Background and Objectives: Cardiac Syndrome X (CSX), a clinical entity within the Ischaemia with Non-Obstructive Coronary Arteries (INOCA) spectrum, is increasingly recognised as an inflammatory and systemic vascular disorder. Remnant cholesterol (RC) and inflammation are emerging contributors to residual cardiovascular risk; however, their combined role in microvascular angina remains unclear. This study aimed to evaluate the association between the remnant cholesterol inflammation index (RCII), integrating RC and high-sensitivity C-reactive protein (hs-CRP), and the clinical presence of CSX. Methods: This single-centre, retrospective observational study included 392 individuals who underwent coronary angiography between January 2023 and January 2025. The study population comprised 197 patients diagnosed with CSX and 195 control subjects with normal coronary anatomy and no objective evidence of myocardial ischaemia. RC was calculated as total cholesterol minus the sum of LDL-C and HDL-C, and RCII was derived as RC × hs-CRP. Importantly, invasive microvascular testing (e.g., CFR or IMR) was not performed. Logistic regression analyses were performed to identify independent predictors of CSX, and receiver operating characteristic (ROC) curve analysis was used to evaluate diagnostic performance. Results: Patients with CSX exhibited significantly higher levels of hs-CRP, SII, and RCII compared with controls (all p < 0.001). In the multivariable logistic regression analysis, RCII demonstrated an independent association with CSX (odds ratio 1.095, 95% confidence interval 1.060–1.131; p < 0.001). ROC curve analysis showed that RCII provided moderate but significant discrimination for CSX (area under the curve [AUC] 0.765, 95% CI 0.695–0.795). Pairwise comparisons confirmed that RCII had a significantly higher AUC than RC, hs-CRP, or SII individually. Conclusions: Higher RCII levels appear to be significantly associated with the clinical diagnosis of CSX. By integrating atherogenic remnant cholesterol burden and systemic inflammation, RCII may serve as a valuable composite biomarker for identifying residual inflammatory lipid risk. Rather than acting as a definitive diagnostic tool, these findings warrant further validation in large-scale prospective cohort studies.

Background and Objectives: Although chronic total occlusion (CTO) often presents with varying degrees of coronary collateral circulation (CCC), the biological factors accompanying inadequate collateralization are not fully established. The Remnant Cholesterol Inflammation Index (RCII) is a composite metric integrating atherogenic lipid load and systemic inflammation. This study examined the association between RCII and CCC and the discriminative ability of RCII for identifying insufficient collateral networks in patients with CTO. Materials and Methods: This retrospective, single-center analysis evaluated 359 patients with at least one major epicardial CTO who underwent diagnostic coronary angiography between 15 January 2023 and 15 January 2026. Participants were stratified via the Rentrop scoring system into poor (grades 0–1; n = 168) and good (grades 2–3; n = 191) CCC cohorts. RCII was calculated as [remnant cholesterol (mg/dL) × high-sensitivity C-reactive protein (hs-CRP, mg/L)]/10, with remnant cholesterol derived as total cholesterol minus LDL-C and HDL-C. Univariable and multivariable logistic regression models, together with receiver operating characteristic (ROC) curve analysis, were used to assess the association of RCII with poor CCC and its discriminative ability. Results: Patients with poor CCC exhibited significantly higher RCII values compared with the good CCC cohort (19.7 ± 4.7 vs. 6.5 ± 2.4, p < 0.001). Following multivariable adjustment, higher RCII remained independently associated with poor collateralization (OR 1.120, 95% CI 1.052–1.199; p < 0.001), alongside right coronary artery (RCA) CTO and the systemic immune-inflammation index (SII). RCII showed discriminative ability for poor CCC (AUC 0.792, 95% CI 0.745–0.835; p < 0.001), which was greater than that of remnant cholesterol, hs-CRP, or SII considered separately. In this cohort, an RCII threshold above 12.3 identified poor CCC with 80% sensitivity and 71% specificity. Conclusions: In this retrospective cohort, higher RCII was independently associated with inadequate coronary collateralization in the setting of CTO. RCII may represent a candidate marker of the combined residual lipid and inflammatory burden; prospective studies and external validation, together with formal assessment of clinical utility, are required before any clinical application can be considered.