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

## TL;DR

This study uses a computational model to show how acute liver injury harms heart function by reducing blood flow and increasing resistance, leading to weakened cardiac performance.

## Contribution

A closed-loop cardiovascular model reveals the hemodynamic impact of acute liver injury on cardiac function, providing a theoretical basis for liver-heart comorbidities.

## Key findings

- Acute liver injury reduces cardiac output and stroke volume by approximately 17%.
- Increased hepatic vascular resistance raises afterload and decreases left ventricular ejection fraction by about 4%.
- Presinusoidal vascular resistance is the main contributor to cardiac dysfunction in liver injury.

## Abstract

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.

The liver and heart are intimately connected through blood circulation, yet how liver damage directly impacts cardiac function has remained unclear. The liver has a unique dual blood supply (from both the hepatic artery and portal vein), and when injured, its blood vessels stiffen and narrow, forcing the heart to work harder. In this study, we used a computational model of the human circulatory system to investigate how acute liver injury—such as from infections, toxins, or surgery—affects the cardiac function. Our simulations revealed that as acute liver injury worsens, blood flow to the heart decreases, while resistance against pumping increases. This double burden weakens the heart, reducing its pumping efficiency by nearly 20% in severe cases. These findings help explain why liver disease patients often develop heart complications and why heart risks must be carefully assessed before liver surgeries or transplants. By uncovering this liver-heart interaction, our research provides a foundation for better treatments and highlights the need for integrated care in patients with both liver and heart conditions.