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European Heart Journal Advance Access published online on September 4, 2006
European Heart Journal, doi:10.1093/eurheartj/ehl230
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European Heart Journal © The European Society of Cardiology 2006; all rights reserved
Received March 16, 2006
Revised April 8, 2006
Accepted August 17, 2006

Clinical research

Lipoprotein-associated phospholipase A2 activity and risk of heart failure: the Rotterdam Study

Laura C. van Vark 1, Isabella Kardys 1, Gysèle S. Bleumink 2, Anneke M. Knetsch 1, Jaap W. Deckers 3, Albert Hofman 1, Bruno H.Ch. Stricker 1, and Jacqueline C.M. Witteman 1 *

1 Department of Epidemiology and Biostatistics, Erasmus Medical Center, PO Box 2040, 3000 CA Rotterdam, The Netherlands
2 Department of Epidemiology and Biostatistics, Erasmus Medical Center, PO Box 2040, 3000 CA Rotterdam, The Netherlands; Department of Internal Medicine, Albert Schweitzer Hospital, Dordrecht, The Netherlands
3 Department of Cardiology, Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands

* To whom correspondence should be addressed.
Jacqueline C.M. Witteman, E-mail: j.witteman{at}erasmusmc.nl


  Abstract

Aims Evidence is accumulating that inflammation plays a role in the pathophysiology of heart failure. Lipoprotein-associated phospholipase A2 (Lp-PLA2) has pro-inflammatory properties. We investigated whether Lp-PLA2 activity is associated with heart failure.

Methods and results Lp-PLA2 activity was determined in a random sample of 1820 subjects from the Rotterdam Study, a population-based cohort study among persons aged 55 years and over. During a mean follow-up of 6.7 years, 94 heart failure cases occurred. We excluded participants with heart failure or coronary heart disease at baseline and we accounted for incident coronary heart disease during follow-up. We used Cox proportional hazard models to compute hazard ratios adjusted for age, sex, non-HDL cholesterol, HDL cholesterol, body mass index, systolic blood pressure, diastolic blood pressure, hypertension, diabetes mellitus, smoking, and C-reactive protein. The hazard ratio per unit increase of Lp-PLA2 activity was 1.03 [95% confidence interval (95% CI 1.01-1.05]; P for trend was 0.011. Hazard ratios for the second, third, and fourth quartiles were 1.06 (95% CI 0.55-2.04), 1.43 (95% CI 0.73-2.81), and 2.33 (95% CI 1.21-4.49), respectively, using the lowest quartile of Lp-PLA2 activity as the reference category.

Conclusion This study suggests that Lp-PLA2 activity is independently associated with incident heart failure.

Keywords: Heart failure; Inflammation; Epidemiology.
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