Nonalcoholic Fatty Liver Disease and Cardiovascular Diseases: The Heart of the Matter

Abstract

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most frequent cause of liver disease worldwide, comprising a plethora of conditions, ranging from steatosis to end-stage liver disease. Cardiovascular disease (CVD) has been associated with NAFLD and CVD-related events represent the main cause of death in patients with NAFLD, surpassing liver-related mortality. This association is not surprising as NAFLD has been considered a part of the metabolic syndrome and has been related to numerous CVD risk factors, namely, insulin resistance, abdominal obesity, dyslipidemia, hyperuricemia, chronic kidney disease, and type 2 diabetes. Moreover, both NAFLD and CVD present similar pathophysiological mechanisms, such as increased visceral adiposity, altered lipid metabolism, increased oxidative stress, and systemic inflammation that could explain their association. Whether NAFLD increases the risk for CVD or these diagnostic entities represent distinct manifestations of the metabolic syndrome has not yet been clarified. This review focuses on the relation between NAFLD and the spectrum of CVD, considering the pathophysiological mechanisms, risk factors, current evidence, and future directions.

Positive Effects of Exercise Intervention without Weight Loss and Dietary Changes in NAFLD-Related Clinical Parameters: A Systematic Review and Meta-Analysis

“…The main cause of death in NAFLD individuals is cardiovascular diseases (CVDs) [ 71 ]. One reason for developing CVDs is atherogenic dyslipidemia, which is characterized by a low HDL-C concentration and high LDL-C, TC, and TG concentrations [ 71 ].…”

“…The main cause of death in NAFLD individuals is cardiovascular diseases (CVDs) [ 71 ]. One reason for developing CVDs is atherogenic dyslipidemia, which is characterized by a low HDL-C concentration and high LDL-C, TC, and TG concentrations [ 71 ]. Our analysis with five studies showed that HDL-C did not change after exercise, which is consistent with another SR. LDL-C was significantly decreased after exercise, but no changes were observed in aerobic exercise alone.…”

Prognostic impact of liver fibrosis and steatosis by transient elastography for cardiovascular and mortality outcomes in individuals with nonalcoholic fatty liver disease and type 2 diabetes: the Rio de Janeiro Cohort Study

“…In another cohort study with a very long follow-up (33 years), advanced histological NAFLD fibrosis stages were predictors of all-cause and disease-specific mortality, including CVD, while inflammatory activity grade was not associated with mortality risk [ 31 ]. The pathophysiological mechanisms behind the association of liver fibrosis in NAFLD with cardiovascular disease are still incompletely understood and may involve other pathways besides insulin resistance, such as oxidative stress, inflammation, and gut microbiota [ 32 ]. Another possible physiopathological link between advanced liver fibrosis and atherosclerotic disease development in diabetes was the finding that individuals with NAFLD and diabetes who increased or persisted with abnormally high aortic stiffness during follow-up were also at particular risk of having advanced liver fibrosis [ 23 ].…”

IL-1β and IL-10: diagnostic and prognostic potential of cytokines in the assessment of progression of non-alcoholic fatty liver disease in patients with hypertension

“…It is produced to protect against excessive immune response, limits organ damage, in particular, plays a protective role in liver fibrogenesis and prevents the progression of hepatic steatosis. [11][12][13]. In the liver, IL-10 was detected in hepatocytes, stellate cells, and Kupffer cells, but only a few studies have been performed to investigate the role of endogenous IL-10 in the progression of NAFLD [14].…”