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Published on: May 10, 2021
Cholesterol efflux promoting function of high-density lipoproteins in calcific aortic valve stenosis
Duygu Kocyigit1, Francesca Zimetti2, Kadri M Gurses3
1Department of Cardiology, Hacettepe University Faculty of Medicine, Ankara, Turkey.
Insights
Cholesterol efflux capacity (HDL-CEC) is reduced in moderate-severe calcific aortic valve stenosis (CAVS). Lower HDL-CEC correlates with CAVS severity and may offer novel therapeutic targets.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Metabolomics
Background:
- Cholesterol efflux capacity (HDL-CEC) is a key measure of reverse cholesterol transport.
- The role of HDL-CEC in calcific aortic valve stenosis (CAVS) remains incompletely understood.
- CAVS is a progressive disease affecting aortic valve function.
Purpose of the Study:
- To investigate the relationship between HDL-CEC and CAVS severity.
- To explore associations between HDL-CEC, osteogenic biomarkers, and metabolites in CAVS patients.
- To identify potential therapeutic targets for CAVS.
Main Methods:
- Evaluated HDL-CEC in patients with varying degrees of CAVS using echocardiography and cardiac CT.
- Measured biomarkers of osteogenic activity and tissue remodeling.
- Analyzed dietary and gut microbiota-derived metabolites.
Main Results:
- Patients with moderate-severe CAVS exhibited significantly lower HDL-CEC compared to controls.
- HDL-CEC negatively correlated with CAVS severity indicators (aortic jet velocity, calcium score).
- HDL-CEC showed independent associations with aortic valve calcium score, GFR, and total cholesterol.
Conclusions:
- Impaired HDL-CEC is associated with moderate-severe CAVS.
- Findings suggest HDL-CEC may be a potential therapeutic target for CAVS management.
- Further research into HDL-CEC modulation could benefit CAVS patients.
Background And Aims:
Cholesterol efflux capacity is a functional property of high-density lipoproteins (HDL) reflecting the efficiency of the atheroprotective reverse cholesterol transport process in humans. Its relationship with calcific aortic valve stenosis (CAVS) has not been fully assessed yet.
Methods:
We evaluated HDL-CEC in a patient population with varying degrees of aortic valvular calcific disease, assessed using echocardiography and cardiac computed tomography. Measurement of biomarkers that reflect osteogenic and tissue remodeling, along with dietary and gut microbiota-derived metabolites were performed.
Results:
Patients with moderate-severe CAVS had significantly lower HDL-CEC compared to both control and aortic sclerosis subjects (mean: 6.09%, 7.32% and 7.26%, respectively). HDL-CEC displayed negative correlations with peak aortic jet velocity and aortic valve calcium score, indexes of CAVS severity (ρ = -0.298, p = 0.002 and ρ = -0.358, p = 0.005, respectively). In multivariable regression model, HDL-CEC had independent association with aortic valve calcium score (B: -0.053, SE: 0.014, p < 0.001), GFR (B: -0.034, SE: 0.012, p = 0.007), as well as with levels of total cholesterol (B: 0.018, SE: 0.005, p = 0.002).
Conclusion:
These results indicate an impairment of HDL-CEC in moderate-severe CAVS and may contribute to identify potential novel targets for CAVS management.
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