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

 Mücahid Yılmaz * and Çetin Mirzaoğlu

Department of Cardiology, University of Health Sciences, Elazığ Fethi Sekin City Hospital, Turkey/Elazig.
 
Research Article
World Journal of Biology Pharmacy and Health Sciences, 2024, 18(01), 012–020.
Article DOI: 10.30574/wjbphs.2024.18.1.0160
Publication history: 
Received on 19 February 2024; revised on 01 April 2024; accepted on 04 April 2024
 
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.
 
Keywords: 
Epicardial fat tissue thickness; Smoking; Monocyte to the HDL cholesterol ratio
 
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