Why the study?
The remnant cholesterol inflammatory index (RCII) is a recently proposed biomarker combining remnant cholesterol and high-sensitivity C-reactive protein, but its role in cardiometabolic risk and cardiovascular mortality in elderly patients with aortic stenosis had not yet been evaluated.
Population
Elderly patients with severe aortic stenosis
Comparison
Remnant cholesterol inflammatory index (RCII) levels
Follow-up
Mean 19 ± 4 months
May aid mortality risk stratification in elderly aortic stenosis; hypothesis-generating and requires prospective validation before clinical use.
Background Inflammaging activates a vicious cycle common to the progression of structural cardiovascular alterations, cardiometabolic diseases as well as degenerative aortic stenosis (AoS). The remnant cholesterol inflammatory index (RCII) is a new recently proposed biomarker that combines remnant cholesterol and high-sensitivity C-reactive protein, resembling inflammaging. However, the role of RCII in terms of cardiometabolic risk and cardiovascular mortality in AoS elderly patients has not been evaluated still now. Aim to assess the association between RCII and cardiovascular risk factors and mortality in AoS elderly patients. Results RCII levels correlated with systemic inflammation biomarkers (closer correlation with interleukin-6), glucose, creatinine, vascular endothelial growth factor and frailty in AoS patients. Inverse correlations were observed with albumin (typically reduced in inflammatory states) and with HDL concentration. The Kaplan-Meier survival estimates showed significantly worse survival in patients with elevated RCII levels (p<0.01) (mean follow-up 19 ± 4 months). In an exploratory multivariable Cox analysis, higher RCII was associated with cardiovascular mortality (HR = 3.5, 95% CI: 1.0–12.0). Conclusion RCII is associated with cardiometabolic risk and adverse prognosis in elderly patients with AoS, providing an additional perspective on the prognostic implications of the coexistence of lipid abnormalities and low-grade inflammation in this population. However, the limited number of cardiovascular deaths warrants cautious interpretation of this estimate. Moreover, external validation, standardized thresholds, serial measurements, and comparison with established risk models are needed before RCII clinical implementation.
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Mazzone et al. (2026) studied this question.
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