Epicardial fat in heart failure patients with mid‐range and preserved ejection fraction

Abstract

Aims Adipose tissue and inflammation may play a role in the pathophysiology of patients with heart failure (HF) with mildly reduced or preserved ejection fraction. We therefore investigated epicardial fat in patients with HF with preserved (HFpEF) and mid‐range ejection fraction (HFmrEF), and related this to co‐morbidities, plasma biomarkers and cardiac structure. Methods and results A total of 64 HF patients with left ventricular ejection fraction >40% and 20 controls underwent routine cardiac magnetic resonance examination. Epicardial fat volume was quantified on short‐axis cine stacks covering the entire epicardium and was related to clinical correlates, biomarkers associated with inflammation and myocardial injury, and cardiac function and contractility on cardiac magnetic resonance. HF patients and controls were of comparable age, sex and body mass index. Total epicardial fat volume was significantly higher in HF patients compared to controls (107 mL/m 2 vs. 77 mL/m 2 , P <0.0001). HF patients with atrial fibrillation and/or type 2 diabetes mellitus had more epicardial fat than HF patients without these co‐morbidities (116 vs. 100 mL/m 2 , P =0.03, and 120 vs. 97 mL/m 2 , P =0.001, respectively). Creatine kinase‐MB, troponin T and glycated haemoglobin in patients with HF were positively correlated with epicardial fat volume (R =0.37, P =0.006; R =0.35, P =0.01; and R =0.42, P =0.002, respectively). Conclusion Heart failure patients had more epicardial fat compared to controls, despite similar body mass index. Epicardial fat volume was associated with the presence of atrial fibrillation and type 2 diabetes mellitus and with biomarkers related to myocardial injury. The clinical implications of these findings are unclear, but warrant further investigation.

Myocardial adiposity in heart failure with preserved ejection fraction: the plot thickens

“…Moreover, patients with HFpEF showed increased volumes of the visceral fat adjacent to the heart (e.g. epicardial fat) compared to controls, a finding which has been confirmed in the current study. This is particularly interesting, since epicardial fat and the underlying myocardium share a common, contiguous microcirculation, with no basal layer separating the two tissues .…”

Evaluation of the effects of sodium–glucose co‐transporter 2 inhibition with empagliflozin on morbidity and mortality in patients with chronic heart failure and a preserved ejection fraction: rationale for and design of the EMPEROR‐Preserved Trial

“…A wide range of systemic inflammatory states lead to the accumulation and inflammation of epicardial adipose tissue and perivascular fat, which act as transducers for the transmission of the inflammatory process to the myocardium and aorta . The inflammation of myocardial and vascular tissues causes disruption of the microvascular blood supply, cardiac and adventitial fibrosis and impaired distensibility of the cardiac chambers and great vessels . The inflammatory process can also trigger the release of various cell‐signalling molecules and enzymes from adipose tissue, including aldosterone, neprilysin and leptin; the resulting sodium retention and expansion of plasma volume lead to a disproportionate increase in cardiac filling pressures when the left ventricle cannot expand as a result of microvascular rarefaction and fibrosis .…”

“…The principal biological processes that characterize HFrEF are cardiomyocyte loss and stretch; the resulting enlargement of the left ventricle promotes the activation of neurohormonal systems that cause sodium retention, systemic vasoconstriction and adverse chamber remodelling, leading to further cardiomyocyte loss and systolic dysfunction . In contrast, the principal biological processes that characterize HFpEF are systemic inflammation, epicardial adipose tissue accumulation, coronary microcirculatory rarefaction, myocardial fibrosis and vascular stiffness; the resulting impairment of left ventricular and aortic distensibility (especially when accompanied by impaired glomerular function and sodium retention) causes increases in cardiac filling pressures and exertional dyspnoea despite the relative preservation of left ventricular ejection fraction (LVEF) . The systemic inflammation in HFpEF can also cause changes in mitochondrial function and in the mass and composition of skeletal muscle, which can contribute to exercise intolerance in this disorder.…”

Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

“…Changes in epicardial fat and its secretory products are also associated with worsening of glomerular function and proteinuria, suggesting that the inflammatory process in the epicardium may extend to other organs affected by obesity and diabetes . The systemic inflammatory process that parallels the expanded epicardial fat mass helps to explain why comorbidities are so common in subjects with obesity and type 2 diabetes who have HFpEF, especially those with coexistent AF …”