Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl


Preferences help
enabled [disable] Abstract
Number of results


2009 | 4 | 1 | 26-31

Article title

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


Title variants

Languages of publication



In 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.










Physical description


1 - 3 - 2009
11 - 2 - 2009


  • Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
  • Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
  • Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
  • Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
  • Department of Pathophysiology, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
  • Department of Experimental Medicine, Faculty of Medicine, Safarik University, 04066, Košice, Slovakia
  • Eastern Slovak Cardiovascular Institute, 04001, Košice, Slovakia
  • Eastern Slovak Cardiovascular Institute, 04001, Košice, Slovakia


  • [1] 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 http://dx.doi.org/10.1073/pnas.86.12.4695[Crossref]
  • [2] Grech E.D., Jackson M.J., Ramsdale D.R., Reperfusion injury after acute myocardial Infarction, Br. Med. J., 1995, 77, 477–478
  • [3] 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.
  • [4] 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 http://dx.doi.org/10.1016/S0002-8703(96)90344-0[Crossref]
  • [5] 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 http://dx.doi.org/10.1056/NEJM199303113281001[Crossref]
  • [6] 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 http://dx.doi.org/10.1056/NEJM199303113281002[Crossref]
  • [7] 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
  • [8] 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
  • [9] Rice Evans C., Miller N.J.: Total antioxidant status in plasma and body fluids, Methods Enzymol. 1994, 234, 279–293 http://dx.doi.org/10.1016/0076-6879(94)34095-1[Crossref]
  • [10] 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 http://dx.doi.org/10.1097/00019501-199309000-00003[Crossref]
  • [11] 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
  • [12] 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 http://dx.doi.org/10.1016/S0002-9149(01)02237-8[Crossref]
  • [13] 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 [Crossref]
  • [14] 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 http://dx.doi.org/10.1016/0891-5849(95)94361-G[Crossref]
  • [15] 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 http://dx.doi.org/10.1080/10715760400028027[Crossref]
  • [16] 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 http://dx.doi.org/10.3109/10715769809097873[Crossref]
  • [17] 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 http://dx.doi.org/10.1080/14017430260180409[Crossref]
  • [18] 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 http://dx.doi.org/10.1016/S0002-9149(98)00688-2[Crossref]
  • [19] 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 http://dx.doi.org/10.1016/0002-8703(94)90368-9[Crossref]
  • [20] 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 http://dx.doi.org/10.1016/S0002-9149(96)90580-9[Crossref]
  • [21] 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
  • [22] 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
  • [23] 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
  • [24] 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 http://dx.doi.org/10.1016/j.cardiores.2006.12.007[WoS][Crossref]
  • [25] 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 http://dx.doi.org/10.1152/ajpheart.00223.2005[Crossref]

Document Type

Publication order reference


YADDA identifier

JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.