Epicardial Fat Thickness in Heart Failure and Other Clinical Conditions

Abstract

In this issue of Angiology, Karayannis et al report that epicardial fat thickness (EFT) is related to anthropometric characteristics (body mass index [BMI], waist, or thigh perimeter) in both non-cachectic congestive heart failure (CHF) patients and controls. In addition, they found that in healthy individuals, decreased plasma ghrelin and increased high-sensitivity C-reactive protein (hsCRP) levels significantly predicted increased EFT, even after adjustment for BMI. On the other hand, the positive association of increased leptin with increased EFT in non-cachetic CHF was blunted after adjustment for BMI. Leptin is an adipocyte-derived protein hormone that is elevated in obesity and results in inhibition of food intake. Leptin causes energy consumption through central stimulation of sympathetic activation. Leptin appears to play multiple roles that include: functioning as a growth factor for various cell types, as a mediator of energy expenditure, as a permissive factor for puberty, and as a signal for modulation of fetal–maternal metabolism. Perhaps most importantly, leptin interacts with other hormonal mediators/regulators of energy metabolism such as insulin, glucagon, insulin-like growth factors, growth hormone (GH) and glucocorticoids. The complexity of the leptin axis suggests the unlikely development of simple obesity treatments. On the other hand, ghrelin is an appetite-stimulating peptide that is secreted by the stomach with regulation by food intake and it causes the release of GH. Ghrelin is released and circulates in the bloodstream under fasting conditions with transmission of a hunger signal to the central nervous system. As a peptide predominantly produced by the stomach and with strong GH-releasing activity, ghrelin contributes significantly to the regulation of diverse functions of the gut–brain axis. Therefore, ghrelin plays an important role in maintaining GH release and energy homeostasis in vertebrates. In patients with CHF, ghrelin has been shown to decrease plasma norepinephrine, increase left ventricular (LV) ejection fraction, increase LV mass, decrease LV endsystolic volume, decrease skeletal muscle wasting, and, during exercise, to increase peak workload plus peak oxygen consumption.