European Heart Journal Advance Access published online on April 11, 2005
European Heart Journal, doi:10.1093/eurheartj/ehi222
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1 Department of Nutrition, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Department of Epidemiology, S. Daniel Abraham International Center for Health and Nutrition, Ben-Gurion University, Beer-Sheva, Israel
* To whom correspondence should be addressed. Aims With its homology with plasminogen, lipoprotein(a) [Lp(a)] may be related to thrombosis and inflammation. We assessed the role of Lp(a) in coronary heart diseases (CHD) by a recently developed assay that is not affected by the plasminogen-like Kringle-type- 2 repeats. Methods and results Of 32 826 women from the Nurses' Health Study, who provided blood at baseline, we documented 228 CHD events during 8 years of follow-up. Each case was compared with two matched controls. In a multivariable model adjusted for body mass index, family history, hypertension, diabetes, post-menopausal hormone use, physical activity, blood drawing characteristics, and alcohol intake, the odd ratio (OR) for Lp(a) levels Conclusion Lp(a) levels >30 mg/dL are associated with twice the risk of CHD events among women and may be related to thrombosis and inflammation.
Received May 21, 2004
Revised December 21, 2004
Accepted February 17, 2005
Clinical research
Lipoprotein (a) and coronary heart disease among women: beyond a cholesterol carrier?
2 Department of Nutrition, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Channing Laboratory, Department of Medicine, Brigham Women Hospital and Harvard Medical School, Boston, MA, USA
3 Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Channing Laboratory, Department of Medicine, Brigham Women Hospital and Harvard Medical School, Boston, MA, USA
4 Merck Research Laboratories, Merck & Co. Inc., Whitehouse Station, NJ, USA
5 Channing Laboratory, Department of Medicine, Brigham Women Hospital and Harvard Medical School, Boston, MA, USA
6 Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Channing Laboratory, Department of Medicine, Brigham Women Hospital and Harvard Medical School, Boston, MA, USA; Division of preventive medicine, Department of Medicine, Brigham Women Hospital and Harvard Medical School, Boston, MA, USA
7 Department of Laboratory Medicine, Children's Hospital and Harvard Medical School, Boston, MA, USA
Iris Shai, E-mail: ishai{at}hsph.harvard.edu
Abstract 
30 mg/dL was 1.9(95% CI: 1.3-3.0) when compared with those with Lp(a)<30 mg/dL. Women with high levels of both Lp(a) (30 mg/dL) and fibrinogen (400 mg/dL) had an OR of 3.2(95% CI: 1.6-6.5) for CHD, when compared with the combination of low levels (P interaction=0.05). Women with high levels of both Lp(a) and C-reactive protein (3 mg/L) had an OR of 3.67(95% CI: 2.03-6.64) for CHD, when compared with the combination of low levels (P interaction=0.06).
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