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Published on: November 10, 2017
Moderate statin treatment reduces prebeta-1 high-density lipoprotein levels in dyslipidemic patients
Alex G Quinn1, Rachel Schwemberger1, Eveline Oestreicher Stock2
1Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Insights
Statin therapy significantly reduces prebeta-1 high-density lipoprotein (HDL), a marker linked to coronary heart disease risk. This reduction is associated with decreased triglycerides, suggesting a beneficial impact on cholesterol efflux.
Area of Science:
- Cardiovascular Medicine
- Lipid Metabolism
- Pharmacology
Background:
- Elevated prebeta-1 high-density lipoprotein (HDL) is linked to increased atherosclerotic coronary heart disease risk.
- Prebeta-1 HDL is the primary acceptor of cholesterol effluxed from macrophages.
Purpose of the Study:
- To evaluate the impact of a 6-week moderate-dose statin treatment on prebeta-1 HDL levels.
- To understand the relationship between statin therapy, lipid profiles, and prebeta-1 HDL.
Main Methods:
- 101 patients with hypercholesterolemia or combined hyperlipidemia were treated with statins (mean atorvastatin potency equivalence 23.6 mg/d) for 6 weeks.
- Prebeta-1 HDL levels were measured using immunofixation of agarose gels with anti-apolipoprotein A-1 antibody before and after treatment.
- Lipid profiles, including LDL cholesterol and triglycerides, were assessed.
Main Results:
- Statin treatment resulted in a 42.0% reduction in LDL cholesterol and a 22.3% decrease in triglycerides.
- Prebeta-1 HDL levels significantly decreased by 17.9% post-treatment (P < .001).
- The reduction in prebeta-1 HDL was strongly correlated with triglyceride reduction, not LDL cholesterol reduction.
Conclusions:
- Statin therapy effectively reduces prebeta-1 HDL levels, a marker associated with coronary heart disease.
- The observed reduction in prebeta-1 HDL may be partly due to decreased triglycerides and potentially a direct beneficial effect on cholesterol efflux.
- These findings highlight a potential mechanism for statins' cardioprotective effects beyond LDL reduction.
Background:
Elevated plasma levels of prebeta-1 high-density lipoprotein (HDL), the principal acceptor of cholesterol effluxed from macrophages, are associated with increased risk of atherosclerotic coronary heart disease and myocardial infarction.
Objective:
The objective of the study was to assess the effects on prebeta-1 HDL levels of 6-week moderate-dose statin treatment.
Methods:
We studied 101 patients (mean age 52.7 years; 53.5% female; 63 with primary hypercholesterolemia; 38 with combined hyperlipidemia) before and after treatment with statins. Mean atorvastatin potency equivalence was 23.6 mg/d. Prebeta-1 HDL plasma levels were measured by immunofixation of agarose gels using anti-apolipoprotein A-1 antibody.
Results:
We observed a 42.0% reduction of low-density lipoprotein cholesterol (181 ± 56 vs 105 mg/dL, P < .001). Triglyceride (TG) levels decreased by 22.3% (157 vs 122 mg/dL, P < .001), HDL cholesterol levels remained similar (56.0 vs 57.1, P = NS). Levels of prebeta-1 HDL were significantly reduced by 17.9% after statin treatment (mean 11.4 vs 9.4 mg apoA-1/dL, P < .001). The magnitude of this decrease was similar with each of 3 statins (atorvastatin, simvastatin, and rosuvastatin). The decrease in prebeta-1 HDL was strongly associated with the decline in TG, but not with the decline in low-density lipoprotein cholesterol.
Conclusions:
The association of high prebeta-1 HDL with coronary heart disease identifies it as an inferential measure of the rate of cholesterol efflux from the artery wall. Our observations demonstrate a reduction of prebeta-1 HDL with statin therapy, partially reflecting the reduced TGs, and probably reflecting a direct beneficial impact on cholesterol efflux.
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