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Normal levels of inflammatory markers in treated patients with familial hypercholesterolaemia: a cross-sectional
Mary Seed1, D John Betteridge, Jackie Cooper
1Imperial College Health Services, Charing Cross Hospital , London , UK.
Insights
Inflammatory markers were linked to coronary artery disease (CAD) in familial hypercholesterolaemia patients, but these associations diminished after adjusting for factors like smoking and apoB. Newer risk markers did not prove useful for identifying symptomatic CAD in this study.
Area of Science:
- Cardiovascular Medicine
- Clinical Chemistry
- Genetics and Heredity
Background:
- Familial hypercholesterolaemia (FH) is a genetic disorder leading to high low-density lipoprotein (LDL) cholesterol levels.
- Patients with FH have an increased risk of premature coronary artery disease (CAD).
- Inflammatory processes play a role in the development and progression of atherosclerosis.
Purpose of the Study:
- To investigate the association between inflammatory risk markers and the presence of clinical coronary artery disease (CAD) in patients with treated heterozygous familial hypercholesterolaemia.
- To determine if novel inflammatory markers could serve as predictors of CAD in this specific patient population.
Main Methods:
- A cross-sectional study involving 211 men and 199 women with heterozygous familial hypercholesterolaemia from six UK hospital outpatient clinics.
- Analysis included conventional risk factors and concentrations of high-sensitivity C-reactive protein (hsCRP), lipoprotein(a), serum intercellular adhesion molecule (sICAM), interleukin-6 (IL-6), and lipoprotein-associated phospholipase A2 (LpPLA2).
Main Results:
- Univariate analysis showed associations between CAD and age, male sex, smoking, IL-6, sICAM, and inversely with LDL and LpPLA2.
- Multivariate analysis identified age, smoking, low LDL, and low LpPLA2 as associated with CAD.
- After adjustments for apoB and aspirin, LpPLA2 was no longer significantly associated with CAD. Age and smoking were independently associated in men, while IL-6 and lipoprotein(a) were associated in women.
Conclusions:
- While initial univariate analyses suggested links between inflammatory markers and CAD in FH patients, most associations, including hsCRP, were not significant after adjusting for smoking and apoB.
- The lack of association might be due to quiescent atherosclerotic plaques in statin-treated patients or the effect of aspirin.
- Novel risk markers were not found to be usefully associated with the presence or absence of symptomatic CAD in this observational study.
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), interleukin-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.
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