Previous research has denoted the existence of a pathophysiological link between both conditions, with NAFLD distinctly increasing the risks of cardiac arrhythmias and myocardial remodelling. Large community-based cohort studies also report independent associations between surrogate markers of NAFLD, including high serum gamma-glutamyltransferase levels, and higher risks of new-onset HF events.
This review aimed to characterise the association between NAFLD and new-onset HF. It further described putative biological mechanisms underpinning this association and explored NAFLD-targeted pharmacotherapies with the potential to improve cardiac complications.
According to recent observational cohort studies, patients with NAFLD possess a 1.5-fold higher risk of developing new-onset HF. This association was stronger for HF with preserved ejection fraction (HFpEF) than for HF with reduced ejection fraction (HFrEF) and retained its statistical significance even after adjusting for patient- and diagnosis-specific confounders. Moreover, the risk of new-onset HF increased with NAFLD severity, particularly with higher fibrosis stage. Higher non-invasive liver fibrosis scores, including the FIB-4 index, were further found to be associated with higher risks of hospitalisation for HF. Ultimately, the pathophysiological link between both conditions may be explained by low-grade inflammation, which characterises NAFLD and may contribute to myocardial remodelling and hypertrophy. Pharmacotherapies targeting proinflammatory cytokines, including interleukin-1, may thus improve NAFLD severity and cardiac contractility in patients with simultaneous HF.