Hemodynamic impact of acute liver injury on cardiac function: An in silico study via a closed-loop cardiovascular model.

Acute liver injury and cardiovascular disease interact, forming a mutually exacerbating vicious cycle. However, the dynamic influence of hepatic vascular impedance on cardiac function has not been systematically elucidated. To address this gap, a closed-loop hemodynamic model based on lumped parameters was developed, encompassing the heart, liver, and the systemic arterial and venous circulation. This model was used to analyze how alterations in hepatic vascular impedance influence cardiac function and to provide a theoretical foundation for understanding liver-heart comorbidities. Healthy subjects served as the control group, while acute liver injury was simulated by proportionally increasing hepatic microvascular resistance. Changes in cardiovascular hemodynamic parameters were then systematically compared across conditions. As the severity of acute liver injury increases, the peak aortic flow and total cardiac output significantly decrease, with stroke volume reduced by approximately 17%. The left ventricular end-diastolic volume and stroke work are markedly diminished. Effective arterial elastance increases by about 20.7%, and the left ventricular ejection fraction decreases by approximately 4%. Furthermore, the change in hepatic arterial flow is considerably greater than that in portal vein flow. This closed-loop hemodynamic model reveals that acute liver injury leads to a reduction in preload and an increase in afterload, thereby causing abnormalities in both systolic and diastolic cardiac function. Global sensitivity analysis demonstrated that changes in presinusoidal vascular resistance serve as the major contributors to the resulting cardiac dysfunction. These findings provide a theoretical basis for understanding the interplay between liver and heart, and offer a feasible method for pre-assessing cardiovascular risk in patients prior to liver resection or transplantation.