LAUSR

In this issue of Angiology, Randrianarisoa et al compared peribrachial adipose tissue (PBAT) with periaortic adipose tissue (PAAT) mass in 95 participants participating in the Tübingen Lifestyle Intervention Program. Although in univariate analyses PBAT was strongly correlated with PAAT (P < .0001), after adjustment for several variables, their correlation with carotid intima–media thickness (an indicator of risk of vascular events) and insulin sensitivity differed. The authors concluded that PAAT may be more associated with atherosclerosis, while PBAT better reflects insulin sensitivity. Therefore, fat around the brachial artery or the aorta may have a different significance not only for the local vasculature but also for systemic metabolic factors. The findings of Randrianarisoa et al lead to the concept of different roles attributed to abnormal peri-organ or intra-organ fat (APIFat) deposition. Several organs are surrounded by fat or may, in pathological circumstances, increase their intraorgan fat content such as intrahepatic, epicardial, perivascular, intramuscular, peripancreatic, and perirenal fat. A well-documented example of abnormal APIFat is nonalcoholic fatty liver disease (NAFLD) and its more advanced form, nonalcoholic steatohepatitis (NASH). Both NAFLD and NASH can progress to liver cirrhosis and even hepatocellular carcinoma, but most patients will die from a vascular etiology before cirrhosis and carcinoma occur. Therefore, it follows that these patients require appropriate treatment to prevent both hepatic and vascular events. The role of statins in achieving both objectives is promising, but appropriately designed trials are absent. Apart from therapeutic lifestyle changes and weight loss, there is currently no definitive, evidence-based treatment for NAFLD/NASH. It is also relevant that there is a high prevalence of NAFLD/NASH worldwide, which is likely to rise even further due to the epidemics of obesity and diabetes. Epicardial fat is thought to adversely affect cardiac function. The close proximity of epicardial fat to the myocardium may allow a direct transfer of harmful mediators (eg, cytokines). Several cardiometabolic risk factors, including obesity, diabetes, and dyslipidemia, as well as and inflammatory cytokines, may increase epicardial adiposity. Patients with increased pericardial fat may also have NAFLD/NASH. This link may be a factor that accounts for the increased vascular risk observed in patients with NAFLD/NASH. Perivascular fat was considered by Randrianarisoa et al. Furthermore, “regional differences” between arteries may not only relate to the varying role of perivascular fat but also to differences in local receptor types and density. There are multiple other potentially relevant forms of fat deposition. Skeletal muscle and intramuscular fat are thought to play a key role in glucose homeostasis. However, there is more to insulin resistance than just the fat content of muscles; specific lipid intermediates may also be relevant. Furthermore, the proportion of fat in the muscle tissue may be involved in the development of sarcopenia. Periand intrapancreatic fat may increase the risk of diabetes and worsen acute pancreatitis. Perirenal fat may contribute to the increased risk of hypertension in obese people. Metabolic syndrome (MetS) is associated with NAFLD as well as increased perirenal and epicardial fat. There are probably several other similar associations between APIFat and MetS. It follows that APIFat may turn out to be a relatively poorly documented characteristic of MetS which accounts, at least in part, for the increased risk of vascular events associated with MetS. In addition to the examples discussed above, we must not forget the well-established relevance of the type of fat (eg, brown fat) and subcutaneous versus visceral fat in relation to vascular risk. Abnormal peri-organ or intra-organ fat may also turn out to be relevant to other diseases and involve organs not mentioned above.