Normal levels of inflammatory markers in treated patients with familial hypercholesterolaemia: a cross-sectional study

Author:

Seed Mary1,Betteridge D John2,Cooper Jackie3,Caslake Muriel4,Durrington Paul N5,Thompson Gilbert R6,Sattar Naveed7,Humphries Steve E3,Neil H Andrew W8

Affiliation:

1. Imperial College Health Services, Charing Cross Hospital, London, UK

2. Department of Medicine, Royal Free and University College London Medical School, London, UK

3. Centre for Cardiovascular Genetics, British Heart Foundation Laboratories, Royal Free and University College London Medical School, London, UK

4. College of Medicine, Veterinary and Life Sciences, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK

5. Cardiovascular Research Group, School of Clinical and Laboratory Sciences, University of Manchester, Manchester, UK

6. Imperial College School of Medicine, Hammersmith Hospital, London, UK

7. Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK

8. Department of Primary Care Health Sciences, University of Oxford, Oxford, UK

Abstract

Objective To assess the relationship of levels of inflammatory risk markers to presence of clinical coronary artery disease (CAD) in patients with treated heterozygous familial hypercholesterolaemia. Design A cross-sectional study of patients on the Simon Broome Familial Hyperlipidaemia Register. Setting Six hospital outpatient clinics in the UK. Participants A total of 211 men and 199 women with heterozygous familial hypercholesterolaemia. Main outcome measures Analysis of conventional risk factors and concentrations of high-sensitivity C-reactive protein (hsCRP), lipoprotein (a), serum intercellular adhesion molecule (sICAM), interIeukin-6 (IL-6) and lipoprotein-associated phospholipase A2 (LpPLA2) mass. Results CAD was present in 104 men and in 55 women; the mean ages of onset were 43.1 and 46.5 years, respectively. On univariate analysis there was a positive relationship of CAD with age, male sex, smoking, IL-6 and sICAM, and an inverse relationship with low-density lipoprotein (LDL) and LpPLA2. On multivariate analysis, age, smoking, low LDL and low LpPLA2 were associated with CAD. When LpPLA2 values were adjusted for apoB and aspirin usage, there was no significant difference between those with and without CAD. Only age and smoking were independently associated with CAD in men, and IL-6 and lipoprotein(a) in women. Conclusions Although on univariate analysis inflammatory marker levels were associated with CAD in these patients, the majority of the associations, including that for hsCRP, disappeared when corrected for smoking and apoB. This may be because atherosclerotic plaques in these statin-treated patients were quiescent or an effect of aspirin usage. In this observational study newer risk markers were not usefully associated with the presence or absence of symptomatic CAD.

Publisher

SAGE Publications

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