ST elevasyonlu akut koroner sendromlu hastalarda artmış tiyol/disülfid oranı

Year 2019, Volume: 44 Issue: Supplement 1, 20 - 25, 29.12.2019

Fatih Esad Topal , Zeynep Karakaya , Pınar Yeşim Akyol , Umut Payza , Murat Çalışkan Firdevs Topal Saliha Aksun , Serpil Erdoğan , Salim Neşelioğlu

https://doi.org/10.17826/cumj.527542

Abstract

Amaç: Bu çalışmanın amacı, sağlıklı gönüllüler ile ST elevasyonlu miyokart enfarktüsü (STEMI) şikayeti ile acil servise kabul edilen hastalar arasında tiyol / disülfit hemostaz düzeylerini karşılaştırmaktır.

Gereç ve Yöntem: Bu vaka kontrol çalışması Acil Tıp Anabilim Dalı'nda yapılmıştır. Katılımcılar, 48 sağlıklı gönüllüden ve 48 hastanede yatan STEMI hastalarından oluşmaktadır. Her çalışma grubunda tiyol / disülfit seviyesi değerlendirildi. STEMI'li hastalarda Tiyol düzeylerinin (doğal/toplam) birlikteliği değerlendirildi.

Bulgular: STEMI'li hastalar ile sağlıklı gönüllüler arasında yaşlarına ve cinsiyetlerine göre anlamlı bir fark bulunmadı. Disülfit (SS) seviyelerinin her iki grupta da benzer olduğu saptandı. Gönüllülere kıyaslandığında STEMI hastalarında total tiyol (TT) ve doğal tiyol (SH) seviyelerinin çok daha düşük ve SS/TT seviyelerinin ise daha yüksek olduğu saptandı.

Sonuç: Bu çalışma, STEMI hastalarında oksidan/antioksidan oranının oksidatif tarafa kaydığını ortaya çıkarmıştır. Anormal bir tiyol/disülfit dengesi, patogenezde ve tedavi yanıtının izlenmesinde önemli bir faktör olarak düşünülebilir. Tiyol kaynakları, STEMI'nin teşhisi için kullanılabilir.

Keywords

STEMI, Acute Coronary Syndrome, oxidative stress, thiol / disulphide

Increased thiol/disulphide ratio in patients with ST elevation-acute coronary syndromes

Abstract

Purpose: The aim of this study was to compare thiol/disulphide haemostasis levels between healthy volunteers and the patients who were admitted to emergency with the complaint of ST Elevation myocardial infarction (STEMI).

Materials and Methods: This case-control study was carried out in the Department of Emergency Medicine. The participants consisted of 48 healthy volunteers and 48 hospitalized patients with STEMI. The thiol / disulphide level was evaluated in each study group. The association of Thiol levels (native/total) was evaluated in patients with STEMI.

Results: No significant difference was found between the patients with STEMI and healthy volunteers regarding their age or gender. The disulphide (SS) levels were similar in both groups. The total thiol (TT) and native thiol (SH) levels were much lower and the SS/TT levels were much higher in the patients with STEMI when compared with the volunteers. 

Conclusion: This study revealed that the oxidant/antioxidant ratio was shifted to the oxidative side in patients with STEMI. An abnormal thiol/disulphide state might be considered as an important factor in the pathogenesis and in monitoring the treatment response. The thiol resources may be used for diagnosis of STEMI.

References

• 1. Young I, Woodside J. Antioxidants in health and disease. Journal of clinical pathology. 2001;54:176-86.
• 2. Dzau VJ, Antman EM, Black HR, Hayes DL, Manson JE, Plutzky J, et al. The cardiovascular disease continuum validated: clinical evidence of improved patient outcomes part i: pathophysiology and clinical trial evidence (risk factors through stable coronary artery disease). Circulation. 2006;114:2850-70.
• 3. Kasap S, Gönenç A, Şener DE, Hisar İ. Serum cardiac markers in patients with acute myocardial infarction: oxidative stress, C-reactive protein and N-terminal probrain natriuretic peptide. Journal of clinical biochemistry and nutrition. 2007;41:50.
• 4. Cremers CM, Jakob U. Oxidant sensing by reversible disulfide bond formation. Journal of Biological Chemistry. 2013;288:26489-96.
• 5. Jones DP, Liang Y. Measuring the poise of thiol/disulfide couples in vivo. Free Radical Biology and Medicine. 2009;47:1329-38.
• 6. Gur M, Aslan M, Yildiz A, Demirbag R, Yilmaz R, Selek S, et al. Paraoxonase and arylesterase activities in coronary artery disease. European journal of clinical investigation. 2006;36:779-87.
• 7. Go Y-M, Jones DP. Cysteine/cystine redox signaling in cardiovascular disease. Free Radical Biology and Medicine. 2011;50:495-509.
• 8. Maritim AC, Sanders RA, Watkins JB. Diabetes, oxidative stress, and antioxidants: a review. J Biochem Mol Toxicol. 2003; 17(1): 24–38
• 9. Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. FreeRadicBiolMed. 2010;48(6):749-62.
• 10. Biswas S, Chida AS, Rahman I. Redox modifications of protein-thiols: emerging roles in cell signaling. Biochem Pharmacol. 2006;71(5):551-64.
• 11. Erel O, Neselioglu S. A novel and automated assay for thiol/disulphide homeostasis. Clinical Biochemistry. 2014;47(18):326–332.
• 12. Acet H, Ertaş F, Akıl MA, et al. Novel predictors of infarct-related artery patency for ST-segment elevation myocardial infarction: Platelet-to-lymphocyte ratio, uric acid, and neutro- phil-to-lymphocyte ratio. Anatol J Cardiol. 2015; 15(8): 648–656.
• 13. Roffi M, Patrono C, Collet JP, et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016; 37(3): 267–315
• 14. Freeman BA, Crapo JD. Biology of disease: free radicals and tissue injury. Lab Invest. 1982; 47(5): 412–426.
• 15. Lunec J, Blake D. Oxygen free radicals: Their relevance to disease processes. , London 1990: 189–212
• 16. Kundi H, Ates I, Kiziltunc E, et al. A novel oxidative stress marker in acute myocardial infarction; thiol/disulphide homeo- stasis. Am J Emerg Med. 2015; 33(11): 1567–1571.
• 17. Levy Y, Bartha P, Ben-Amotz A, Gerald Brook J, Dankner G, Lin S, et al. Plasma antioxidants and lipid peroxidation in acute myocardial infarction and thrombolysis. Journal of the American College of Nutrition. 1998;17:337-41.
• 18. Demirbag R, Rabus B, Sezen Y, Taskın A, Kalaycı S. The plasma and tissue oxidative status in patients with coronary artery disease: oxidative stress and coronary artery disease. Turkish J Thorac Cardiovasc Surg. 2010;18:079-82.
• 19. Sezen Y, Bas M, Polat M, Yildiz A, Buyukhatipoglu H, Kucukdurmaz Z, et al. The relationship between oxidative stress and coronary artery ectasia. Cardiology journal. 2010;17:488-94.
• 20. Mallika V, Goswami B, Rajappa M. New risk factor-atherosclerosis pathophysiology and the role of novel risk factors: A clinicobiochemical perspective. Angiology, 2007;58:513-22.
• 21. Morrow JD. Quantification of isoprostanes as indices of oxidant stress and the risk of atherosclerosis in humans. Arterioscler Thromb Vasc Biol, 2005;25: 279-86.
• 22. Yong QC, Lee SW, Foo CS, Neo KL, Chen X, Bian JS. Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning. Am J Physiol Heart Circ Physiol. 2008;295(3):H1330-H40.
• 23. Elrod JW, Calvert JW, Morrison J, Doeller JE, Kraus DW, Tao L, et al. Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. Proc Natl Acad Sci USA. 2007;104(39):15560-5.
• 24. Koprivica Z, Djordjevic D, Vuletic M, et al. Von Willebrand factor and oxidative stress parameters in acute coronary syndromes. Oxid Med Cell Longev. 2011; 2011: 918312,
• 25. CircuML,AwTY.Reactiveoxygenspecies,cellularredoxsystems,andapoptosis.Free Radic Biol Med 2010;48(6):749–62.
• 26. Matteucci E, Giampietro O. Thiol signalling network with an eye to diabetes. Molecules 2010;15(12):8890–903.
• 27. Kuo LM, Kuo CY, Lin CY, Hung MF, Shen JJ, Hwang TL. Intracellular glutathione de- pletion by oridonin leads to apoptosis in he- patic stellate cells. Molecules 2014;19(3): 3327-44.
• 28. Kundi H, Erel Ö, Balun A, et al. Association of thiol/disulfide ratio with syntax score in patients with NSTEMI. Scand Cardiovasc J. 2015; 49(2): 95–100.
• 29. Sivri S, Kasapkara HA, Polat M, et al. Dynamic thiol/disulphide homeostasis and its prognostic value in patients with non-ST elevation-acute coronary syndromes. Kardiol Pol. 2018; 76(2): 426–432.