98%
921
2 minutes
20
Background: Residual cholesterol (RC), a key indicator of lipid metabolism disorders, has been increasingly implicated in atherosclerotic progression. However, its association with vulnerable thin-cap fibroatheromas (TCFA) in non-culprit coronary lesions (NCCLs) and the subsequent risk of major adverse cardiovascular events (MACE) remains insufficiently explored.
Methods: In this prospective observational study conducted between June 2022 and September 2023, patients diagnosed with TCFA within NCCLs were followed for at least 12 months. Participants were grouped according to MACE occurrence. Spearman correlation and multivariate logistic regression were used to examine associations between RC levels, plaque vulnerability features, and MACE.
Results: RC showed significant correlations with key vulnerability markers-negatively with fibrous cap thickness (rs = -0.61, P < 0.001) and positively with lipid arc (rs = 0.75, P < 0.001). In univariate analysis, elevated RC was associated with a 1.88-fold increased risk of MACE. RC remained an independent risk factor in multivariate analysis (OR = 1.127, 95% CI: 1.101-1.593, P = 0.031). ROC analysis yielded moderate predictive value (AUC = 0.720).
Conclusion: Elevated RC is associated with greater plaque vulnerability and increased MACE risk in patients with NCCL-TCFA. These findings suggest RC's potential role in cardiovascular risk stratification, warranting further validation in larger studies.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394060 | PMC |
http://dx.doi.org/10.3389/fendo.2025.1603907 | DOI Listing |
J Clin Invest
September 2025
Metabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, United States of America.
Background: Statin therapy lowers the risk of major adverse cardiovascular events (MACE) among people with HIV (PWH). Residual risk pathways contributing to excess MACE beyond low-density lipoprotein cholesterol (LDL-C) are not well understood. Our objective was to evaluate the association of statin responsive and other inflammatory and metabolic pathways to MACE in the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE).
View Article and Find Full Text PDFAm J Prev Cardiol
September 2025
Division of Cardiovascular Medicine, University of California San Diego, La Jolla, CA, USA.
Elevated lipoprotein(a) [Lp(a)] is well established as a common risk factor for atherosclerotic cardiovascular disease (ASCVD). Lp(a) levels are >90 % genetically determined. However, Lp(a) remains very underrecognized as a cardiovascular risk factor with low rates of testing.
View Article and Find Full Text PDFLipids
September 2025
Ecotera Health, Blue Ash, Ohio, USA.
Per- and polyfluoroalkyl substances (PFAS) are persistent environmental pollutants increasingly implicated in cardiometabolic risk. This study evaluates the association between serum PFAS exposure and lipid dysregulation, focusing on low-density lipoprotein cholesterol (LDL-C), a key cardiovascular risk factor. We analyzed 998 adults from the 2017 to 2020 National Health and Nutrition Examination Survey (NHANES), representing a weighted sample of 240 million US adults.
View Article and Find Full Text PDFEur Heart J
September 2025
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.
Cardiovascular disease remains a major global health challenge, with dyslipidaemia being a key modifiable risk factor. While low density lipoprotein cholesterol (LDL-C) is the primary target for lipid-lowering therapies, recent evidence highlights the importance of triglycerides, apolipoprotein B (apoB), and lipoprotein(a) [Lp(a)] for residual cardiovascular risk. Current lipid-lowering therapies target key enzymes and proteins involved in cholesterol and lipid metabolism.
View Article and Find Full Text PDFJACC Asia
September 2025
Cardiovascular Center, Osaka Medical and Pharmaceutical University, Takatsuki, Japan.
Homozygous familial hypercholesterolemia (HoFH) is a rare situation where biallelic genetic disturbance of low-density lipoprotein (LDL) metabolism leads to extreme elevation of LDL cholesterol. There is a great variety of severity in their phenotype, where some patients exhibit premature supravalvular aortic stenosis at their early childhood, whereas others experience myocardial infarction at their adolescence. In addition, there is a set of familial hypercholesterolemia (FH) patients whose phenotype fall into between heterozygous FH and HoFH.
View Article and Find Full Text PDF