Abstract

Left ventricular diastolic dysfunction (LVDD) can be affected by many factors, including epicardial adipose tissue (EAT), obesity and type-2 diabetes mellitus (T2DM). The aim of this study was to establish and validate an easy-to-use nomogram that predicts the severity of LVDD in patients with T2DM. This is a retrospective study of 84 consecutive subjects with T2DM admitted to the Endocrinology Department, the First People’s Hospital of Zunyi City between January 2015 and October 2020. Several echocardiographic characteristics were used to diagnose diastolic dysfunction according to the 2016 diastolic dysfunction ASE guidelines. Anthropometric, demographic, and biochemical parameters were collected. Through a least absolute shrinkage and selection operator (LASSO) regression model, we reduced the dimensionality of the data and determined factors for the nomogram. The mean follow-up was 25.97 months. Cases were divided into two groups, those with LVDD (31) and those without (53). LASSO regression identified total cholesterol (Tol.chol), low-density lipoprotein (LDL), right ventricular anterior wall (RVAW) and epicardial adipose tissue (EAT) were identified as predictive factors in the nomogram. The ROC curve analysis demonstrated that the AUC value for most clinical paramerters was higher than 0.6. The nomogram can be used to promote the individualized prediction of LVDD risk in T2DM patients, and help to prioritize patients diagnosed with echocardiography.

Highlights

  • Under normal conditions, epicardial adipose tissue (EAT) can release massive adrenomedullin as a potential peptide, a potent vasodilator

  • No statistical differences were found in gender, age, diastolic blood pressure (DBP), Weight, body mass index (BMI), triglyceride, low-density lipoprotein (LDL) cholesterol, glycated hemoglobin (HbA1C)

  • According to the above‐defined criteria, 31 subjects were defined as group with Left ventricular diastolic dysfunction (LVDD) and 53 subjects are with normal LVDF

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Summary

Introduction

Epicardial adipose tissue (EAT) can release massive adrenomedullin as a potential peptide, a potent vasodilator. Angiotensin II induced oxidative stress is antagonized by adrenomedullin which inhibits release of endothelial cell apoptosis and endothelin-1, and suppresses migration and proliferation of vascular smooth muscle cells (VSMCs) [1]. EAT is believed to affect left ventricular (LV) function [3–5]. Minkyung Kim [5] found greater EAT in patients with metabolic syndrome (MetS) and it has significant correlation with LV dysfunction in those with MetS. No such related studies have been published about the relation of EAT and LV function in subjects with type-2 diabetes mellitus (T2DM)

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