Monocyte to HDL cholesterol ratio and smoking are predictors of epicardial fat tissue thickness

Abstract

Objective: Smoking stimulates lipid accumulation and causes non-alcoholic fatty liver disease. Epicardial Fat Tissue (EFT) resides between the visceral pericardium and myocardium. The aim of this study was to determine whether if smoking may accumulate Epicardial Fat Tissue thickness (EFTt). Material and methods: 266 smoking and 500 non-smoking subjects were included in the study. The subjects were chosen to be healthy individuals, without any cardiovascular/systemicdisorders or risk factors for atherosclerosis (except hyperlipidemia). Transthoracic echocardiography (TTE) was applied to all subjects, and EFTt was measured in both diastole and systole (EFTtd and EFTts respectively). Results: EFTtd, EFTts, low-density lipoprotein cholesterol, triglyceride, and monocyte to the HDL cholesterol ratio (MHR) values were found to be significantly increased in the smoking group when compared to the non-smoking group. Pearson’s correlation analyses revealed that EFTtd and EFTts were related to pack.year, low-density lipoprotein cholesterol, triglyceride, MHR, BMI, and age. Linear regression analysis results showed that smoking, pack.year, BMI, age, and MHR were independent predictors of EFTtd, EFTts. Conclusions: The study results showed that smoking increases the EFTtd and EFTts. Smoking and MHR were independent predictors of EFTt. Evaluating blood parameters together with EFTt may guide primary prevention in smokers.