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Author Spotlight: Assessing the Cardiovascular Profile of Patients with Metabolic Syndrome
Published on: September 27, 2024
Elevated Epicardial Adipose Tissue and Ischemic Stroke Risk: A Systematic Review and Meta-Analysis
Arankesh Mahadevan1, Monitha Pinnamaneni2, Manaswini Krishnakumar3
1Department of Neurology, University of Utah Health, Salt Lake City, UT 84132, USA.
None:
Introduction: Epicardial adipose tissue (EAT), a fat depot between the myocardium and pericardium, produces pro-inflammatory adipokines, contributing to inflammation, insulin resistance, and endothelial dysfunction. EAT has been recognized as an independent risk factor for cardiovascular diseases, including atrial fibrillation (AFib) and acute ischemic stroke (AIS). This study explores the association between EAT and AIS risk, with a focus on populations with cardiovascular comorbidities. Material and Methods: This meta-analysis adhered to MOOSE and PRISMA guidelines. A comprehensive search of PubMed, SCOPUS, and Embase databases was conducted, targeting studies evaluating the association between EAT and AIS. Inclusion criteria encompassed RCTs, cohort, case-control, and cross-sectional studies. Quality assessment was performed using appropriate tools, and statistical analysis involved pooled odds ratios (ORs) with 95% confidence intervals (CIs) using a binary random-effects model. Results: The search identified 711 studies, eight of which met the inclusion criteria, yielding 7412 participants. Analysis revealed that increased EAT thickness significantly correlated with higher odds of AIS (aOR: 3.60 [2.26-5.74], I2 = 74.24%). Sensitivity analysis confirmed the robustness of these findings despite publication bias. Higher epicardial adipose volume was also associated with an increased AIS risk (aOR: 1.17 [1.03-1.34], I2 = 49.54%). Conclusions: Increased EAT thickness and volume are associated with a higher risk of AIS in populations with cardiovascular comorbidities, including AFib. EAT's pro-inflammatory and pro-thrombotic properties may contribute to stroke pathophysiology. These findings highlight the potential utility of EAT measurement in stroke risk stratification and support further research to integrate EAT assessment into clinical practice.
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