In the last decades, the interest in the role of Epicardial Fat Thickness (EFT) in the cardiovascular and metabolic diseases has increased exponentially. Epicardial Fat (EF) is defined as the true visceral depot of the heart and is located between the myocardium and the visceral pericardium. EF, similar to the intra-abdominal fat, embryologically evolves from the brown adipose tissue and is responsible for the production of many molecules (proinflammatory and ant-inflammatory). A unique anatomic characteristic of the EF is the close connection with the coronary vessels, with whom it shares the vascularization. Robust evidence supports the importance of a paracrine interaction between epicardial fat and coronaries, thus the role of EF in cardioovascular diseases. Nonalcoholic Fatty Liver Disease (NAFLD) is the most common hepatic disease worldwide. NAFLD represents a broad spectrum of conditions, ranging from steatosis to nonalcoholic steatohepatitis (NASH), which is characterized by hepatic necroinflammation
with a potential of evolution to fibrosis and even to cirrhosis. Oxidative stress is considered of primary importance in the progression from fatty liver to NASH, representing one of the most plausible mechanisms involved in the progression of liver damage. This study aims to explore the interplay between oxidative stress, endothelial dysfunction, and EFT in patients affected by NAFLD.
To our knowledge, this will be the first study to assess the relationship between EFT, oxidative stress, and severity of liver disease. To date, EFT and oxidative stress have been studied only in a cohort of patients affected by hypothyroidism. Although there is evidence that EFT may correlate with the severity of liver disease, no data is available on the interplay between EF, oxidative stress, and progression of the NAFLD. Our study proposes a novel approach to the problem. In fact, through
the quantification of the oxidative stress burden, the endothelial function and the EFT in patients affected by different stages of NAFLD and controls, we will be able to demonstrate the interplay between EF and liver disease, which would provide a reasonable starting point for future researches, aiming at determining the underlining mechanisms which link EFT to liver disease and
cardiovascular diseases. Moreover, a correlation between oxidative stress and EFT and endothelial dysfunction would highlight the
importance of EF quantification in the clinical stratification of patients affected by NAFLD. EFT, thanks to its easy and precise quantification during a standard echocardiogram, could represent a new ideal echographic marker to reflect the global oxidative stress burden, which would help the clinician to take into account an unrecognized risk factor for both cardiovascular and liver diseases pathogenesis and progression.
In this scenario, EFT would be represent perfect marker to follow the disease progression and eventually the efficacy of the therapy. To date, the only effective therapeutic option to treat NASH is weight reduction. Many studies have been conducted with differents molecules (Vitam E, Pioglitazon, GLP1-Inhibitor and others) with poor outcomes on the severity of the liver disease. Our study could help to clarify the physiopathology behind this complex disease and address a new potential therapeutic target to treat these patients.