Cardiovascular Risk in NAFLD: An Intimate Relationship?

Nonalcoholic fatty liver disease (NAFLD) is an umbrella definition that designates a wide spectrum of histological liver changes ranging from uncomplicated simple steatosis (nonalcoholic fatty liver disease [NAFLD]) to nonalcoholic steatohepatitis, (NASH) with or without fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), which are closely and mutually interrelated with the metabolic syndrome, in the absence of significant alcohol consumption and other competing causes of chronic liver disease [1]. The development and the progression of the entire histopathological spectrum of NAFLD is affected by several physiological and pathological modifiers, notably including age, sex, ethnicity, abdominal obesity, and diabetes [2]. The natural course of NAFLD is typically characterized by an increased risk of developing liver-related complications and extrahepatic diseases. Indeed, the presence of NAFLD-related cirrhosis is predominantly more conducive to liver-related complications, i.e., hepatic decompensation (ascites or upper gastrointestinal bleeding secondary to portal hypertension or hepatic encephalopathy) or HCC, whereas the presence of histological “bridging” liver fibrosis is more closely associated with an increased risk of developing major vascular events (myocardial infarction, heart failure requiring hospitalization, angina, aneurysm dissection, cardiac arrest, and ischemic or hemorrhagic stroke) and extrahepatic cancers [3]. Of the three key histological elementary lesions of NAFLD/NASH [1], the amount of liver fat content (LFC) and the severity of liver fibrosis can be accurately assessed with several noninvasive imaging techniques, including magnetic resonance imaging-based proton density fat fraction (MRI-PDFF) and shear wave elastography (SWE), respectively [4, 5].