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The association between the monocyte-to-HDL cholesterol ratio and coronary collateral circulation in patients with chronic total occlusion #MMPMID41353274
Yanik A; Boyaci F; Sahin MK
BMC Cardiovasc Disord 2025[Dec]; ? (?): ? PMID41353274show ga
BACKGROUND: Coronary collateral circulation (CCC) plays a crucial role in preserving myocardial perfusion in patients with chronic total occlusion (CTO) of the coronary arteries. However, the extent of collateral vessel development varies widely and cannot be explained solely by anatomical or hemodynamic factors. Systemic inflammation and lipid metabolism are critical modulators of arteriogenesis. The monocyte-to-high-density lipoprotein cholesterol ratio (MHR) has been proposed as a novel biomarker reflecting the balance between proinflammatory activity and anti-atherogenic protection. This study aimed to investigate the relationship between the MHR and the adequacy of the CCC in patients with stable coronary artery disease and angiographically confirmed CTO. METHODS: This retrospective study included 143 patients with stable angina who were diagnosed with at least one CTO lesion via coronary angiography. CCC was assessed via the Rentrop classification and categorized as poor (grades 0-1) or good (grades 2-3). Demographic, clinical, and laboratory data, including monocyte count, HDL cholesterol, and high-sensitivity C-reactive protein (hs-CRP) values, were collected. MHR values were calculated and compared between the groups. Logistic regression and receiver operating characteristic (ROC) curve analyses were performed to identify independent predictors and determine the diagnostic performance of the MHR. RESULTS: Patients with poor CCCs presented significantly higher MHR values (17.3 +/- 4.7 vs. 12.0 +/- 4.7, p < 0.001), higher hs-CRP levels, and lower HDL cholesterol concentrations. In the multivariate analysis, both the MHR (adjusted odds ratio [aOR]: 1.283, p < 0.001) and the hs-CRP level (aOR: 4.272, p = 0.009) emerged as independent predictors of poor collateral development. The MHR demonstrated good discriminative performance for poor CCC (AUC = 0.808, 95% CI: 0.735-0.881), with an optimal cutoff value of 13.8 (sensitivity 74%, specificity 71%). CONCLUSIONS: An elevated MHR is significantly associated with poor CCC development in patients with CTO. As a readily available and cost-effective biomarker, it has potential clinical utility for identifying patients at risk of insufficient arteriogenesis. Further prospective studies are needed to validate its prognostic utility and explore its therapeutic implications in ischemic heart disease.
BMC+Cardiovasc+Disord 2025 ; ? (?): ?
