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European Heart Journal 2004 25(10):847-853; doi:10.1016/j.ehj.2004.03.015
Copyright © 2004 by the European Society of Cardiology.
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Clinical research

Influence of isoprostane F2{alpha}-III on reflow after myocardial infarction

Kim Greavesa, Simon R Dixonb, Ivan O'Brien Cokerc, Anthony I Malletc, Metin Vkiranb, Michael J Shattocka, Martin J Fejkab, William W O'Neillb, Roxy Seniord, Simon Redwooda and Michael S Marbera,*

a Department of Cardiology, The Cardiovascular Division, King's College London, St. Thomas' Hospital, London, UK
b Division of Cardiology, William Beaumont Hospital, MI, USA
c Department of Biochemistry, University of Greenwich, London, UK
d Northwick Park Hospital, London, UK

Received June 12, 2003; revised February 26, 2004; accepted March 11, 2004 * Corresponding author. Tel.: +44-207-922-8191; fax: +44-207-960-5659
E-mail address: mike.marber{at}kcl.ac.uk

Aims To investigate whether the vasoconstrictor isoprostane -III (iP-III), released during myocardial reperfusion, contributes to the low/no reflow phenomenon observed following acute myocardial infarction (AMI).

Methods and results Thirteen patients undergoing primary percutaneous coronary intervention (PCI) for AMI had iP-III measured by high-performance liquid and gas chromatography–mass spectrometry. Isoprostane -III concentrations were significantly higher following PCI than in controls (1.5±1.3 vs.16±0.06 nM, ). Mean iP-III concentration correlated positively with ST-segment resolution at 90 min (, ). In the isolated murine heart: (a) coronary vasoconstriction occurred at, or above, iP-III concentrations of 1 µM. From 1 to 10 µM, iP-III induced dose-dependent vasoconstriction () with reduction in coronary flows (f) of 57±5% and 31±4% (percentage baseline), respectively; (b) SQ29548 1 µM completely reversed the vasoconstrictive effects of iP-III 10 µM; (c) SQ29548 1 µM infused during reperfusion following 30 min ischaemia had no effect on CF or infarct volume.

Conclusion Concentrations of iP-III released into the venous circulation during reperfusion following AMI in humans are significantly lower than those required to diminish coronary flow in the murine heart; increased levels indicate successful reperfusion. Inhibition of iP-III has no effect on coronary flow or infarct size in the murine heart, suggesting that iP-III alone does not account for the low/no reflow phenomenon observed following AMI.

Key Words: Myocardial infarction • Isoprostanes • Reperfusion


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J.-L. Cracowski and O. Ormezzano
Isoprostanes, emerging biomarkers and potential mediators in cardiovascular diseases
Eur. Heart J., October 1, 2004; 25(19): 1675 - 1678.
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