Copyright © 1993 by the European Society of Cardiology.
© 1993 The Europen Society of Cardiology
Lipid peroxidation and antioxidant status following thrombolytic therapy for acute myocardial infarction


*Department of Clinical Biochemistry, Queen's University of Belfast Belfast, N. Ireland
Regional Medical Cardiology Centre, Royal Victoria Hospital Belfast, N. Ireland
Received 16 November 1993; revised 18 February 1993; .
Correspondence: Dr I. Young, Department of Clinical Biochemistry, Institute of Clinical Science, Royal Victoria Hospital, Grosvenor Road, Belfast BT12 6BA, Northern Ireland
Abstract
We have investigated the timescale of increased lipid peroxidation following successful early thrombolytic therapy for acute myocardial infarction and report for the first time reciprocal changes in plasma chain-breaking antioxidants. Sixty-seven patients were recruited following a first acute myocardial infarction within 6 h of the onset of symptoms and received 70 or 100 mg of recombinant tissue plasminogen activator (Actilyse) as two intravenous bolus injections 30 min apart. Serial blood samples were taken before administration of thrombolytic therapy and after 30 min, 60 min, 90 min, 6 h and 24 h. Coronary artery patency was assessed at 90 min by coronary angiography. Malondialdehyde (MDA), a marker of lipid peroxidation, and the chain-breaking antioxidants alpha-tocopherol, retinol and ascorbate were measured by high performance liquid chromatography. When the coronary artery was patent there was an early rise in plasma MDA (time 0.091 ± 0.05 µmol.l1) with levels peaking at 90 min (1.02 ± 0.06, P<0.05) and returning to baseline by 6 h (0.85 ± 0.06), accompanied by reciprocal decreases in alpha-tocopherol (time 0 7.13 ± 0.34 µmol.mmol1 cholesterol, 90 min 6.64±0.33, P<0.05) and retinol (time 0 1.99±0.10 µmol.l1, 90 min 1.81 ± 0.08, P<0.05). Ascorbate levels did not change significantly until 24 h (time 0 29.5 ± 4.9 µmol.l1, 24 h 22.6 ± 4.4, P<0.05). Where the coronary artery was occluded no changes in these parameters were found except for a late (24 h) fall in ascorbate (time 0 18.5 ± 2.0 mol.l1, 24 h 12.2 ± 2.2, P<0.05). The timescale of changes in MDA and antioxidants supports a role for increased free radical production following successful early thrombolytic therapy for acute myocardial infarction.
Key Words: Free radicals antioxidants myocardial infarction thrombolysis
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
V. P. Palace, M. F. Hill, F. Farahmand, and P. K. Singal Mobilization of Antioxidant Vitamin Pools and Hemodynamic Function After Myocardial Infarction Circulation, January 12, 1999; 99(1): 121 - 126. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. R. Thom, M. Kang, D. Fisher, and H. Ischiropoulos Release of glutathione from erythrocytes and other markers of oxidative stress in carbon monoxide poisoning J Appl Physiol, May 1, 1997; 82(5): 1424 - 1432. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. A. Arstall, J. Yang, I. Stafford, W. H. Betts, and J. D. Horowitz N-Acetylcysteine in Combination With Nitroglycerin and Streptokinase for the Treatment of Evolving Acute Myocardial Infarction : Safety and Biochemical Effects Circulation, November 15, 1995; 92(10): 2855 - 2862. [Abstract] [Full Text] |
||||

