The Heart of NAFLD

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Background

Non-alcoholic fatty liver disease (NAFLD) is rapidly emerging as the most common liver disease worldwide with an estimated global prevalence rate of 25%. The NAFLD epidemic mirrors the rising rates of metabolic syndrome. It results from the accumulation of fat in the liver, in the absence of alcohol consumption or other secondary aetiologies of fat accumulation. The disease spectrum ranges from non-alcoholic fatty liver and non-alcoholic steatohepatitis (NASH), typically differentiated by evidence of hepatic necroinflammation and hepatocyte injury found in NASH. With disease progression, advanced fibrosis can develop, eventually leading to cirrhosis, liver failure and hepatocellular carcinoma (HCC). NAFLD has been traditionally described as the hepatic manifestation of metabolic syndrome. While NAFLD is associated with a host of complications including cirrhosis and malignancy, there is emerging evidence on the extra-hepatic complications of NAFLD, with its increasing recognition as a multisystem disease. Cardiovascular diseases (CVD) are the leading cause of mortality amongst NAFLD patients, followed by extra-hepatic cancers and then liver related complications. The presence of NAFLD is not only associated with several cardiovascular manifestations, but studies have also demonstrated a positive correlation between the severity of NAFLD and CVD.

Although the direct causal relationship between NAFLD and CVD has yet to be definitively established, NAFLD is associated with atherosclerosis independent of the traditional cardiovascular risk factors. The combination of insulin resistance and the proinflammatory milieu affects the lipogenesis cycle and glucose metabolism, predisposing to atherogenesis and eventually CVD. This complex interplay of vasoactive, thrombogenic, inflammatory and oxidative factors may all contribute to atherosclerosis, coronary artery disease, structural changes to the myocardium and cardiomyopathy, valvular calcification and even defects in the conduction system. While the presence of obesity and metabolic syndrome in NAFLD has been a primary driver in the development of CVD, a subset of NAFLD (known as lean NAFLD) has gained much interest as preliminary evidence suggests it to be associated with increased risk of CVD. Moreover, the severity of liver histology, in particular hepatic fibrosis, has been shown to be positively correlated with increased cardiovascular-related fatal and nonfatal events. Indeed the interdependence and crosstalk between the liver and other organs, increases cardiovascular risk in NAFLD patients through multiple pathophysiology mechanisms. The current evidence primarily describes the pathophysiology hypotheses on the associations of NAFLD and CVD. More studies interrogating the bi-directional causal relationship between the two entities will be the next important step.

Treatment strategies should be targeted towards NAFLD and CVD, as well as addressing insulin resistance and its related metabolic dysfunction. Treatment strategies require a multifaceted approach focusing on lifestyle modifications, with increasing attention on pharmacological interventions. There are emerging data on the utility of antidiabetic medications (such as pioglitazone, glucagon-like peptide receptor agonist and sodium-glucose transporter-2 inhibitors) and antioxidants (Vitamin E and newer drugs targeting downstream NAFLD pathways such as obeticholic acid) on NAFLD in the presence of CVD. More studies are needed to evaluate the optimal timing and methods of screening cardiovascular disease in NAFLD, as well as the efficacy and safety profile of these pharmacological therapies.

Keywords: Non-alcoholic fatty liver disease, NAFLD, Cardiovascular diseases, insulin resistance, metabolic dysfunction

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