Key result
Elevated cardiometabolic index linked to ~40% greater odds of TCFA and macrophage infiltration in ACS.
Why the study?
The associations between the cardiometabolic index and vulnerable plaque, along with the role of inflammation, were not well defined in acute coronary syndrome.
Does an elevated cardiometabolic index predict vulnerable plaque characteristics assessed by OCT in patients with acute coronary syndrome?
Cross-Sectional (n=270)
No
Does an elevated cardiometabolic index predict vulnerable plaque characteristics assessed by OCT in patients with acute coronary syndrome?
Effect estimate: OR 1.40 (95% CI 1.25-2.89)
Absolute Event Rate: 26.7% vs 10%
p-value: p=0.003
An elevated cardiometabolic index is associated with vulnerable plaque characteristics in ACS patients, a relationship that is partially mediated by systemic inflammation.
Elevated CMI was associated with vulnerable plaques in ACS; leaves open causal links and therapeutic implications.
BACKGROUND: As 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. METHODS: This 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. RESULTS: CMI 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]. CONCLUSIONS: CMI 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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Yan et al. (2025) conducted a cross-sectional in Acute Coronary Syndrome (n=270). Cardiometabolic index (CMI) vs. Lower CMI tertiles was evaluated on Prevalence of thin-cap fibroatheromas (TCFA) (OR 1.40, 95% CI 1.25-2.89, p=0.003). Elevated cardiometabolic index independently predicted a higher prevalence of thin-cap fibroatheromas (OR 1.40) and macrophage infiltration in patients with acute coronary syndrome.
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