Evaluation of oxidant status in both systolic and diastolic heart failure

Yıl 2018, Cilt: 5 Sayı: 10, 350 - 356, 30.10.2018

Ramazan Asoglu , Hatice Sezen Muslihittin Emre Erkus , Halil Altiparmak , Zekeriya Kaya , Emin Asoglu Ozgur Gunebakmaz , Recep Demirbag , Yusuf Sezen

https://doi.org/10.17546/msd.458810

Öz

Objective:  Oxidative stress status in subgroup of heart failure (HF) syndrome still remains unknown. We aimed to study Total Antioxidant Status (TAS), Total Oxidant Status (TOS) and Oxidative Stress Index (OSI) in both systolic and diastolic HF, and also in both ischemic and non-ischemic HF. Materials and Methods: Consecutive 123 chronic HF patients were included in this cross-sectional study. Group 1 consisted of 73 systolic HF patients (50 ischemic patients and 23 non-ischemic patients) and group 2 consisted of 50 diastolic HF patients. As a control group (group 3), 37 healthy subjects were included. Echocardiographic evaluation was performed and TAS, TOS and OSI were studied in all patients. Results: The highest TAS value (1.10±0.24) was found in Group 1, but the lowest in Group 2 (0.90±0.14). Diastolic HF group had the highest TOS value (37.2±10.41) while systolic HF group (32.9±7.26) and control group (26.19±8.00) followed it. OSI was found the highest in diastolic HF group (4.37±1.24) and the lowest in systolic HF group (2.24±0.80). TOS and OSI were similar between ischemic and non-ischemic subgroups of systolic HF but TAS was statistically higher in non-ischemic (p:0.0005). Conclusions: We found higher oxidative stress in HF patients, predominantly in diastolic HF patients. The difference between diastolic and systolic HF with regard to oxidative and antioxidative status seems to come from distinct drugs usage between the groups, which have potential effects on oxidative and antioxidative parameters. To reduce, at least, oxidative stress in diastolic HF patients, medical therapy is needed.

Anahtar Kelimeler

sistolic heart failure, diastolic heart failure, oxidative stress

Kaynakça

• 1. McMurray JJ V, Adamopoulos S, Anker SD, Auricchio A, Bohm M, Dickstein K, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart. Eur Heart J. 2012 Jul 2;33(14):1787–847.
• 2. Go AS, Mozaffarian D, Roger VL, MEMBERS WG, Go AS, Mozaffarian D, et al. Heart disease and stroke statistics--2014 update: a report from the American Heart Association. Circulation. 2014;129(3):e28–292.
• 3. Halliwell B. The role of oxygen radicals in human disease, with particular reference to the vascular system. Pathophysiol Haemost Thromb. 1993;23(Suppl. 1):118–26.
• 4. Dalle-Donne I, Rossi R, Colombo R, Giustarini D, Milzani A. Biomarkers of oxidative damage in human disease. Clin Chem. 2006 Apr 16;52(4):601–23.
• 5. Peluso I, Morabito G, Urban L, Ioannone F, Serafi M. Oxidative stress in atherosclerosis development: the central role of LDL and oxidative burst. Endocrine, Metab Immune Disord Targets (Formerly Curr Drug Targets-Immune, Endocr Metab Disord. 2012 Oct 1;12(4):351–60.
• 6. Touyz RM. Reactive oxygen species, vascular oxidative stress, and redox signaling in hypertension. Hypertension. 2004;44(3):248–52.
• 7. Elahi MM, Kong YX, Matata BM. Oxidative stress as a mediator of cardiovascular disease. Oxid Med Cell Longev 2009. Oxid Med Cell Longev. 2009;2(5):259–69.
• 8. Rodrigo R, Cereceda M, Castillo R, Asenjo R, Zamorano J, Araya J, et al. Prevention of atrial fibrillation following cardiac surgery: basis for a novel therapeutic strategy based on non-hypoxic myocardial preconditioning. Pharmacol Ther. 2008 Apr;118(1):104–27.
• 9. Belch JJ, Bridges AB, Scott N, Chopra M. Oxygen free radicals and congestive heart failure. Endocrine, Metab Immune Disord Targets (Formerly Curr Drug Targets-Immune, Endocr Metab Disord. 1991 May 1;52(5):547–55.
• 10. Amir O, Paz H, Rogowski O, Barshai M, Sagiv M, Shnizer S, et al. Serum oxidative stress level correlates with clinical parameters in chronic systolic heart failure patients. Clin Cardiol. 2009 Apr 1;32(4):199–203.
• 11. Ellidag HY, Eren E, Yılmaz N, Cekin Y. Oxidative stress and ischemia-modified albumin in chronic ischemic heart failure. Redox Rep. 2014 May 13;19(3):118–23.
• 12. Erel O. A novel automated direct measurement method for total antioxidant capacity using a new generation, more stable ABTS radical cation. Clin Biochem. 2004;37(4):277–85.
• 13. Erel O. A novel automated method to measure total antioxidant response against potent free radical reactions. Clin Biochem. 2004;37(2):112–9.
• 14. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989 Mar 4;2(5):358–67.
• 15. Schiller NB, Acquatella H, Ports TA, Drew D, Goerke J, Ringertz H, et al. Left ventricular volume from paired biplane two-dimensional echocardiography. Circulation. 1979 Sep 1;60(3):547–55.
• 16. Redfield MM, Jacobsen SJ, Burnett Jr JC. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. Jama. 2003;289(2):194–202.
• 17. Mancia G. The task force for the management of arterial hypertension of the European Society of Hypertension and the task force for the management of arterial hypertension of the European Society of Cardiology, 2007 Guidelines for the management of arterial hyperte. Eur Hear J. 2007;28:1462–536.
• 18. IDF Clinical Guidelines Task Force. Global {Guideline} for {Type} 2 {Diabetes}: recommendations for standard, comprehensive, and minimal care. Diabet Med A J Br Diabet Assoc. 2006;23(6):579–93.
• 19. European Association for Cardiovascular Prevention & Rehabilitation, Reiner Z, Catapano AL. {ESC}/{EAS} {Guidelines} for the management of dyslipidaemias: the {Task} {Force} for the management of dyslipidaemias of the {European} {Society} of {Cardiology} ({ESC}) and the {European} {Atherosclerosis} {Society} ({EAS}). Eur Heart J. 2011;32(14):1769–818.
• 20. Yancy CW, Jessup M, Bozkurt B, Butler J, Jr DEC, Drazner MH. 2013 ACCF/AHA guideline for the management of heart failure. Circulation. 2013;128:e240–327. 21. Hill MF, Singal PK. Right and left myocardial antioxidant responses during heart failure subsequent to myocardial infarction. Circulation. 1997;96(7):2414–20.
• 22. Mallat Z, Philip I, Lebret M, Chatel D, Maclouf J, Tedgui A. Elevated Levels of 8-iso-Prostaglandin F2 in Pericardial Fluid of Patients With Heart Failure : A Potential Role for In Vivo Oxidant Stress in Ventricular Dilatation and Progression to Heart Failure. Circulation. 1998 Apr 28;97(16):1536–9.
• 23. Demirbag R, Yilmaz R, Erel O. The relationship between potency of oxidative stress and severity of dilated cardiomyopathy. Can J Cardiol. 2005;21(10):851–5.
• 24. Tsutsui H, Kinugawa S, Matsushima S. Oxidative stress and heart failure. Am J Physiol Circ Physiol. 2011 Dec;301(6):H2181–90.
• 25. Shah A, Passacquale G, Gkaliagkousi E, Ritter J, Ferro A. Platelet nitric oxide signalling in heart failure: role of oxidative stress. Cardiovasc Res. 2011;91(4):625–31.
• 26. Matsushima S, Kinugawa S, Yokota T. Increased myocardial NAD (P) H oxidase-derived superoxide causes the exacerbation of postinfarct heart failure in type 2 diabetes. Am J Physiol Circ Physiol. 2009;297(1):H409–16.
• 27. Cappola TP, Kass DA, Nelson GS, Berger RD, Rosas GO, Kobeissi ZA, et al. Allopurinol improves myocardial efficiency in patients with idiopathic dilated cardiomyopathy. Circulation. 2001 Jul 13;297(1):2407–11.
• 28. Borchi E, Bargelli V, Stillitano F, Giordano C, Sebastiani M, Nassi PA, et al. Enhanced ROS production by NADPH oxidase is correlated to changes in antioxidant enzyme activity in human heart failure. Biochim Biophys Acta (BBA)-Molecular Basis Dis. 2010 Mar 1;1802(3):331–8.
• 29. Khaper N, Kaur K, Li T, Farahmand F, Singal PK. Antioxidant enzyme gene expression in congestive heart failure following mycardial infarction. Mol Cell Biochem. 2003;251(1):9–15.
• 30. Li J-MJ-M, Gall NP, Grieve DJ, Chen M, Shah AM. Activation of NADPH oxidase during progression of cardiac hypertrophy to failure. Hypertens (Dallas, Tex 1979). 2002 Oct 1;40(4):477–84.
• 31. Takayama T, Wada A, Tsutamoto T. Contribution of vascular NAD (P) H oxidase to endothelial dysfunction in heart failure and the therapeutic effects of HMG-CoA reductase inhibitor. Circ J. 2004;68(11):1067–75.
• 32. Paulus WJ, Bronzwaer JGF. Nitric oxide9s role in the heart: control of beating or breathing? Am J Physiol Circ Physiol. 2004;287(1):H8–13.
• 33. Beckman JS, Koppenol WH. Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and ugly. Am J Physiol Physiol. 1996;271(5):C1424–37.
• 34. Mihm MJ, Coyle CM, Schanbacher BL. Peroxynitrite induced nitration and inactivation of myofibrillar creatine kinase in experimental heart failure. Cardiovasc Res. 2001 Mar;49(4):798–807.
• 35. Ungvári Z, Gupte SA, Recchia FA, Bátkai S, Pacher P. Role of oxidative-nitrosative stress and downstream pathways in various forms of cardiomyopathy and heart failure. Curr Vasc Pharmacol. 2005 Jul;3(3):221–9.