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Published on: October 12, 2017
Serum- and HDL3-serum amyloid A and HDL3-LCAT activity are influenced by increased CVD-burden
Jane McEneny1, Peter McKavanagh2, Edmund York1
1Centre for Public Health, Queen's University Belfast, Belfast, United Kingdom.
Insights
Increased serum amyloid-A (SAA) inflammation is linked to higher cardiovascular disease (CVD) burden. SAA may negatively impact high-density lipoprotein (HDL) function, suggesting its potential as a CVD biomarker.
Area of Science:
- Cardiovascular Medicine
- Inflammation Research
- Lipoprotein Metabolism
Background:
- High-density lipoproteins (HDL) are protective against cardiovascular disease (CVD).
- Increased serum amyloid-A (SAA) related inflammation may counteract HDL's protective effects.
- The relationship between SAA and CVD burden requires further investigation.
Purpose of the Study:
- To investigate the association between SAA and the burden of CVD.
- To determine if SAA levels correlate with atherosclerotic plaque presence and severity.
- To explore the impact of SAA on HDL subfractions and their function.
Main Methods:
- 240 subjects from a chest pain clinic underwent CT angiography for atherosclerotic burden assessment.
- Subjects were categorized into no-CVD, non-obstructive-CVD (<50% stenosis), and moderate/significant-CVD (≥50% stenosis) groups.
- HDL subfractions (HDL2, HDL3) were isolated, and SAA concentration and LCAT activity were measured.
Main Results:
- Moderate/significant CVD group showed higher serum SAA and HDL3-SAA, and lower HDL3-LCAT activity compared to other groups.
- Positive correlations were found between serum SAA and HDL3-SAA, and between CVD burden and SAA markers.
- Negative correlations were observed between HDL3-LCAT activity and SAA markers, and CVD burden.
Conclusions:
- Elevated SAA-related inflammation is associated with increased CVD burden.
- SAA appears to diminish the antiatherogenic properties of HDL.
- SAA may serve as a potential biomarker for increased CVD burden, warranting further research.
Background:
High density lipoproteins (HDL) protect against cardiovascular disease (CVD). However, increased serum amyloid-A (SAA) related inflammation may negate this property. This study investigated if SAA was related to CVD-burden.
Methods:
Subjects referred to the rapid chest pain clinic (n = 240) had atherosclerotic burden assessed by cardiac computerised tomography angiography. Subjects were classified as: no-CVD (n = 106), non-obstructive-CVD, stenosis<50% (n = 58) or moderate/significant-CVD, stenosis ≥50% (n = 76). HDL was subfractionated into HDL2 and HDL3 by rapid-ultracentrifugation. SAA-concentration was measured by ELISA and lecithin cholesterol acyltransferase (LCAT) activity measured by a fluorimetric assay.
Results:
We illustrated that serum-SAA and HDL3-SAA-concentration were higher and HDL3-LCAT-activity lower in the moderate/significant-CVD-group, compared to the no-CVD and non-obstructive-CVD-groups (percent differences: serum-SAA, +33% & +30%: HDL3-SAA, +65% and +39%: HDL3-LCAT, -6% & -3%; p < 0.05 for all comparisons). We also identified a positive correlation between serum-SAA and HDL3-SAA (r = 0.698; p < 0.001) and a negative correlation between HDL3-SAA and HDL3-LCAT-activity (r = -0.295; p = 0.003), while CVD-burden positively correlated with serum-SAA (r = 0.150; p < 0.05) and HDL3-SAA (r = 0.252; p < 0.001) and negatively correlated with HDL3-LCAT-activity (r = -0.182; p = 0.006). Additionally, multivariate regression analysis adjusted for age, gender, CRP and serum-SAA illustrated that HDL3-SAA was significantly associated with modifying CVD-risk of moderate/significant CVD-risk (p < 0.05).
Conclusion:
This study has demonstrated increased SAA-related inflammation in subjects with moderate/significant CVD-burden, which appeared to impact on the antiatherogenic potential of HDL. We suggest that SAA may be a useful biomarker to illustrate increased CVD-burden, although this requires further investigation.
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