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Effect of atorvastatin on lipid parameters, LDL subtype distribution, hemorrheological parameters and adhesion
1Medical Department II, Ludwig-Maximilians-University, Munich, Germany.
Insights
Atorvastatin therapy improved low-density lipoprotein (LDL) profiles and reduced blood viscosity in hypertriglyceridemic patients. While it lowered cholesterol, it did not significantly decrease triglyceride levels.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Hypertriglyceridemia is a risk factor for atherosclerosis.
- It is associated with adverse lipid profiles, increased adhesion molecules, and impaired hemorrheology.
- Lipid-lowering therapy may influence these risk markers.
Purpose of the Study:
- To investigate the effects of atorvastatin on risk markers in hypertriglyceridemic patients.
- To assess changes in lipoproteins, LDL subtypes, hemorrheology, and adhesion molecules.
Main Methods:
- Nineteen patients with primary hypertriglyceridemia received 10 mg of atorvastatin daily for four weeks.
- Measurements included lipid levels, LDL subtypes, hemorrheological parameters, and adhesion molecules before and after treatment.
Main Results:
- Total cholesterol and LDL cholesterol decreased significantly (25% and 24%, respectively).
- Cholesterol was reduced across all LDL subfractions.
- Plasma and blood viscosity decreased, but triglyceride levels and adhesion molecules showed no significant change.
Conclusions:
- Atorvastatin (10 mg/day) improved LDL subtype profile and reduced plasma and blood viscosity.
- The therapy effectively lowered atherogenic lipoproteins but did not significantly reduce triglyceride concentrations.
Background And Aim:
Hypertriglyceridemia is a risk factor for atherosclerosis that is typically associated with high concentrations of adhesion molecules, impaired hemorrheology and an unfavourable low-density lipoprotein (LDL) subtype distribution. We hypothesised that some of these risk markers might be beneficially influenced by lipid-lowering therapy with atorvastatin in hypertriglyceridemic patients.
Methods And Results:
Nineteen patents with primary hypertriglyceridemia were given 10 mg of atorvastatin per day for four weeks. Their cholesterol, triglyceride, LDL and high-density lipoprotein cholesterol (HDL-C) levels, LDL subtype profile, hemorrheological parameters and E-selectin, vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 concentrations were measured before and at the end of atorvastatin therapy. The levels of total and LDL cholesterol respectively decreased by 25% and 24% (both p < 0.001). Furthermore, cholesterol was reduced by 8-29% in all seven LDL subfractions (density range: 1.020-1.066 g/mL) (p < 0.05). The reduction in triglyceride concentrations was of marginal significance (9%, p = 0.1), but its degree positively correlated with the reduction of small-dense LDL (r = 0.5, p < 0.025). Plasma viscosity and blood viscosity at low shear rates were respectively reduced by 2% and 16% (both p < 0.05). The effect of the treatment on the concentrations of HDL-C, fibrinogen and adhesion molecules was not significant.
Conclusions:
Atorvastatin (10 mg/day) not only reduced the plasma concentrations of atherogenic lipoproteins but also improved the LDL-subtype profile and reduced plasma and blood viscosity in patients with hypertriglyceridemia; however, it failed to significantly lower triglyceride concentrations.
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