The Liver–Heart Axis: Linking Liver Stiffness to Early Cardiac Dysfunction in MASLD

Background and Aims Metabolic dysfunction–associated steatotic liver disease (MASLD) is increasingly recognized as a systemic disorder with cardiovascular consequences. Conventional measures such as left ventricular ejection fraction fail to identify early myocardial impairment. The present prospective study was undertaken to evaluate subclinical myocardial dysfunction in MASLD using global longitudinal strain (GLS), assess its correlation with liver stiffness measurement (LSM), and identify its independent predictors. Methods This prospective cross-sectional study included 128 patients with MASLD. GLS was assessed by speckle-tracking echocardiography, and liver stiffness was measured using vibration-controlled transient elastography (FibroScan). A GLS value ≥ 18% was considered abnormal (indicative of subclinical left ventricular dysfunction). Correlation and regression analyses were performed to identify predictors of subclinical myocardial dysfunction. Results Subclinical myocardial dysfunction (GLS ≥ 18%) was detected in 74.2% of MASLD patients despite preserved ejection fraction. Liver stiffness correlated strongly with impaired GLS (r = 0.722, p < 0.001). Patients with abnormal GLS had significantly higher liver stiffness (8.98 ± 1.24 kPa vs. 6.95 ± 0.85 kPa, p < 0.001). Fibrosis stage showed a graded association with worsening GLS. On regression analysis, liver stiffness and body mass index (BMI) emerged as independent predictors of subclinical myocardial dysfunction, while steatosis (CAP) did not correlate with GLS. Conclusions MASLD patients demonstrate a high prevalence of early cardiac dysfunction that is strongly associated with liver stiffness. Myocardial strain imaging combined with liver stiffness measurement offers a valuable approach for early cardio-hepatic risk stratification and integrated care of MASLD patients. Impact and Implications MASLD confers a "silent" cardiac burden, with nearly three-quarters of patients showing subclinical left ventricular dysfunction despite normal ejection fraction. Our study identifies liver stiffness as the key correlate of this cardiac impairment, whereas steatosis alone was not correlated with myocardial dysfunction. These findings suggest that integrating myocardial strain imaging and liver stiffness assessment can enable earlier identification of at-risk MASLD patients, underscoring the need for multidisciplinary management bridging hepatology and cardiology. Clinical Trial Registration CTRI/2024/02/062960 (Clinical Trials Registry – India)