Atherosclerosis
Applied
Type
AdditionConfidence
85%
Created
Mar 27, 2026
Evidence
1 source
Rationale
The new evidence from Basios et al. (2025) is a meta-analysis focusing on statin adherence. While the original text was purely pathophysiological, integrating the clinical reality of treatment adherence provides a necessary bridge between the mechanism (LDL-driven plaque formation) and clinical management. I also expanded the abbreviation for LDL on its first occurrence as required.
Evidence
Content Changes
removedadded
Endothelial dysfunction allows LDLlow-density lipoprotein (LDL) to penetrate the intima, where it undergoes oxidation. Monocytes adhere, migrate, and differentiate into macrophages, forming foam cells. Smooth muscle proliferation and extracellular matrix deposition lead to fibrous cap formation. Plaque rupture triggers platelet activation and thrombus formation, which can result in acute ischemic events [@libby2021]. While lipid-lowering therapies are central to stabilizing plaques and reducing cardiovascular risk, the clinical effectiveness of these interventions is frequently compromised by poor patient adherence to statin therapy [@basios2025-prevalence].