No increase of plasma malondialdehyde after primary coronary angioplasty for acute myocardial infarction.

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Aström Olsson, Karin (author)

No increase of plasma malondialdehyde after primary coronary angioplasty for acute myocardial infarction.

Article/chapterEnglish2002

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2009-07-12
Informa UK Limited,2002

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LIBRIS-ID:oai:lup.lub.lu.se:dbea2743-ec0d-4dc9-b547-e11020b09c44
https://lup.lub.lu.se/record/110436URI
https://doi.org/10.1080/14017430260180409DOI

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Language:English
Summary in:English

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Subject category:ref swepub-contenttype

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OBJECTIVE: Free radicals formed after coronary artery occlusion and reperfusion are assumed to produce myocardial stunning and possibly other forms of reperfusion injury as well. Malondialdehyde (MDA) is an end product in the lipid peroxidation chain reaction and is frequently used as a marker for free oxygen radical production. Increased levels of plasma MDA have been found following successful thrombolytic therapy. The aim of this study was to investigate whether plasma MDA levels also increase after successful primary percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI). DESIGN: In 23 patients with AMI, treated with primary PTCA, plasma MDA was analysed using a high-performance liquid chromatography method (HPLC). The results obtained with this method were compared with those obtained with a fluorimetric assay of thiobarbituric acid reactive substances (TBARS). This assay measures MDA but with a lower specificity. RESULTS: We found a significant decrease of plasma MDA from baseline 0.99 to 0.87 micro mol/l at 30 min and to 0.90 micro mol/l at 90 min following the primary PTCA (p = 0.048 and 0.014, respectively). No significant changes in TBARS method levels were observed. CONCLUSION: Instead of the expected increase in MDA following reperfusion we found a significant decrease. The results from measurements of MDA and TBARS were significantly incompatible. The results raise serious doubts as to the usefulness of increased plasma levels of MDA as a marker of oxidative stress caused by coronary reperfusion in patients treated with angioplasty.

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Harnek, JanLund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)drad-jha (author)
Öhlin, Ann-KristinLund University,Lunds universitet,Avdelningen för klinisk kemi och farmakologi,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Chemistry and Pharmacology,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)kkem-ako (author)
Pavlidis, Natascia (author)
Thorvinger, BjörnLund University,Lunds universitet,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)drad-bth (author)
Öhlin, HansLund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)kard-hoh (author)
KardiologiSektion II (creator_code:org_t)

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In:Scandinavian Cardiovascular Journal: Informa UK Limited36:4, s. 237-2401651-20061401-7431

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