Journals / Anadolu Kardiyoloji Dergisi / 2010 / Cilt: 10 - Sayı: 5

Fibrinolitik tedavi alan hastalarda homosistein düzeyleri ile enfarktüsle ilişkili arterin açıklığı ve akım hızının ilişkisi

Relation of homocysteine levels with patency and flow rate of infarct related artery in patients receiving fibrinolytic therapy

Pages
410–415
Publication Date
2022-10-10
DOI
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In addition, we found a significant positive correlation between CTFC and plasma homocysteine levels (r=0.415; p

📌 3 Key Takeaways

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Objective & Hypothesis:Objective:Elevated homocysteine levels induce a hypercoagulable state and make the clot more resistant to fibrinolysis.
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Key Findings & Data:Methods: Sixty-one patients who received fibrinolytic therapy for a first ST elevation myocardial infarction (STEMI) within 12 hours of chest pain were included.
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Conclusion & Impact:In addition, we found a significant positive correlation between CTFC and plasma homocysteine levels (r=0.415; p
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective:Elevated homocysteine levels induce a hypercoagulable state and make the clot more resistant to fibrinolysis. In this prospective observational study, we investigated the influence of homocysteine levels on infarct-related artery (IRA) patency and flow as determined with regard to thrombolysis in myocardial infraction (TIMI) flow grade and corrected TIMI frame count (CTFC). Methods: Sixty-one patients who received fibrinolytic therapy for a first ST elevation myocardial infarction (STEMI) within 12 hours of chest pain were included. Coronary angiography was performed according to the Judkins technique within 72 hours after fibrinolytic therapy. Total plasma homocysteine level was determined by the high-performance liquid chromatography method with fluorescence detection. Statistical analysis was performed using Chi-square, Student’s t and Pearson correlation tests. Logistic regression analysis was used to determine the predictors of IRA occlusion. Results: Of the 61 patients, 22 (36.1%) had an occluded IRA (group 1), 39 (63.9%) had a patent IRA (group 2). Mean plasma homocysteine levels were found to be significantly higher in the group 1 compared to the group 2 (18.5±9.6 µmol/L vs 14.3±5 µmol/L, p=0.04). In addition, we found a significant positive correlation between CTFC and plasma homocysteine levels (r=0.415; p

Özet

Amaç:Yüksek homosistein düzeyleri mevcut pıhtıyı fibrinolize daha dirençli hale getirmektedir. Bu prospektif gözlemsel çalışmada, homosistein düzeylerinin, TIMI (thrombolysis in myocardial infarction) akım derecesi ve TIMI kare sayısına göre değerlendirilen enfarktüs ile ilişkili arter (EİA) açıklık ve akım hızı üzerine etkisini araştırdık.Yöntemler: ST yükselmeli miyokart enfarktüsü nedeniyle, göğüs ağrısının ilk 12 saati içinde fibrinolitik tedavi alan 61 hasta çalışmaya alındı. Fibrinolitik tedavi sonrası 72 saat içinde Judkins tekniği ile koroner anjiyografi yapıldı. Total plazma homosistein düzeyi flörosan saptama ile yüksek performanslı likit kromatografi metodu ile belirlendi. İstatistiksel analiz Ki-kare, Student t test, Pearson korelasyon testi kullanılarak yapıldı. EİA oklüzyonu öngördürücülerinin belirlemesinde lojistik regresyon analizi kullanıldı. Bulgular: Çalışmaya alınan 61 hastanın 22'sinde (%36.1) EİA tıkalı (grup 1), 39'unda (%63.9) EİA açık (grup 2) saptandı. Ortalama plazma homosistein düzeyleri grup 1 de grup 2 ile kıyaslandığında daha yüksekti (18.5±9.6 µmol/L’ye karşın 14.3±5 µmol/L, p=0.04). Ayrıca düzeltilmiş TIMI kare sayısıyla plazma homosistein düzeyleri arasında anlamlı bir pozitif korelasyon vardı (r=0.415; p

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Cite This Article

AYHAN, H., KELEŞ, T., DURMAZ, T., AKÇAY, M., YETER, E., BAYRAM, A. N., BOZKURT, E. (2022). Fibrinolitik tedavi alan hastalarda homosistein düzeyleri ile enfarktüsle ilişkili arterin açıklığı ve akım hızının ilişkisi. Anadolu Kardiyoloji Dergisi, Cilt: 10 - Sayı: 5, 410–415. https://ajindex.com/articles/436737

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References (13)

  1. Clarke R, Daly R, Robinson K, Naughten E, Cahalane S, Fowler B, et al. Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med 1991; 324: 1149-55
  2. The Homocysteine Studies Collaboration. Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA 2002; 288: 2015-22
  3. De Jong SC, Stehouwer CD, Van Der Berg M, Visher UM, Rauwerda JA, Emeis JJ. Endothelial marker proteins in hyperhomocysteinemia. Thromb Haemost 1997; 78: 1332-7
  4. Al-Obaidi MK, Philippou H, Stubbs PJ, Adami A, Amersey R, Noble MM, et al. Relationships between homocysteine, factor VIIa, and thrombin generation in acute coronary syndromes. Circulation 2000; 101: 372-7
  5. Kuch B, Bobak M, Fobker M, Junker R, von Eckardstein A, Marmot M, et al. Associations between homocysteine and coagulation factors-a cross-sectional study in two populations of central Europe. Thromb Res 2001; 103: 265-73
  6. Schreiner PJ, Wu KK, Malinow MR, Stinson VL, Szklo M, Nieto FJ, et al. Hyperhomocyst(e)inemia and hemostatic factors: the atherosclerosis risk in communities study. Ann Epidemiol 2002; 12: 228-36
  7. Tofler GH, D’agostino RB, Jacques PF, Bostom AG, Wilson PW, Lipinska I, et al. Association between increased homocysteine levels and impaired fibrinolytic potential: potential mechanism for cardiovascular risk. Thromb Haemost 2002; 88: 799-804
  8. Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS, Dalen J, et al. Thrombolysis in Myocardial Infarction Trial, Phase I (TIMI). A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Circulation 1987; 76: 142-54
  9. Gibson CM, Cannon CP, Daley WL, Dodge JT Jr, Alexander B Jr, Marble SJ, et al. TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation 1996; 93: 879-88
  10. Rodgers SM, Conn MT. Homocysteine, an atherogenic stimulus, reduces protein C activation by arterial and venous endothelial cells. Blood 1990; 75: 895-901
  11. Hayashi T, Honda G, Suzuki K. An atherogenic stimulus homocysteine inhibits cofactor activity of thrombomodulin and enhances thrombomodulin expression in human umbilical vein endothelial cells. Blood 1992; 79: 2930-6
  12. Nishinaga M, Ozawa T, Shimada K. Homocysteine, a thrombogenic agent, suppresses anticoagulant heparin sulfate expression in cultured porcine aortic endothelial cells. J Clin Invest 1993; 92: 1381-6
  13. Hajjar KA. Homocysteine-induced modulation of tissue plasminogen activator binding to its end