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Association of Epicardial Adipose Tissue and High‐Risk Plaque Characteristics: A Systematic Review and Meta‐Analysis

BACKGROUND: Epicardial adipose tissue (EAT) is hypothesized to alter atherosclerotic plaque composition, with potential development of high‐risk plaque (HRP). EAT can be measured by volumetric assessment (EAT‐v) or linear thickness (EAT‐t). We performed a systematic review and random‐effects meta‐an...

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Detalles Bibliográficos
Autores principales: Nerlekar, Nitesh, Brown, Adam J., Muthalaly, Rahul G., Talman, Andrew, Hettige, Thushan, Cameron, James D., Wong, Dennis T. L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5586465/
https://www.ncbi.nlm.nih.gov/pubmed/28838916
http://dx.doi.org/10.1161/JAHA.117.006379
Descripción
Sumario:BACKGROUND: Epicardial adipose tissue (EAT) is hypothesized to alter atherosclerotic plaque composition, with potential development of high‐risk plaque (HRP). EAT can be measured by volumetric assessment (EAT‐v) or linear thickness (EAT‐t). We performed a systematic review and random‐effects meta‐analysis to assess the association of EAT with HRP and whether this association is dependent on the measurement method used. METHODS AND RESULTS: Electronic databases were systematically searched up to October 2016. Studies reporting HRP by computed tomography or intracoronary imaging and studies measuring EAT‐v or EAT‐t were included. Odds ratios were extracted from multivariable models reporting the association of EAT with HRP and described as pooled estimates with 95% confidence intervals (CIs). Analysis was stratified by EAT measurement method. Nine studies (n=3772 patients) were included with 7 measuring EAT‐v and 2 measuring EAT‐t. Increasing EAT was significantly associated with the presence of HRP (odds ratio: 1.26 [95% CI, 1.11–1.43]; P<0.001). Patients with HRP had higher EAT‐v than those without (weighted mean difference: 28.3 mL [95% CI, 18.8–37.8 mL]; P<0.001). EAT‐v was associated with HRP (odds ratio: 1.19 [95% CI, 1.06–1.33]; P<0.001); however, EAT‐t was not (odds ratio: 3.09 [95% CI, 0.56–17]; P=0.2). Estimates remained significant when adjusted for small‐study effect bias (odds ratio: 1.13 [95% CI, 1.03–1.28]; P=0.04). CONCLUSIONS: Increasing EAT is associated with the presence of HRP, and patients with HRP have higher quantified EAT‐v. The association of EAT‐v with HRP is significant compared with EAT‐t; however, a larger scale study is still required, and further evaluation is needed to assess whether EAT may be a potential therapeutic target for novel pharmaceutical agents. CLINICAL TRIAL REGISTRATION: URL: https://www.crd.york.ac.uk/. Unique identifier: CRD42017055473.