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Association of Volumetric Epicardial Adipose Tissue Quantification and Cardiac Structure and Function
BACKGROUND: Epicardial adipose tissue (EAT) is in immediate apposition to the underlying myocardium and, therefore, has the potential to influence myocardial systolic and diastolic function or myocardial geometry, through paracrine or compressive mechanical effects. We aimed to review the associatio...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6405553/ https://www.ncbi.nlm.nih.gov/pubmed/30571602 http://dx.doi.org/10.1161/JAHA.118.009975 |
Sumario: | BACKGROUND: Epicardial adipose tissue (EAT) is in immediate apposition to the underlying myocardium and, therefore, has the potential to influence myocardial systolic and diastolic function or myocardial geometry, through paracrine or compressive mechanical effects. We aimed to review the association between volumetric EAT and markers of myocardial function and geometry. METHODS AND RESULTS: PubMed, Medline, and Embase were searched from inception to May 2018. Studies were included only if complete EAT volume or mass was reported and related to a measure of myocardial function and/or geometry. Meta‐analysis and meta‐regression were used to evaluate the weighted mean difference of EAT in patients with and without diastolic dysfunction. Heterogeneity of data reporting precluded meta‐analysis for systolic and geometric associations. In the 22 studies included in the analysis, there was a significant correlation with increasing EAT and presence of diastolic dysfunction and mean e′ (average mitral annular tissue Doppler velocity) and E/e′ (early inflow / annular velocity ratio) but not E/A (ratio of peak early (E) and late (A) transmitral inflow velocities), independent of adiposity measures. There was a greater EAT in patients with diastolic dysfunction (weighted mean difference, 24.43 mL; 95% confidence interval, 18.5–30.4 mL; P<0.001), and meta‐regression confirmed the association of increasing EAT with diastolic dysfunction (P=0.001). Reported associations of increasing EAT with increasing left ventricular mass and the inverse correlation of EAT with left ventricular ejection fraction were inconsistent, and not independent from other adiposity measures. CONCLUSIONS: EAT is associated with diastolic function, independent of other influential variables. EAT is an effect modifier for chamber size but not systolic function. |
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