ABC | Volume 112, Nº1, January 2019

Original Article Enhos et al Atherosclerosis and MB Arq Bras Cardiol. 2019; 112(1):12-17 artery were enrolled in the study. The patients’ angiographic, demographic and clinic characteristics of the patients were reviewed from medical records. Patients with acute coronary syndrome, previous cardiac surgery, known coronary artery disease, concomitant valvular disease, cardiomyopathy, heart failure, atrial fibrillation, congenital heart defects, renal or hepatic disease, malignancy, hematological disorders, and acute or chronic inflammatory disorders were excluded from this study. The study was approved by the local ethics committee. Angiographic analysis Coronary angiography was performed using the standard Judkins’ technique with a biplane cineangiography system. Coronary arteries in the left and right oblique planes and in the cranial and caudal angles were demonstrated. Iopromide (Ultravist-370; Schering AG, Berlin, Germany) was used as the contrast agent, and it was manually injected (4–6ml of contrast agent in each position) during the coronary arteriography. All of the angiograms were evaluated by two experienced physicians. The presence of MB was defined according to the following criteria: narrowing of coronary vessel lumen during systole and dilation during diastole; no evidence of coronary vasospasm. Based on the findings of coronary angiography, the patients were divided in two subgroups: group A (n = 84) with normal coronary arteries; and group B (n = 76) with MB. Laboratory measurements Blood sample was collected from the antecubital vein using a 21-gauge sterile syringe in laboratory. Monocytes and HDL‑cholesterols were measured via complete blood count. MHR was calculated as the ratio of the absolute monocyte count to the HDL-cholesterol value. Statistical analysis All the statistical data were analyzed using SPSS 15.0 for Windows (SPSS Inc., Chicago, IL, USA). Continuous data were expressed as mean ± standard deviation, and the categorical data were expressed as percentages. Continuous variables were tested for normal distribution using Kolmogorov-Smirnov test. Both groups were compared using chi-square test or Fisher’s exact test for qualitative variables when appropriate, and independent t-test for normally distributed continuous variables. The non-normally distributed continuous variables are presented as median and interquantile range. Pearson test was used in the correlation analysis between parametric variables. Receiver-operating characteristic (ROC) analysis was performed for MHR in order to determine optimal cut‑off values and to obtain the sensitivity and specificity for each variable to predict the presence of MB. A multivariate logistic regression model was performed by including the parameters that differed significantly between the groups in order to identify the independent predictor of patients with MB. A p-value of < 0.05 was considered significant. Results Seventy-six MB (mean age: 52.3 ± 11.7 years, 82.0%male) and 84 age- and gender-matched control participants with normal coronary arteries (mean age: 53.8 ± 12.2 years, 75.0% male) were enrolled in this study. Both groups’ baseline demographics, as well as their clinic and laboratory characteristics, are summarized in Table 1. Diabetes mellitus and smoking were found to be lower in the MB group compared to the control group. There was no difference between two groups in terms of other demographic or clinic findings. When laboratory parameters were compared, creatinine, white blood cell and neutrophil were significantly higher in the MB group compared to the control group. However, HDL and total cholesterol were found to be significantly lower in the MB patients. Moreover, the monocyte/ HDL ratio was found to be significantly higher in the MB group compared to the control group. The remaining laboratory parameters did not differ between both groups. MHR values were divided into three tertiles as follows: lower (8.25 ± 1.61); moderate (13.11 ± 1.46); and higher (21.21 ± 4.30) tertile (Table 2). We found the frequency of MB (p = 0.002), male gender (p = 0.04) and the WBC count (p < 0.001) to increase as the MHR tertiles rose. A receiver operating curve (ROC) was generated for sensitivity and specificity, with the respective areas under the curve (AUC), to investigate the predictive value of monocyte/ HDL ratio for the presence of MB (Figure 1). The Monocyte/ HDL ratio with a cut‑point of 13.35 had 59.0% sensitivity and 65.0% specificity (ROC area under curve: 0.687, 95% CI: 0.606–0.769, p < 0.001) in accurately predicting MB diagnosis. In a univariate regression analysis, age, gender, total cholesterol, neutrophil to lymphocyte ratio (NLR), and hemoglobin were significantly related with MB. In the multivariate analysis, MHR (p = 0.013) was found to be significant as the independent predictor of MB, after adjusting for other risk factors (Table 3). Discussion The main findings of the present study were as follows: 1) A raised monocyte/HDL ratio was found to be significantly higher in patients with MB; 2) The monocyte/HDL ratio with a cut-point of 13.35 had moderate sensitivity and specifity to diagnose MB; and 3) MHR was found to be a significant independent predictor for presence of MB, after adjusting for other risk factors in multivariate analysis. Myocardial bridging, which is the compression of a coronary artery segment during systole, is generally accepted to be clinically benign, but it can result in a wide clinical spectrum, from angina to myocardial infarction. 12,14-16 In general, the coronary vessel segment proximal to the bridge has been reported to develop atherosclerosis at an increased rate – up to 90%. 12,14 However, one study has also demonstrated diffuse intimal thickening in the tunneled segment. 16 Besides the tunneled and proximal artery segments, other parts of the same coronary artery, as well as different arteries, could show atheroslerosis. 16 Endothelial cell morphology variations occur before and after tunneled segment due to blood flow shear stress. 1 Endothelial dysfunction, inflammation and unknown increased expression of vasoactive agents, such as endothelial nitric oxide synthase, endothelin-1, and angiotensin, all of which 13