. MN Kardiyoloji, Cilt: 17 - Sayı: 1, 19–25. https://ajindex.com/articles/297432

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References (14)

  1. Hefler L, Jirecek S, Heim K, Grimm C, Antensteiner G, Zeil - lin ger R ve ark. Genetic polymorphisms associated with thrombophilia and vascular disease in women with unexplained late intrauterine fetal death: a multicenter study. J Soc Gynecol Investig. 2004
  2. 4 2. Diz-Kucukkaya R, Hancer VS, Inanc M, Nalcaci M, Pekcelen Y. Factor XIII Val34Leu polymorphism does not contribute to the prevention of thrombotic complications in patients with antiphospholipid syndrome.Lupus. 2004
  3. Attié-Castro FA, Zago MA, Lavinha J, Elion J, Rodriguez- Delfin L, Guerreiro JF ve ark. Ethnic heterogeneity of the factor XIII Val34Leu polymorphism.Thromb Haemost. 2000
  4. Marín F, Corral J, Roldán V, González-Conejero R, del Rey ML, Sogorb F ve ark. Factor XIII Val34Leu polymorphism modulates the prothrombotic and inflammatory state associated with atrial fibrillation. J Mol Cell Cardiol. 2004
  5. 704 5. Kakko S, Elo T, Tapanainen JM, Huikuri HV, Savolainen MJ. Polymorphisms of genes affecting thrombosis and risk of myocardial infarction. Eur J Clin Invest. 2002
  6. Franco RF, Pazin-Filho A, Tavella MH, Simões MV, Marin- Neto JA, Zago MA. Factor XIII val34leu and the risk of myocardial infarction. Haematologica. 2000
  7. Canavy I, Henry M, Morange PE (Genetic polymorphisms and coronary artery disease in the south of France. Thromb Haemost 2000
  8. 6 8. Gensini GG, Kelly AE. Incidence and progression of coronary artery disease. Arch Intern Med 1972
  9. 23 9. Gensini GG. A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol 1983
  10. Sullivan DR, Marwick TH, Freedman SB. A new method of scoring coronary angiograms to reflect extent of coronary atherosclerosis and improve correlation with major risk factors. Am Heart J 1990
  11. Zaacks SM, Allen JE, Calvin JE, Schaer GL, Palvas BW, Parrillo JE ve ark.Value of The American College of Cardiology/American Heart Association Stenosis Morp - ho logy Classification for Coronary Interventions in the Late 1990s Am J Cardiol 1998
  12. 9 12. Markis JE, Joffe CD, Cohn PF, Feen DJ, Herman MV, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol. 1976
  13. Nordlie MA, Wold LE, Kloner RA. Genetic contributors toward increased risk for ischemic heart disease. J Mol Cell Cardiol. 2005
  14. Heng CK, Lal S, Saha N, Low PS, Kamboh MI. The impact of factor XIIIa V34L polymorphism on plasma