ArticleLipids in health and disease2025
Inflammation mediates the relationship between cardiometabolic index and vulnerable plaque in patients with acute coronary syndrome.
Article in Lipids in health and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Genetic and epidemiological insights into the role of neutrophil percentage in heart failure risk: a Mendelian randomization and NHANES study.Molecular and cellular biochemistry · 2026Article
- Associations between the atherogenic index of plasma and coronary heart disease in hypertensive patients: results from NHANES 2005-2018.BMC cardiovascular disorders · 2025Article
- Predicting major amputation risk in diabetic foot ulcers using comparative machine learning models for enhanced clinical decision-making.Scientific reports · 2025Article
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8 authors.
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Abstract
backgroundAs a novel indicator reflecting metabolic status and visceral adiposity distribution, the cardiometabolic index (CMI) has gained attention in cardiovascular risk stratification. This investigation employed optical coherence tomography (OCT) to examine potential associations between CMI and vulnerable plaque, as well as the role of inflammation.
methodsThis study conducted a cross-sectional analysis of 270 acute coronary syndrome (ACS) patients who had OCT imaging evaluation. Patients were categorized based on CMI tertiles, with CMI calculated using the formula [waist (cm)/height (cm)]×[triglycerides (mmol/L)/HDL-C (mmol/L)]. OCT was used to assess plaque events in culprit lesions and plaque components in non-culprit lesions, and inflammatory markers were measured. A mediation analysis framework was implemented to investigate inflammatory pathways in CMI-vulnerable plaque relationships.
resultsCMI tertiles were linked to vulnerable plaque traits: thin-cap fibroatheromas (TCFA), macrophages (Tertiles1 vs. Tertiles2 vs. Tertiles3, TCFA: 10.0% vs. 20.0% vs. 26.7%, P = 0.016; macrophages: 17.8% vs. 28.9% vs. 36.7%, P = 0.019). Multivariate regression demonstrated CMI elevation independently predicted a higher prevalence of TCFA (OR:1.40, 95%CI: 1.25-2.89, P = 0.003), more macrophage infiltration (OR:1.61, 95% CI:1.09-2.37, P = 0.017), reduced FCT (β:-30.65, 95% CI:-50.72-10.57, P = 0.003), and enlarged maximum lipid arc (β:20.78, 95% CI:6.55-35.01, P = 0.004). Moreover, CMI was positively related to hsCRP, WBC, and neutrophils. Mediation analysis revealed that hsCRP mediated about 17.0% of the association between CMI and minimum FCT [Indirect effect=-5.21, 95% CI=(-12.70, -1.27), P = 0.016].
conclusionsCMI is a key forecaster of vulnerable plaque in patients with ACS. Systemic inflammation is associated with the relationship between CMI and vulnerable plaque features, suggesting a potential mechanistic link.
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