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C-reactive protein gene haplotypes and risk of coronary heart disease: the Rotterdam Study

Isabella Kardys1, Moniek P M de Maat, André G Uitterlinden

  • 1Department of Epidemiology and Biostatistics, Erasmus MC, PO Box 1738, 3000 DR Rotterdam, The Netherlands.

European Heart Journal
|May 10, 2006
PubMed

Insights

C-reactive protein (CRP) gene variations influence CRP levels but do not appear to significantly impact coronary heart disease risk. This study found no strong genetic link between CRP haplotypes and heart disease occurrence.

Area of Science:

  • Genetics
  • Cardiovascular Medicine
  • Immunology

Background:

  • C-reactive protein (CRP) is a known risk factor for cardiovascular disease (CVD).
  • It remains unclear if CRP is merely a marker of CVD severity or actively participates in its pathogenesis.
  • Understanding the genetic influence on CRP is crucial for elucidating its role in CVD.

Purpose of the Study:

  • To investigate the relationship between C-reactive protein gene haplotypes and the risk of coronary heart disease (CHD).
  • To determine if common variations in the CRP gene influence the occurrence of CHD.

Main Methods:

  • The Rotterdam Study, a prospective population-based cohort of individuals aged 55 and older.
  • Analysis of four common C-reactive protein haplotypes and their association with CHD risk.
  • Assessment of C-reactive protein serum levels across different haplotypes.

Main Results:

  • Elevated C-reactive protein levels were associated with an increased risk of coronary heart disease (HR 1.9).
  • Significant differences in C-reactive protein serum levels were observed among the four C-reactive protein haplotypes.
  • However, C-reactive protein haplotypes were not found to be associated with coronary heart disease.

Conclusions:

  • C-reactive protein gene haplotypes influence steady-state C-reactive protein serum levels.
  • Despite CRP being a strong risk factor for cardiovascular disease, common variations in the CRP gene do not appear to have a substantial effect on the incidence of coronary heart disease.
Abstract

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