Atherogenic, dense low-density lipoproteins. Pathophysiology and new therapeutic approaches.
Level 5 - mechanism / opinion, no new human data
Narrative review with embedded uncontrolled before-after intervention data
What was done
The authors reviewed the pathophysiology of small, dense low-density lipoproteins (LDL) and presented findings from an intervention in patients with combined hyperlipidaemia. Patients received micronized fenofibrate (200 mg/day) for 8 weeks to evaluate changes in lipoprotein subfractions (VLDL, dense LDL, HDL-cholesterol) and cholesteryl ester transfer rates between HDL, VLDL, and LDL.
What was found
After 8 weeks of fenofibrate treatment: - Plasma VLDL concentrations decreased by 37% (P < 0.005). - Dense LDL concentrations decreased by 21.5% (P < 0.05). - HDL-cholesterol increased by 19% (P < 0.0001). - Cholesteryl ester transfer from HDL to VLDL decreased by 38%, with no change in transfer between HDL and LDL. - The LDL profile shifted from small, dense LDL toward intermediate-density, larger LDL particles.
Why it matters
Small, dense LDL particles are prone to arterial retention and oxidative modification, driving foam cell formation. This study demonstrates that fenofibrate reduces small dense LDL and normalizes lipoprotein remodeling toward receptor-active particles.
Limits
The abstract does not state the sample size, control group details, blinding, or patient demographics. Clinical cardiovascular outcomes were not evaluated.
Cited by
- supports Small LDL particles are cleared less efficiently by LDL receptors than larger LDL particles.