Acute-on-chronic liver failure: the heart and systemic hemodynamics

Purpose of review Circulatory abnormalities in cirrhosis include hyperdynamic circulation and cirrhotic cardiomyopathy. The extent of circulatory abnormalities is further exaggerated in acute-on-chronic liver failure (ACLF). The mechanism remains unclear and management also needs to be evaluated. Recent findings The predominant mechanism of ACLF is thought to be a systemic inflammatory reaction. Cardiovascular-active factors such as tumor necrosis factor and nitric oxide are increased and cortisol is decreased; the former further dilates the vasculature and the latter decreases the sensitivity to vasoconstrictors. The exaggerated vasodilatation further decreases the cardiac afterload. However, no study has yet demonstrated the benefit of vasodilators/vasoconstrictors in the management of ACLF. Standard medical treatment in this setting is associated with high mortality. Patients treated with molecular adsorbent recirculating system (MARS) had improved serum levels of inflammatory mediators such as tumor necrosis factor alpha and interleukin-6, but this was not associated with improved survival. Liver transplantation eventually reverses the cardiovascular abnormalities. Summary Circulatory abnormalities are exaggerated in ACLF. The predominant mechanism is a systemic inflammatory reaction. Modalities such as MARS improve serum markers of inflammation, but not survival. Liver transplantation is the definitive treatment of the cardiovascular abnormalities of ACLF.