The blood monocyte to high density lipoprotein cholesterol ratio (MHR) is a possible marker of carotid artery plaque

Abstract

Abstract Background MHR is the ratio of monocyte to high-density lipoprotein cholesterol (HDL-C). It has been reported that MHR changes are associated with cardiovascular and cerebrovascular disease. Carotid plaque is a common vascular lesion of the carotid artery and is a manifestation of atherogenesis. This study investigated the relationships between the MHR and the incidence of carotid plaques. Methods The data of 3848 physical examiners were analyzed for retrospective analysis, which included 1428 patients with noncarotid plaque, 1133 patients with single carotid plaque, and 1287 patients with bilateral or multiple carotid plaques. Statistical analysis was performed on SPSS 22.0 0 software and statistical software R and its GAM package. Results The difference was statistically significant in the levels of MHR, body mass index (BMI), high-sensitivity C-reactive protein (hs-CRP), blood lipids (HDL-C, low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglyceride (Tg)), blood glucose (Glu), hemoglobin A1c (HbA1c), renal function (urea, creatinine (Crea)), estimated glomerular filtration rate (eGFR), and uric acid (Ua) in the carotid plaque groups (P < 0.001, respectively). There was no significant difference between the sex (P = 0.635) and age (P = 0.063) in the different groups. MHR levels were positively correlated with BMI (r = 0.364, P < 0.001), hs-CRP (r = 0.320, P < 0.001), Tg (r = 0.417, P < 0.001), Crea (r = 0.323, P < 0.001), eGFR (r = − 0.248, P < 0.001), Ua (r = 0.383, P < 0.001) and HbA1c (r = 0.197, P < 0.001). Levels of TC, Glu, and urea were slightly correlated with the MHR level (r = − 0.150, P < 0.001; r = 0.187, P < 0.001; r = 0.137, P < 0.001, respectively). The MHR level increased with elevated severity of carotid plaque in subjects without hypertension or diabetes (P < 0.001). In adjusted models, with the rise of MHR level, the probability of occurrence of carotid plaque had a 1.871-fold (95% CI: 1.015–3.450, P = 0.045) increase; the probability of multiple occurrences of carotid plaques had a 2.896-fold (95% CI: 1.415–5.928, P < 0.001) increase. The GAM curve showed a nonlinear correlation between the normalized MHR and the probability of carotid plaque occurrence. Conclusions MHR could be used as a possible marker for plaque formation and severity.