These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Association between epicardial adipose tissue thickness and parameters of target organ damage in patients undergoing coronary angiography. Author: Rhee TM, Kim HL, Lim WH, Seo JB, Kim SH, Zo JH, Kim MA. Journal: Hypertens Res; 2019 Apr; 42(4):549-557. PubMed ID: 30573811. Abstract: Epicardial adipose tissue (EAT), metabolically active visceral fat, is easily measurable using transthoracic echocardiography (TTE). This study aimed to clarify the relationship between EAT thickness and parameters for target organ damage (TOD). A total of 338 consecutive patients (64.5 ± 10.9 years, 58.0% men) undergoing invasive coronary angiography in a stable condition were prospectively enrolled. TTE was performed, and the EAT thickness was measured perpendicular to the right ventricular free wall at end-systole. We investigated TOD parameters, including the estimated glomerular filtration rate, proteinuria, left ventricular (LV) mass index (LVMI), septal e' velocity, E/e', brachial-ankle pulse wave velocity, ankle-brachial index, aortic pulse pressure (APP), and presence of coronary artery disease (CAD). APP and CAD were assessed by invasive cardiac catheterization. Most patients (77.5%) had significant CAD (≥50% stenosis). In Pearson's bivariate correlation analyses, the EAT thickness was significantly correlated with the septal e' velocity (r = -0.203, P < 0.001) and E/e' (r = 0.217, P < 0.001), but not with other TOD parameters (P > 0.05). Multiple linear regression analysis showed that the correlations of the EAT thickness with septal e' velocity (β = -0.172, P = 0.047) and E/e' (β = 0.207, P = 0.011) remained significant even after adjusting for potential confounders. EAT thickness is more closely related to LV diastolic function than other TOD parameters, including renal function, LVMI, arterial stiffness, peripheral artery disease, and CAD. These findings provide additional evidence for the potential role of EAT in the pathogenesis of LV diastolic dysfunction.[Abstract] [Full Text] [Related] [New Search]