» Articles » PMID: 23644090

Changes in Plaque Lipid Content After Short-term Intensive Versus Standard Statin Therapy: the YELLOW Trial (reduction in Yellow Plaque by Aggressive Lipid-lowering Therapy)

Overview
Date 2013 May 7
PMID 23644090
Citations 88
Authors
Affiliations
Soon will be listed here.
Abstract

Objectives: This study sought to determine the impact of short-term intensive statin therapy on intracoronary plaque lipid content.

Background: Statin therapy significantly reduces the risk for thrombotic events. Whether or not these benefits are attributable to reduction in plaque lipid content remains to be properly documented in human obstructive coronary artery disease (CAD).

Methods: We randomized 87 patients with multivessel CAD undergoing percutaneous coronary intervention and at least 1 other severely obstructive (fractional flow reserve [FFR] ≤0.8) nontarget lesion (NTL) to intensive (rosuvastatin 40 mg daily) or standard-of-care lipid-lowering therapy. NTLs were evaluated at baseline and after 7 weeks of therapy with FFR, near-infrared spectroscopy, and intravascular ultrasound. The primary endpoint was the change in lipid-core burden index at the 4-mm maximal segment (LCBI4mm max), wherever this occurred within the lesion.

Results: Upon follow-up, median reduction (95% confidence interval) in LCBI4mm max was significantly greater in the intensive versus standard group (-149.1 [-210.9 to -42.9] vs. 2.4 [-36.1 to 44.7]; p = 0.01). Results remained consistent after adjustment for baseline differences in LCBI between groups and use of change in LCBI across the entire lesion as the dependent outcome.

Conclusions: Short-term intensive statin therapy may reduce lipid content in obstructive lesions. These hypothesis-generating findings warrant confirmation in larger studies with longer follow-up. (Reduction in YEllow Plaque by Aggressive Lipid LOWering Therapy [YELLOW]); NCT01567826).

Citing Articles

Highlights of Cardiovascular Disease Prevention Studies Presented at the 2024 American Heart Association Scientific Sessions.

Hermel M, Minhas A, Hinkamp C, Inam M, Murthy N, Chai Z Curr Atheroscler Rep. 2025; 27(1):30.

PMID: 39913067 DOI: 10.1007/s11883-025-01276-0.


Long-Term Carotid Plaque Progression and the Role of Intraplaque Hemorrhage: A Deep Learning-Based Analysis of Longitudinal Vessel Wall Imaging.

Guo Y, Akcicek E, Hippe D, HashemizadehKolowri S, Wang X, Akcicek H medRxiv. 2024; .

PMID: 39711698 PMC: 11661346. DOI: 10.1101/2024.12.09.24318661.


Reversal of Atherosclerotic Plaque Growth and Vulnerability: Effects of Lipid-Modifying and Anti-Inflammatory Therapeutic Agents.

Papafaklis M, Koros R, Tsigkas G, Karanasos A, Moulias A, Davlouros P Biomedicines. 2024; 12(11).

PMID: 39595002 PMC: 11591594. DOI: 10.3390/biomedicines12112435.


Impact of hypertension on coronary artery plaques and FFR-CT in type 2 diabetes mellitus patients: evaluation utilizing artificial intelligence processed coronary computed tomography angiography.

Xi Y, Xu Y, Shu Z Front Artif Intell. 2024; 7:1446640.

PMID: 39507325 PMC: 11537896. DOI: 10.3389/frai.2024.1446640.


Targeting Unc5b in macrophages drives atherosclerosis regression and pro-resolving immune cell function.

Schlegel M, Cyr Y, Newman A, Schreyer K, Barcia Duran J, Sharma M Proc Natl Acad Sci U S A. 2024; 121(44):e2412690121.

PMID: 39436659 PMC: 11536151. DOI: 10.1073/pnas.2412690121.