Relationship between Oxidative Stress Markers and Cardiac Syndrome X

Year 2012, , 174 - 180, 01.06.2012

Durmuş Yıldıray Şahin Zafer Elbasan Mustafa Gür Caner Türkoğlu Betül Özaltun Zehra Sümbül Murat Çaylı

https://doi.org/10.5799/ahinjs.01.2012.02.0139

Cited By: 3

Abstract

Objectives: To investigate the alterations of oxidative and antioxidative status in patients with cardiac syndrome X (CSX). Materials and methods: Thirty-three patients with CSX (CSX group), 27 patients without CSX (NSX) and 20 healthy volunteers as control group were included into the study. Oxidative status of serum was evaluated by measuring total oxidant status (TOS), lipid hydroperoxide levels (LOOH) and oxidative stress index (OSI) of serum, and antioxidative status of serum was evaluated by measuring total antioxidant capacity (TAC). Also, hsCRP and other biochemical markers were measured in all subjects. Results: The oxidants (TOS, LOOH and OSI) and CRP levels were higher, and TAC was lower in the patients with CSX than NSX group and control group. Also, the oxidants (TOS, LOOH and OSI) and hsCRP levels, a marker of chronic inflammation, were higher, and TAC was lower in the patients with NSX than control group. In addition, in patients with CSX, a significant positive correlation (ß =0.606, p

Keywords

Oxidative stress, oxidant, antioxidant, cardiac syndrome X

Relationship between Oxidative Stress Markers and Cardiac Syndrome X

Abstract

Amaç: Biz bu çalışmada kardiyak sendrom X\'li (CSX) hastalarda oksidatif ve antioksidatif durumlardaki değişimi araştırdık. Gereç ve yöntem: Çalışmamıza 33 CSX\'li hasta, 27 CSX tanısı olmayan (NSX) hasta ve kontrol grubu olarak 20 sağlıklı gönüllüyü dahil ettik. Serumun oksidatif durumu total oksidan durum (TOS), lipid hidroperoksid seviyesi (LOOH) ve serum oksidatif stres indeksi ölçülerek (OSİ) değerlendirildi. Serumun antioksidatif durumu ise total antioksidan kapasite (TAC) ölçülerek değerlendirildi. Ayrıca tüm vakalarda hsCRP ve diğer biyokimyasal belirteçler ölçüldü. Bulgular: CSX grubunda NSX ve kontrol grubuna göre oksidan seviyeleri (TOS, LOOH ve OSI) ve CRP seviyeleri daha yüksekken, TAC seviyeleri daha düşük bulundu. Ayrıca NSX grubunda kontrol grubuna göre oksidanlar (TOS, LOOH ve OSI) ve kronik enflamasyonun bir belirteci olan hsCRP seviyeleri daha yüksekken TAC seviyeleri daha düşük olarak saptandı. Bunlara ek olarak CSX\'li hastalarda OSİ seviyesi ve ST depresyonu arasında istatistiksel olarak anlamlı bir korelasyon mevcuttu (r; 0.784, ß =0,606, p

Keywords

Oksidatif stres, oksidan, antioksidan, kardiyak sendrom X.

References

• Cannon RO, Epstein SE. ‘‘Microvascular angina’’ as a cause of chest pain with angiographically normal cor- onary arteries. Am J Cardiol 1988; 61 (15):1338-43.
• Crea F, Lanza GA. Angina pectoris and normal coro- nary arteries: cardiac syndrome X. Heart 2004; 90 (4):457-63.
• Dominguez-Rodriguez A, Garcia-Gonzalez M, Abreu- Gonzalez P. Cardiac syndrome X: diagnosis, patho- genesis and management. Am J Cardiovasc Drugs 2004; 4 (6):423-4.
• Bugiardini R, Pozzati A, Ottani F, Morgagni GL, Puddu P. Vasotonic angina: a spectrum of ischemic syn- dromes involving functional abnormalities of the epi- cardial and microvascular coronary circulation. J Am Coll Cardiol 1993; 22 (2):417-25.
• Buus NH, Bottcher M, Botker HE, Sorensen KE, Nielsen TT, Mulvany MJ. Reduced vasodilator capac- ity in syndrome X related to structure and function of resistance arteries. Am J Cardiol 1999; 83 (2):149-54.
• Egashira K, Inou T, Hirooka Y, Yamada A, Urabe Y, Takeshita A. Evidence of impaired endothelium-de- pendent coronary vasodilatation in patients with angi- na pectoris and normal coronary angiograms. N Engl J Med 1993; 328 (23): 1659-64.
• Vane JR, Anggard EE, Botting RM. Regulatory func- tions of the vascular endothelium. N Engl J Med 1990; 323 (1): 27-36.
• Osamichi S, Kouji K, Yoshimaro I, et al. Myocardial glucose metabolism assessed by positron emission tomography and the histopathologic findings of mi- crovessels in syndrome X. Circ J 2004; 68 (3): 220-6.
• Cannon RO III. Leon MB, Watson RM, Rosing DR, Ep- stein SE. Chest pain and ‘normal’ coronary arteries - role of small coronary arteries. Am J Cardiol 1985; 55 (3): 50B-60B.
• Panting JR, Gatehouse PD, Yang GZ, et al. Abnormal subendocardial perfusion in cardiac syndrome X de- tected by cardiovascular magnetic resonance imag- ing. N Engl J Med 2002; 346 (25): 1948-53.
• Lanza GA, Sestito A, Cammarota G, et al. Assess- ment of Systemic Inflammation and Infective Patho- gen Burden in Patients With Cardiac Syndrome X. Am J Cardiol 2004; 94 (1):40-4.
• Vermeltfoort IA, Raijmakers PG, Riphagen II, et al. Definitions and incidence of cardiac syndrome X: re- view and analysis of clinical data. Clin Res Cardiol 2010; 99 (8):475-81.
• Lekakis JP, Papamichael CM, Vemmos CN, Voutsas AA, Stamatelopoulos SF, Moulopoulos SD. Peripheral vascular endothelial dysfunction in patients with an- gina pectoris and normal coronary arteriograms. J Am Coll Cardiol 1998; 31 (3): 541-6.
• Asbury EA, Creed F, Collins P. Distinct psychosocial differences between women with coronary heart dis- ease and cardiac syndrome X. Eur Heart J 2004; 25 (19): 1695-701.
• Halliwell B, Gutteridge JMC. Free radicals in biology and medicine. Third ed. Oxford: Oxford Science Pub- lications; 2000: 617-24.
• Young IS, McEneny J. Lipoprotein oxidation and ath- erosclerosis. Biochem Soc Transact 2001; 29 (2):358- 62.
• Salonen RM, Nyyssonen K, Kaikkonen J, et al. Six- year effect of combined vitamin C and E supplemen- tation on atherosclerotic progression: the Antioxi- dant Supplementation in Atherosclerosis Prevention (ASAP) Study. Circulation 2003 25; 107 (7):947-53.
• Witztum JL, Steinberg D. The oxidative modification hypothesis of atherosclerosis: does it hold for hu- mans? Trends Cardiovasc Med 2001; 11 (3-4):93-102.
• Tribble DL. AHA Science Advisory. Antioxidant con- sumption and risk of coronary heart disease: empha- sis on vitamin C, vitamin E, and beta-carotene. A state- ment for healthcare professionals from the American Heart Association. Circulation 1999; 99 (4):591-5.
• Erel O. A novel automated method to measure total antioxidant response against potent free radical reac- tions. Clin Biochem 2004; 37 (2):112- 9.
• Aydın M, Selcoki Y, Nazlı Y, et al. Relationship be- tween total antioxidant capacity and the severity of coronary artery disease. J Clin Exp Invest 2012;3 (1); 22-8.
• Kosecik M, Erel O, Sevinc E, Selek S. Increased oxi- dative stress in children exposed to passive smoking. Int J Cardiol 2005; 100 (1):61-4.
• Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem 2005; 38 (12):1103-11.
• Gürbüz GD, Ulaş T, Paksoy F, et al. The effect of in- travenous iron therapy on total antioxidant capacity in patients with iron deficiency anemia. J Clin Exp Invest 2011;2 (3); 287-91.
• Arab K, Steghens JP. Plasma lipid hydroperoxides measurement by an automated xylenol orange meth- od. Analytical Biochemistry 2004; 325 (1):158-63.
• Demirbag R, Yilmaz R, Erel O, Gultekin U, Asci D, Elbasan Z. The relationship between potency of oxi- dative stress and severity of dilated cardiomyopathy. Can J Cardiol 2005; 21(10):851-5.
• Stringer MD, Görög PG, Freeman A, Kakkar VV. Lipid peroxides and atherosclerosis. Br Med J 1989; 298 (6669):281-4.
• Kovacs IB, Jahangiri M, Rees GM, Görög P. Elevated plasma lipid hydroperoxides in patients with coronary artery disease. Am Heart J 1997; 134 (3):572-6.
• Kashyap MK, Yadav V, Sherawat BS, et al. Different antioxidants status, total antioxidant power and free radicals in essential hypertension. Mol Cell Biochem 2005; 277 (1-2):89-99.
• Robertson RP, Harmon J, Tran PO, Tanaka Y, Taka- hashi H. Glucose toxicity in beta-cells: Type 2 diabe- tes, good radicals gone bad, and the glutathione con- nection. Diabetes 2003; 52 (3): 581-7.
• Fang JC, Kinlay S, Beltrame J, et al. Effect of vita- mins C and E on progression of transplant-associated arteriosclerosis: a randomized trial. Lancet 2002;359 (9312):1108-13
• Rueckschloss U, Quinn MT, Holtz J, Morawietz H. Dose-dependent regulation of NAD(P)H oxidase expression by angiotensin II in human endothelial cells: protective effect of angiotensin II type 1 recep- tor blockade in patients with coronary artery disease. Arterioscler Thromb Vasc Biol 2002; 22 (11):1845-51.