The role of epicardial adipose tissue dysfunction in cardiovascular diseases: an overview of pathophysiology, evaluation, and management

Abstract

In recent decades, the epicardial adipose tissue (EAT) has been at the forefront of scientific research because of its diverse role in the pathogenesis of cardiovascular diseases (CVDs). EAT lies between the myocardium and the visceral pericardium. The same microcirculation exists both in the epicardial fat and the myocardium. Under physiological circumstances, EAT serves as cushion and protects coronary arteries and myocardium from violent distortion and impact. In addition, EAT acts as an energy lipid source, thermoregulator, and endocrine organ. Under pathological conditions, EAT dysfunction promotes various CVDs progression in several ways. It seems that various secretions of the epicardial fat are responsible for myocardial metabolic disturbances and, finally, leads to CVDs. Therefore, EAT might be an early predictor of CVDs. Furthermore, different non-invasive imaging techniques have been proposed to identify and assess EAT as an important parameter to stratify the CVD risk. We also present the potential therapeutic possibilities aiming at modifying the function of EAT. This paper aims to provide overview of the potential role of EAT in CVDs, discuss different imaging techniques to assess EAT, and provide potential therapeutic options for EAT. Hence, EAT may represent as a potential predictor and a novel therapeutic target for management of CVDs in the future.

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“…However, it appears to be a metabolically active tissue that secretes adipokines and plays an important role in the storage of free fatty acids [45,48]. However, dysregulation of and increased EAT, (whose density shifts toward lower values, being a negative number expressed in HU) may play an important role in the development of cardiovascular disease through the pro-atherogenic, pro-thrombotic and pro-inflammatory effects caused by increased epicardial fat [26][27][28][29][30]49]. In common clinical practice, patients with FL undergo a PET/CT scan at disease onset and at the end of treatment.…”

“…Increased EAT appears to have pro-inflammatory, pro-thrombotic and pro-atherogenic effects. Thus, EAT has been associated with coronary artery disease (CAD), arrhythmias, heart failure (HF) and other cardiovascular conditions [27][28][29][30]. EAT is strongly and independently correlated with increased cardiac mortality [31].…”

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“…The inhibition of HMGCR, the rate-limiting enzyme in the mevalonate (MVA) biosynthesis pathway and its downstream isoprene compounds, reduced isoprene and affected cell proliferation and the inflammatory response. Moreover, HMGCR inhibits the PI3K/Akt pathway and attenuates the expression of eNOS and nuclear factor-kappa B (NF-κB) in the mevalonate pathway [ 68 , 69 ]. The signaling pathway activated by eNOS is thought to be a key player in this process.…”

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“…Furthermore, given the fact that a relationship between its volume and the extent of CVD and metabolic syndrome has been established, as well as a correlation between EAT volume and the onset and progression of CAD, this specific marker gained a greater clinical value. For that reason, quantification of this tissue has improved in recent years and even though imaging with cardiac magnetic resonance remains the "gold standard" method, echocardiography and cardiac computed tomography can be used as cost-effective and fast modalities to reveal EAT attenuation in the initial stages, which is associated with coronary artery calcification, AMI, and coronary adverse events [42,43].…”