Literature DB >> 25084691

Preclinical left ventricular diastolic dysfunction in metabolic syndrome.

Nir Ayalon1, Deepa M Gopal1, Deirdre M Mooney1, Juliana S Simonetti2, Jason R Grossman3, Aeshita Dwivedi3, Courtney Donohue1, Alejandro J Perez1, Jill Downing1, Noyan Gokce1, Edward J Miller1, Chang-Seng Liang1, Caroline M Apovian2, Wilson S Colucci1, Jennifer E Ho4.   

Abstract

Metabolic syndrome (MS) is commonly associated with left ventricular (LV) diastolic dysfunction and LV hypertrophy. We sought to examine whether preclinical LV diastolic dysfunction can occur independent of LV hypertrophy in MS. We recruited 90 consecutive participants with MS and without cardiovascular disease (mean age 46 years, 78% women) and 26 controls (no risk factors for MS; mean age 43 years, 65% women). Participants underwent echocardiography with tissue Doppler imaging. In age- and gender-adjusted analyses, MS was associated with higher left atrial (LA) diameter, higher LV mass, lower E/A ratio, and lower mean e' (p <0.001 for all). These associations remained significant after further adjusting for blood pressure, antihypertensive medication use, and body mass index. After adjusting for LV mass, MS remained independently associated with higher LA diameter, lower E/A ratio, and lower mean e' (p ≤0.01 for all). Specifically, subjects with MS had a 1.8 cm/s lower mean e' compared with controls (p = 0.01). Notably, differences in mean e' between those with and without MS were more pronounced at younger ages (p for interaction = 0.003). In conclusion, MS was associated with preclinical LV diastolic dysfunction independent of LV mass, as reflected by higher LA diameter, lower E/A ratio, and lower mean e'. This suggests that MS can lead to the development of diastolic dysfunction through mechanisms independent of hypertrophy. Differences in diastolic function were more pronounced at younger ages, highlighting the potential importance of early risk factor modification and preventive strategies in MS.
Copyright © 2014 Elsevier Inc. All rights reserved.

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Year:  2014        PMID: 25084691      PMCID: PMC4162746          DOI: 10.1016/j.amjcard.2014.06.013

Source DB:  PubMed          Journal:  Am J Cardiol        ISSN: 0002-9149            Impact factor:   2.778


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