The most common causes of chronic
liver disease in the developed world-
nonalcoholic fatty liver disease (
NAFLD) and
nonalcoholic steatohepatitis (NASH)-are the hepatic manifestations of an
insulin-resistant state that is linked to visceral adiposity and systemic
inflammation.
NAFLD and NASH lead to an expansion of epicardial adipose tissue and the release of proinflammatory
adipocytokines that cause microcirculatory dysfunction and
fibrosis of the adjoining myocardium, resulting in
atrial fibrillation as well as
heart failure with a preserved ejection fraction (HFpEF). Inflammatory changes in the left atrium lead to electroanatomical remodeling; thus,
NAFLD and NASH markedly increase the risk of
atrial fibrillation. Simultaneously, patients with
NAFLD or NASH commonly show diastolic dysfunction or latent HFpEF. Interventions include 1)
weight loss by
caloric restriction,
bariatric surgery, or intensive exercise, and 2) drugs that ameliorate fat-mediated
inflammation in both the liver and heart (eg,
statins,
metformin,
sodium-glucose cotransporter 2 inhibitors,
glucagon-like peptide-1 receptor agonists, and
pioglitazone). Patients with
NAFLD or NASH commonly have an
inflammation-related atrial and ventricular
myopathy, which may contribute to symptoms and long-term outcomes.