Mathew P M Graham-Brown1, Gerry P McCann, James O Burton. 1. aJohn Walls Renal Unit University Hospitals Leicester NHS Trust bDepartment of Infection, Immunity and Inflammation cDepartment of Cardiovascular Sciences dNational Institute for Health Research Biomedical Research Unit in Cardiovascular Disease, University Hospitals of Leicester NHS Trust and University of Leicester, Leicester, UK.
Abstract
PURPOSE OF REVIEW: Epicardial adipose tissue (EAT) is the visceral fat of the heart, sharing many of the pathophysiological properties of other visceral fat depots. EAT is a metabolically active paracrine and vasocrine organ that causes local cardiac inflammation and is strongly implicated in the pathogenesis of coronary atherosclerosis. This article highlights the findings of recent observational studies in patients on haemodialysis that link the quantity of EAT to increased rates of cardiovascular and coronary artery disease and review the proposed methods of pathogenesis and the possible role of EAT quantification to improve cardiovascular risk assessment. RECENT FINDINGS: Increasing volumes of EAT in patients on haemodialysis correlate with increased inflammatory mediators, higher rates of cardiovascular disease and coronary artery calcification, independent of general adiposity. EAT is an independent predictor of mortality and a potentially modifiable target for therapeutic interventions. SUMMARY: EAT is likely to play a central role in the pathogenesis of cardiovascular disease in patients on haemodialysis, adds incrementally to conventional cardiovascular risk stratification models and is a potential target for therapeutic intervention.
PURPOSE OF REVIEW: Epicardial adipose tissue (EAT) is the visceral fat of the heart, sharing many of the pathophysiological properties of other visceral fat depots. EAT is a metabolically active paracrine and vasocrine organ that causes local cardiac inflammation and is strongly implicated in the pathogenesis of coronary atherosclerosis. This article highlights the findings of recent observational studies in patients on haemodialysis that link the quantity of EAT to increased rates of cardiovascular and coronary artery disease and review the proposed methods of pathogenesis and the possible role of EAT quantification to improve cardiovascular risk assessment. RECENT FINDINGS: Increasing volumes of EAT in patients on haemodialysis correlate with increased inflammatory mediators, higher rates of cardiovascular disease and coronary artery calcification, independent of general adiposity. EAT is an independent predictor of mortality and a potentially modifiable target for therapeutic interventions. SUMMARY: EAT is likely to play a central role in the pathogenesis of cardiovascular disease in patients on haemodialysis, adds incrementally to conventional cardiovascular risk stratification models and is a potential target for therapeutic intervention.
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