Work

Noninvasive Hemodynamic Characterization of Cardiohepatic Syndrome in the Cardiac Intensive Care Unit

Year: 2025

Type: article

Abstract: Background Patients with cardiohepatic syndrome are at higher risk of adverse outcomes in the cardiac intensive care unit. We hypothesized that cardiohepatic syndrome phenotypes would exhibit differences in their clinical and transthoracic echocardiogram hemodynamic profiles, portending a higher risk of mortality. Methods We included unique CICU patients with an admission diagnosis of heart failure from 2007 to 2018 with available data for 1 or more admission liver function tests. Echocardiographic variables were extracted from patients who had a transthoracic echocardiogram within 1 day of admission. We assigned patients to 1 of 4 mutually exclusive cardiohepatic syndrome phenotype groups: normal, hepatocellular, cholestasis, and combined. Results We included 3992 CICU patients; 2483 had an available transthoracic echocardiogram. Patients with cholestasis had more right ventricular systolic dysfunction and congestion, whereas those with hepatocellular injury had more left ventricular systolic dysfunction and poor forward flow; hemodynamics and biventricular function were worst in the combined group. In‐hospital mortality occurred in 14.6% and was higher for patients with cholestasis or hepatocellular injury, especially those with greater extent/severity and worse biventricular function or poor hemodynamics. After adjustment, only the group with hepatocellular injury (adjusted odds ratio [OR], 1.35 [95% CI, 1.04–1.75], P =0.03) and the combined group (adjusted OR, 1.75 [95% CI, 1.30–2.34], P <0.001) remained at higher risk. One‐year mortality was highest in the combined group (adjusted hazard ratio [HR], 1.29 [95% CI, 1.10–1.51], P =0.002). Conclusions Cardiohepatic syndrome phenotypes are associated with distinct echocardiographic profiles. Patients with the combined cardiohepatic syndrome phenotype were at highest risk of mortality, particularly if this was combined with poor cardiac function.

Source: Journal of the American Heart Association

DOI: 10.1161/jaha.125.043895