Markers of oxidative stress in acute myocardial infarction treated by percutaneous coronary intervention

Walter de Gruyter GmbH - Tập 4 Số 1 - Trang 26-31 - 2009
Eva Sedláková1, Olivér Rácz1, Eva Lovásová1, Roman Beòaèka1, Martin Kurpas1, Anna Chmelařová2, J Sedlák3, Martin Studenèan3
11Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
22Department of Experimental Medicine, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
33Eastern Slovak Cardiovascular Institute, 04001, Košice, Slovakia

Tóm tắt

AbstractIn the current study, we evaluated the dynamics of oxidative stress markers in patients with acute myocardial infarction (AMI) treated by primary percutaneous coronary intervention (PCI). Thirty consecutive patients with AMI with ST elevation were included. Plasma lipid peroxidation end product malondialdehyde (MDA) and total antioxidant capacity (TAC) in blood plasma were evaluated. Peripheral venous blood samples were obtained prior to reperfusion and at five time points after reperfusion. The control group consisted of 20 ischemic patients without acute coronary syndrome. TAC in the AMI group at admission was lower than in control patients (1.26 + 0.32 vs. 1.52 + 0.24 mmol/l). Within 1 h after reperfusion, in most cases, values significantly declined (1 min, 1.10 + 0.33 mmol/l; 1 h, 1.06 + 0.21 mmol/l [p= 0.03]). After 3 h, values began to increase (1.14 + 0.29 mmol/l) and returned to basal values after 3 d (1.29 + 0.24 mmol/l). MDA levels in AMI patients at admission were higher than in control patients (1.66 + 0.55 vs. 1.44 + 0.55 mmol/l) but showed a sustained decrease over the 3 h after reperfusion of the occluded artery (1 min, 1.57 + 0.37 mmol/l; 1 h, 1.50 + 0.35 μmol/l; 3 h, 1.35 + 0.59 μmol/l [p = 0.03]). Reperfusion of the occluded coronary artery by PCI in AMI lead to an immediate decrease in TAC, suggesting formation of reactive oxygen species. However, the MDA level significantly decreased after reperfusion. This may suggests less reperfusion injury after PCI.

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Tài liệu tham khảo

Bolli R., Jeroudi M.O., Patel B.S., DuBose C.M., Lai E.K., Roberts R., et al., Direct evidence that oxygenderived free radicals contribute to postischemic myocardial dysfunction in the intact dog, Proc. Natl. Acad. Sci. USA, 1989, 86, 4695–4699

Grech E.D., Jackson M.J., Ramsdale D.R., Reperfusion injury after acute myocardial Infarction, Br. Med. J., 1995, 77, 477–478

Mužáková V., Kand’ár R., Vojtíšek P., Skalicky J., Vankova R., Cegan A., et al., Antioxidants Vitamin levels and Glutathione Peroxidase Activity During Ischemia/Reperfusion in Myocardial Infarction, Physiol. Res., 2001, 50, 389–396.

Lafont A., Marwick T.H., Chisolm G.M., Van Lente F., Vaska K.J., Whitlow P.L., Decreased free radical scavengers with reperfusion after coronary angioplasty in patient with acute myocardial infarction, Am Heart J. 1996, 131, 219–23

Grines C.L., Browne J.M., Marco J., Rothbaum D., Stone G.W., O’Keefe J., et al., A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction, N. Engl. J. Med., 1993, 10, 673–679

Zijlstra F., De Boer M.J., Hoornje J., Reiffers S., Reiber J.H., Suryapranata H., A Comparison of Immediate Coronary Angioplasty with Intravenous Streptokinase in Acute Myocardial Infarction, N. Engl. J. Med., 1993, 10, 680–684

Yagi K., Assay for serum lipid peroxide level and its clinical significance. In: Yagi K., editor. Lipid peroxides in biology and medicine. New York: New York Academic Press, 1982, 223–242

Miller N.J., Rice-Evans C., Davies M.J., Gopinathan V., Milner A., A novel method for measuring capacity and its application to monitoring the antioxidant status in premature neonates, Clin. Sci., 1993, 84, 407–412

Rice Evans C., Miller N.J.: Total antioxidant status in plasma and body fluids, Methods Enzymol. 1994, 234, 279–293

Grech E.D., Jack C.I., Bleasdale C., Jackson M.J., Baines M., Faragher E.B. et al., Differential freeradical activity after successful and unsuccessful thrombolytic reperfusion in acute myocardial infarction, Coron. Artery Dis., 1993, 4, 769–774

Beard T., Carrie D., Boyer M.J., Boudjemaa B., Ferrières J., Delay M. et al., Production of oxygen free radicals in myocardial infarction treated by thrombolysis. Analysis of glutathione peroxidase, superoxide dismutase and malondialdehyde, Arch. Mal. Coeur. Vaiss., 1994, 87, 1289–1296

Iqbal K., Rauoof M.A., Mir M.M., Tramboo N.A., Malik J.A., Naikoo B.A., et al., Lipid peroxidation during acute coronary syndromes and its intensification at the time of myocardial ischemia reperfusion, Am. J. Cardiol., 2002, 89, 334–337

Young I.S., Purvis J.A., Lightbody J.H., Adgey A.A., Trimble E.R., Lipid peroxidation and antioxidant status following thrombolytic therapy for acute myocardial infarction, Eur. Heart J., 1993, 14, 1027–1033

Pucheu S., Coudray C.H., Vanzetto G., Favier A., Machecourt J., de Leiris J., Assesment of radical activity during the acute phase of myocardial infarction following fibrinolysis: Utility of assaying plasma malondialdehyde, Free Radic. Biol. Med., 1995, 19, 873–881

Berg K., Jynge P., Bjerve K., Skarra S., Basu S., Wiseth R., Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction, Free Radic Res. 2005, 6, 629–636

Tavazzi B., Di Pierro D., Bartolini M., Marino M., Distefano S., Galvano M., et al., Lipid peroxidation, tissue necrosis, and metabolic and mechanical recovery of isolated reperfused rat heart as a function of increasing ischemia, Free Radic. Res., 1998, 1, 25–37

Olsson K.A., Harnek J., Ohlin A.K., Pavlidis N., Thorvinger B., Ohlin H., No increase of plasma malondialdehyde after primary coronary angioplasty for acute myocardial infarction, Scand Cardiovasc J. 2002, 36, 237–40

Ohlin E., Pavlidis N., Ohlin A.K., Effect of intravenous nitroglycerin on lipid peroxidation after thrombolytic therapy for acute myocardial infarction, Am. J. Cardiol., 1998, 82, 1463–1467

Grech E.D., Bellamy C.M., Jackson M.J., Muirhead R.A., Faragher E.B., Ramsdale D.R., Free-radical activity after primary coronary angioplasty in acute myocardial infarction, Am. Heart J., 1994, 127, 1443–1449

Grech E.D., Dodd J.F., Jackson M.J., Morrison W.L., Faragher E.B., Ramsdale D.R., Evidence for free radical generation after primary percutaneous transluminal coronary angioplasty recanalization in acute myocardial infarction, Am J Cardiol. 1996, 77, 122–127

Ceconi C., Cargoni A., Pasini E., Condorelli E., Curello S., Ferrari R., Evaluation of phospholipid peroxidation as malondialdehyde during myocardial ischemia and reperfusion injury, Am. J. Physiol. Heart Circ. Physiol., 1991, 260, H1057–H1061

Tukozkan N., Erdamar H., Seven I., Measurement of total malondialdehyde in plasma and tissues by high-performance liquid chromatography and thiobarbituric acid assay, Firat Tip Dergisi, 2006, 11, 88–92

Janssen M., Koster J.F., Bos E., De Jong J.W., Malondialdehyde and glutathione production in isolated perfused human and rat hearts, Circ. Res., 1993, 73, 681–688

Milei J., Forcada P., Fraga C.G., Grana D.R., Iannelli G., Chiariello M., et al., Relationship between oxidative stress, lipid peroxidation, and ultrastructural damage in patients with coronary artery disease undergoing cardioplegic arrest/reperfusion, Cardiovasc. Res. 2007, 73, 710–719

Angelos M.G., Kutala V.K., Torres C.A., He G., Stoner J.D., Mohammad M., et al.: Hypoxic reperfusion of the ischemic heart and oxygen radical generation, Am. J. Physiol. Heart Circ. Physiol., 2006, 290, H341–347

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Walter de Gruyter GmbH

Tập 4 Số 1

26-31

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