Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease and its prevalence is increasing at an alarming rate, ranging from 15 % to 45 %, particularly high in the Americas and South-East Asia [1], [2], [3]. NAFLD has become the second most common reason for liver transplantation in Western countries [4]. It has emerged as one of the most challenging health issues and is associated with increased economic burdens [5].

NAFLD is defined by an excessive deposition of fat involving more than 5 % of hepatocytes without significant alcohol consumption and other secondary causes of liver steatosis [6]. It encompasses a broad spectrum of liver disease ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), a progressive form of hepatic damage, inflammation, and fibrosis [7]. NAFLD has been considered to be a multisystem disease [8]. For instance, cardiovascular disease is linked to a major cause of death in patients with NAFLD. Interestingly, most of the morbidity and mortality in patients with NAFLD do not result from progressive liver disease but are derived from the increased risk of cardiovascular disease [9], [10], [11].

In addition, growing evidence suggests a possible link between NAFLD and heart function [12,13]. Heart failure (HF) has become an important health issue in recent decades [14]. HF is a major cause for hospitalization [15] and markedly increases all-cause mortality. It is categorized according to left ventricular (LV) ejection fraction (EF) into either HF with reduced EF (HFrEF) or HF with preserved EF (HFpEF), also referred to as LV diastolic dysfunction. The diagnosis and management of HFrEF have been relatively well studied, whereas that of HFpEF has remained incompletely understood. LV diastolic dysfunction has important clinical implications since the prevalence is increasing and almost half of the patients with HF have HFpEF [16,17]. In addition, the prognosis and mortality rate of HFpEF have been similar to HFrEF [18,19]. Recent studies highlighted the potential benefits of dapagliflozin and empagliflozin in reducing the combined risk of worsening HF and cardiovascular death in patients with HFpEF [20,21]. As a result, these medications have been included as class I intervention in the new ESC 2023 guidelines for the treatment of HFpEF [22]. However, the identification of predisposing factors associated with HFpEF remains important for setting up effective prevention strategies.

Previous small cross-sectional studies demonstrated that people with NAFLD had altered LV structure and diastolic dysfunction [23], [24], [25], [26]. Early features of LV diastolic dysfunction have been shown in patients with type 2 diabetes and NAFLD [27,28]. However, due to the predominantly cross-sectional design of most studies, the causal relationship between the two conditions has remained elusive. Recently, systematic review reported that NAFLD was associated with a 1.5-fold higher risk of heart failure with assessed mainly by International Classification of Diseases (ICD) codes [12]. Moreover, there has been limited study evaluating the casual association between hepatic fibrosis and subclinical myocardial dysfunction evaluated by echocardiography. Nevertheless, several underlying pathophysiological processes could potentially elevate the risk of HF in individuals with NAFLD [13]. Thus, this study aimed to investigate the longitudinal effects of hepatic steatosis and fibrosis by abdominal sonography and liver fibrosis prediction models on the development of LV diastolic dysfunction using serial echocardiography in a large population.