Association between monocyte to high-density lipoprotein cholesterol ratio and multi-vessel coronary artery disease: a cross-sectional study

Abstract

Abstract Background Patients with multi-vessel coronary artery disease (MV-CAD) have poorer clinical outcomes than those with single-vessel coronary artery disease (SV-CAD). Solid evidence underlines that high-density lipoprotein cholesterol (HDL-C) plays a protective role and monocyte plays a negative role in coronary artery disease (CAD). However, the monocyte to high-density lipoprotein ratio (MHR) has not been studied in relation to MV-CAD. Methods In this study, 640 patients underwent coronary angiography, of whom 225 had severe coronary artery disease. Then divide the above two groups of patients into three groups based on the MHR tertiles, respectively. Logistic regression and subgroup analysis were carried out to estimate the association between MHR and MV-CAD. The receiver operating characteristic (ROC) curve analysis was constructed by combining classic CAD risk factors with MHR in response to MV-CAD. In addition, the mediating effect of MHR between smoking and MV-CAD in suspected CAD Patients was analyzed. Results Among the three MHR groups, a statistically discrepant was observed in the number of patients with CAD, Severe-CAD and MV-CAD (PCAD < 0.001; PSevere-CAD < 0.001; PMV-CAD = 0.001) in suspected CAD patients. Furthermore, the number of patients with MV-CAD (P < 0.001) was different in Severe-CAD patients among three MHR groups. Non-CAD and CAD patients showed statistically discrepant in MHR levels (P < 0.001), and this difference also was observed between SV-CAD and MV-CAD patients (P < 0.001). In the analysis of suspected CAD patients, a significantly positive relationship was found between MHR and CAD, Severe-CAD, and MV-CAD (P for trend < 0.001). The effect of MHR on MV-CAD was consistent across all subgroups, with no significant randomized factor-by-subgroup interaction (P-interaction = 0.17–0.89). ROC analysis showed that the model constructed with MHR and classic influencing factors of CAD was superior to the model constructed solely based on classic influencing factors of CAD (0.742 vs.0.682, P = 0.002). In the analysis of Severe-CAD patients, patients with higher MHR levels had a higher risk of MV-CAD [OR (95%CI): 2.90 (1.49, 5.62), P for trend = 0.002] compared to patients with lower MHR. The trends persisted after adjusting for demographic (P for trend = 0.004) and classic influencing factors of CAD (P for trend = 0.009). All subgroup factors for patients with MV-CAD had no interaction with MHR (P-interaction = 0.15–0.86). ROC analysis showed that the model combining MHR and classic influencing factors of CAD was superior to the one including only the classic influencing factors of CAD (0.716 vs.0.650, P = 0.046). Assuming that MHR played a mediating effect between smoking and MV-CAD in suspected CAD patients. The results indicated that MHR played a partial mediating effect of 0.48 (P < 0.001). Conclusion A higher MHR was mainly associated with multi-vessel coronary artery disease and MHR partially mediated the association between smoking and MV-CAD.