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Effects of atorvastatin treatment on the oxidatively modified low density lipoprotein in hyperlipidemic patients
1Lipid Research Group, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Insights
Atorvastatin treatment significantly reduced oxidized low-density lipoprotein (LDL) levels and improved vascular function in hyperlipidemic patients. This cholesterol-lowering drug also altered lysophosphatidylcholine (LPC) composition in oxidized LDL, contributing to better endothelial relaxation.
Area of Science:
- Cardiovascular Pharmacology
- Lipid Metabolism
- Endothelial Function
Background:
- Hyperlipidemia is characterized by elevated plasma lipids, including low-density lipoprotein (LDL)-cholesterol.
- Oxidized LDL (oxLDL) plays a critical role in endothelial dysfunction and the development of atherosclerosis.
- Atorvastatin is a potent HMG-CoA reductase inhibitor used to manage hyperlipidemia.
Purpose of the Study:
- To investigate the effect of atorvastatin on the biochemical composition of oxidized LDL (oxLDL) in hyperlipidemic patients.
- To assess whether atorvastatin treatment modifies the ability of oxLDL to impair endothelium-dependent vascular relaxation.
- To explore the relationship between changes in oxLDL composition and endothelial function.
Main Methods:
- A 4-week study involving 19 type IIa hyperlipidemic patients treated with atorvastatin (10 mg/day) plus dietary therapy.
- Comparison of lipid profiles, oxLDL biochemical content, and ex vivo effects of oxLDL on aortic ring relaxation between atorvastatin-treated and diet-only groups.
- Analysis of lysophosphatidylcholine (LPC) levels and acyl group composition (C16:0, C18:0) within oxLDL.
Main Results:
- Atorvastatin significantly reduced total cholesterol (-23%), LDL-cholesterol (-32%), and triacylglycerol (-19%) levels, while increasing high-density lipoprotein (HDL) by ~9%.
- Oxidized LDL from atorvastatin-treated patients showed a significantly reduced capacity to impair endothelium-dependent relaxation compared to the diet-only group.
- Biochemical analysis revealed an 11% reduction in lysophosphatidylcholine (LPC) in oxLDL from the atorvastatin group, with a shift in LPC acyl moieties from C16:0 to C18:0.
Conclusions:
- Atorvastatin treatment improves endothelial function in hyperlipidemic patients, partly by reducing the detrimental effects of oxidized LDL.
- The observed improvement is associated with a reduction in lysophosphatidylcholine (LPC) levels and alterations in its acyl group composition within oxidized LDL.
- These findings suggest that atorvastatin's beneficial effects on vascular tone involve modifications to the atherogenic properties of LDL.
Abstract:
Atorvastatin is an established HMG-CoA reductase inhibitor which effectively reduces the plasma low density lipoprotein (LDL)-cholesterol level in hyperlipidemic patients. The present study was designed to investigate whether atorvastatin treatment can modify the biochemical content of oxidized LDL in hyperlipidemic patients and the ability of oxidized LDL to impair the endothelium-dependent relaxation of blood vessels. With atorvastatin (10 mg/day) treatment for 4 weeks in 19 type IIa hyperlipidemic patients, total cholesterol level was lowered by 23%, LDL-cholesterol was lowered by 32% and triacylglycerol was lowered by 19% as compared with dietary therapy alone. High density lipoprotein levels increased by approximately 9%. The ability of oxidized LDL from hyperlipidemic patients after atorvastatin treatment to impair the endothelium-dependent relaxation was significantly reduced as compared with dietary intervention alone. Analysis of the biochemical contents of oxidized LDL from this group revealed that there was an 11% reduction in lysophosphatidylcholine (LPC) as compared with the group that received only dietary counseling. A decrease in the C16:0 moiety with a corresponding increase in the C18:0 moiety of LPC in the oxidized LDL was also observed in the atorvastatin treated group. We propose that the observed reduction and the change in composition of acyl groups in LPC in the oxidized LDL of the atorvastatin-treated group results from a combination of the continued dietary treatment as well as drug therapy. In view of an observation that both C16:0 and C18:0 LPC species are equally potent in the impairment of endothelium-dependent relaxation of the aortic rings, we feel that the reduced level of LPC in the oxidized LDL produced by atorvastatin treatment is partially responsible for the improvement in endothelium control of vascular tone.
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