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European Heart Journal Advance Access originally published online on March 11, 2005
European Heart Journal 2005 26(9):890-896; doi:10.1093/eurheartj/ehi186
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence short-term prognosis after acute coronary syndrome: results from the MIRACL trial

Anders G. Olsson1,*, Gregory G. Schwartz2, Michael Szarek3, William J. Sasiela3, Michael D. Ezekowitz4, Peter Ganz5, Michael F. Oliver6, David Waters7 and Andreas Zeiher8

1Department of Medicine and Care, Internal Medicine, University of Linköping, SE-58185 Linköping, Sweden
2VA Medical Center and University of Colorado Health Sciences Center, Denver, CO, USA
3Pfizer, New York, NY, USA
4MCP Hahnemann University, Philadelphia, PA, USA
5Brigham and Womens Hospital, Harvard Medical School, Boston, MA, USA
612 Narrow Street, London, UK
7San Francisco General Hospital and University of California, San Francisco, CA, USA
8Johann Wolfgang Goethe University, Frankfurt, Germany

Received 20 October 2004; revised 25 January 2005; accepted 27 January 2005; online publish-ahead-of-print 11 March 2005.

* Corresponding author. Tel: +46 13 222102; fax: +46 13 149991. E-mail address: andol{at}imv.liu.se

See page 853 for the editorial comment on this article (doi:10.1093/eurheartj/ehi218)

Aims Patients with acute coronary syndrome (ACS) in the Myocardial Ischaemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study had diminished cardiovascular events after 16 weeks of treatment of atorvastatin 80 mg daily. We determined whether plasma lipoproteins at baseline and then at 6 weeks after randomization predicted clinical outcome.

Methods and results Cox proportional hazards models were constructed to determine relations between lipoproteins and clinical endpoint events. Baseline LDL cholesterol (LDL-C) did not predict outcome. In contrast, baseline HDL-C predicted outcome with a hazard ratio of 0.986 per mg/dL increment in HDL-C, P<0.001, indicating 1.4% reduction in risk for each 1 mg/dL increase in HDL-C. Atorvastatin treatment profoundly lowered LDL-C, but had minimal effect on HDL-C. Neither Week 6 LDL-C nor absolute change of LDL-C from baseline by Week 6 had any significant impact on clinical endpoints occurring between Week 6 and Week 16 after randomization.

Conclusion Plasma HDL-C, but not LDL-C, measured in the initial stage of ACS predicts the risk of recurrent cardiovascular events over the ensuing 16 weeks. LDL-C reduction does not account for the clinical risk reduction with atorvastatin treatment after ACS. This finding may suggest that the clinical benefit of atorvastatin after ACS is mediated by qualitative changes in the LDL particle and/or by non-lipid (pleiotropic) effects of the drug.

Key Words: Acute coronary syndrome • Intervention study • Lipoprotein • Statin


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