ABC | Volume 112, Nº1, January 2019

Original Article Enhos et al Atherosclerosis and MB Arq Bras Cardiol. 2019; 112(1):12-17 Table 1 – Demographic, clinic and laboratory characteristics of the groups studied Variables Control Myocardial bridge p value Age in years 53.8 ± 12.2 52.3 ± 11.7 0.435 Male gender, n(%) 63(%75) 62(%82) 0.315 Hypertension, n(%) 32(%38) 19(%25) 0.076 Diabetes mellitus, n(%) 18(%21) 6(%8) 0.017 Smoker, n(%) 36(%43) 19(%25) 0.018 Glucose, mg/dl 104 ± 23 97 ± 13 0.088 Creatinine, mg/dl 0.83 ± 0.18 0.95 ± 0.72 0.035 Hemoglobin, gr/dl 13.8 ± 1.8 14.3 ± 1.7 0.077 White blood cell count, x 10 3 /L 7.4 ± 1.8 8.2 ± 2.1 0.018 Neutrophil count, x 10 3 /L 4.28 ± 1.42 4.81 ± 1.57 0.021 Lymphocyte count x 10 3 /L 2.31 ± 0.89 2.44 ± 0.75 0.121 Monocyte count x 10 3 /L 0.56 ± 0.15 0.62 ± 0.21 0.149 RDW 14.4 ± 1.7 14.9 ± 1.6 0.060 PDW 15.2 ± 3.2 17.1 ± 2.9 < 0.001 Platelet count x 10 3 /L 238 ± 59 255 ± 76 0.222 LDL cholesterol, mg/dl 123 ± 32 117 ± 27 0.168 HDL cholesterol, mg/dl 49 ± 12 39 ± 8 < 0.001 TG, mg/dl 152 ± 103 136 ± 54 0.909 Total cholesterol, mg/dl 200 ± 48 186 ± 32 0.021 MHR 12.20 ± 4.87 16.31 ± 6.47 < 0.001 RDW: red cell distribution width; PDW: platelet distribution width; HDL: high density lipoprotein; LDL: low density lipoprotein; TG: triglyceride; MHR: mononcyte count/ HDL cholesterol ratio. convert enzyme in the proximal segment of the MB artery, are the main pathophysiological mechanisms for increased atherosclerotic plaque formation. 13,17 Coronary angiography, intracoronary doppler ultrasonography, intravascular ultrasound, fractional flow reserve and cardiac computed tomography angiography are main tools for diagnosing coronary MB. 18 Monocytes are a source of various cytokines and molecules that interact with endothelial cells, which leads to an aggravation of inflammatory pathways. 19 Inflamation play a major role in atherosclerosis development and progression. 10 HDL cholesterol, which has antiinflammatory, antioxidant, and antithrombotic properties, strongly decreases the endothelial expression of adhesion molecules and prevents monocyte recruitment to the artery wall. 20 Furthermore, HDL decrease pro-inflammatory and pro-oxidant effects of monocytes by inhibiting themigration of macrophages and the oxidation of the low-density lipoprotein (LDL) molecules, as well as by promoting the efflux of cholesterol from these cells. 21 Therefore, it seems logical to combine these two parameters into a single ratio as an MHR, which can reflect the underlying inflammation process. A prognostic value of MHR has been reported in various cardiovascular diseases. 22-24 MHR was found to be related with major cardiovascular adverse events (MACE) including stent thrombosis and mortality after primary percutaneous coronary intervention (PCI) in ST-segment elevationmyocardial infarction (STEMI) patients. 25 Moreover, it has been demonstrated to be a new potential marker for predicting baremetal stent restenosis. 26 An important association between pre-procedural MHR levels and atrial fibrillation recurrence after ablation procedures was demonstrated by the study of Canbolat et al. 24 MHR is alwo well demontrated to be associated with coronary slow flow and coronary actesia, which are different forms of inflammation and atherosclerosis. 10,27 Our study has reported, for the first time, an important relationship between admission MHR and the presence of MB. Moreover, and concordant with previous studies on various cardiovascular diseases, MHR was found to be a significant independent marker associated with MB, with moderate sensitivity and specifity. The main pathophysiological links between MHR and MB can be endothelial dysfunction and inflammation. Inflammation not only leads to monocyte secretion and aggregation, but it also reduces HDL blood levels and its anti-oxidative feature. 10 Increased MHR was associated with systemic inflammation and endothelial dysfunction, and it was defined as a novel inflammation-based prognostic marker in cardiovascular diseases. 22-24 In our study, concordant with previous studies on cardiovascular disease, increased MHR was found to be related with the presence of MB, in whose pathophysiology inflammation plays a significant role. Even though previous studies demonstrated that MHR is associated with systemic inflamation, we found in the present study that MHR is associated with MB. As generally known, a local atherosclerotic process is present in patients with MB, particularly in the proximal and distal segments of 14