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Volume 197, Issue 2, Pages 556-563 (April 2008)


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Paraoxonase activity and coronary heart disease risk in healthy middle-aged males: The PRIME study

J.A. Troughtona, J.V. WoodsideaCorresponding Author Informationemail address, J.W.G. Yarnella, D. Arveilerb, P. Amouyelc, J. Ferrièresd, P. Ducimetièree, C.C. Pattersona, G. Lucf, on behalf of the PRIME Study Group1

Received 10 April 2007; received in revised form 11 August 2007; accepted 20 August 2007. published online 27 September 2007.

Abstract 

Objective

Classic coronary heart disease (CHD) risk factors fail to explain the large gradient in CHD incidence between Northern Ireland and France. The Prospective Epidemiological Study of Myocardial Infarction (PRIME) study, a multicentre prospective study of 10,593 middle-aged males, investigated novel risk factors in these populations. We tested the hypotheses that (1) higher paraoxonase activity is associated with decreased CHD risk and (2) PON55 LL genotype is associated with increased CHD risk.

Methods

Paraoxonase activity was measured in 299 men who had developed CHD at 5-year follow-up and in 576 matched controls. DNA was available from 247 cases and 433 controls for genotyping for the PON55 polymorphism.

Results

There was no significant difference in paraoxonase activity between cases and controls (geometric means 73.8 and 74.2U/l; p=0.81). There was no significant difference in CHD risk between fifths of paraoxonase activity either before (p=0.55) or after adjustment for classical risk factors (p=0.58).

There was no significant association between genotype and CHD risk; relative to the LL genotype, the OR (95% CI) for the LM and MM genotypes were 0.92 (0.66–1.29) and 0.83 (0.50–1.36), respectively. The frequency of the L allele in cases (66.6%) and controls (64.5%) did not differ significantly, p=0.45.

Conclusions

These findings suggest that neither paraoxonase activity nor PON55 genotype is associated with CHD risk in males in the PRIME study.

a Faculty of Medicine, Queen's University Belfast, Belfast, Northern Ireland, UK

b Strasbourg MONICA Project, Department of Epidemiology and Public Health, Faculty of Medicine, Strasbourg, France

c Lille MONICA Project, INSERM U508, Pasteur Institute of Lille, Lille, France

d Toulouse MONICA Project, INSERM U588, Department of Epidemiology, Paul Sabatier-Toulouse Purpan University, Toulouse, France

e Coordinating Center, INSERM U258, Hôpital Paul Brousse, Villejuif, France

f The Department of Atherosclerosis, INSERM U545, Institut Pasteur de Lille, Université de Lille 2, Lille, France

Corresponding Author InformationCorresponding author at: Department of Medicine, Mulhouse Building, Grosvenor Road, Belfast BT12 6BJ, UK. Tel.: +44 28 90632585; fax: +44 28 90235900.

PII: S0021-9150(07)00529-1

doi:10.1016/j.atherosclerosis.2007.08.019


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