P3466Cardiac output in end-stage liver disease increases with the severity of liver dysfunction
Abstract Background End-stage liver disease is associated with significant systemic and haemodynamic alterations that affect cardiac function. Cirrhotic cardiomyopathy remains an ill-defined entity among cardiologists. Understanding the complex interplay between liver dysfunction and cardiac function can lead to a better understanding of the compensatory mechanisms of the heart in liver failure. Purpose To investigate whether severity of liver disease affects baseline cardiac output in a large contemporary cohort of patients undergoing liver transplant work-up. Methods Consecutive patients that underwent pre-liver transplant (LT) workup between 2010–2017 were included. All patients underwent a resting echocardiogram. Cardiac output (CO) was prospectively recorded at baseline by pulsed-wave Doppler examination of the left ventricular outflow tract from the apical window and systemic vascular resistance (SVR) was calculated as 80 x (mean arterial pressure (MAP)/CO). Severity of liver disease was characterized by the model of end-stage liver disease (MELD) and Child-Pugh scores. Results 560 patients were included (mean age 57.5±7.7, 74.8% male). Mean MELD score was 19±7 and Child-Pugh Score was 9±3. There was an inverse linear relationship between the severity of liver disease by the MELD score and baseline SVR (rho 0.40, P<0.001). As SVR reduced, there was also a significant rise in baseline CO with a strong inverse correlation between the two variables (rho 0.86, p<0.001). There was a significant linear correlation between the severity of liver disease and baseline CO with both the scores (MELD Score rho 0.42, p<0.001; Child Pugh rho 0.44, p<0.001) (Figure). Baseline CO in LT Patients by Severity Conclusions Baseline CO increased with the severity of liver dysfunction due to a reduced afterload. A higher resting CO may lead to patients encroaching on their cardiac reserve at rest. This provides a pathophysiological insight suggesting a limited role for beta-blockers, particularly in patients with advanced liver cirrhosis.