Key result
Concomitant hypoxic liver injury and hypoxic hepatitis linked to ~44% higher in-hospital mortality in cardiogenic shock.
Why the study?
The clinical association of hypoxic liver injury with hypoxic hepatitis regarding in-hospital and 12-month mortality in cardiogenic shock patients required investigation.
Does the presence of both hypoxic liver injury at index emergency room visit and hypoxic hepatitis at 48 hours increase the risk of in-hospital mortality in cardiogenic shock patients?
Cohort (n=1,274)
Yes
Does the presence of both hypoxic liver injury at index emergency room visit and hypoxic hepatitis at 48 hours increase the risk of in-hospital mortality in cardiogenic shock patients?
Cardiogenic shock patients presenting with hypoxic liver injury who subsequently develop hypoxic hepatitis at 48 hours have significantly higher risks of both in-hospital and 12-month all-cause and cardiac mortality.
Answers are grounded in this paper and cite their sources.
May aid early risk stratification in cardiogenic shock; hypothesis-generating pending prospective validation.
Aim Current study aim is to investigate the clinical association of hypoxic liver injury with hypoxic hepatitis pertaining to in-hospital and 12 months mortality in cardiogenic shock patients. Material and Method A total of 1,274 cardiogenic shock patients from September of 2019 to August of 2023 were enrolled. 22 tertiary hospitals from South Korea actively participated in this study. Hypoxic liver injury (HLI) was defined as 2-fold increase of the upper limit of hepatic enzyme at index emergency room visit and hypoxic hepatitis (HH) was defined as 20-fold increase of hepatic enzyme at 48hrs from admission. Patients were divided into 4 groups according to their liver injury status; groups 1: HLI (-)/HH (-), group 2: HLI (-)/HH (+), group 3: HLI (+)/HH (-), group 4: HLI (+)/HH (+). Primary end point was in-hospital mortality. Secondary endpoints were in-hospital cardiac mortality, 12 months; all-cause mortality, cardiac mortality, ischemic stroke, readmission for heart failure and major bleeding. Results The prevalence of HLI and HH were 48.9% and 56.9% respectively. Amongst the groups categorized respectful to their liver injury status, group 4 had the highest peak CK-MB (42.79±82.96, 224.35±208.98, 166.69±189.41, 249.49±203.45, p<0.001), lactic acid (3.58±3.51, 4.94±3.43, 6.48±4.89, 7.69±4.79, p<0.001), sequential organ failure assessment (SOFA) score (7.05±3.63, 7.70±3.561, 8.30±3.49, 8.76±3.47, p<0.001) and left ventricular ejection fraction (38.05±17.97, 36.48±16.55, 33.81±16.32, 29.12±15.75, p<0.001) respectfully. Utilization of mechanical support was significantly higher (ECMO: 28.2%, 48.9%, 51.6%, 64.1%, p<0.001; CRRT: 17.5%, 25.3%, 23.9%, 42.2%, p<0.001; mechanical ventilation: 49.7%, 57.0%, 65.1%, 72.1%, p<0.001) in group 4. The risk of in-hospital mortality (HR=1.44, 95% CI=1.001-2.070, p=0.049), in- hospital cardiac mortality (HR=1.562, 95% CI=1.052-2.318, p=0.027) and 12 months all-cause mortality (HR=1.597, 95% CI=1.139-2.239, p=0.007), cardiac mortality (HR=1.756, 95% CI=1.202-2.656, p=0.004) were the highest in group 4 even after adjusting relevant risk factors. Conclusion Cardiogenic shock patients with HLI at index emergency room visit who had developed HH were at a higher risk of in-hospital all-cause/cardiac mortality and 12 months all-cause/cardiac mortality. Identification of HLI at index emergency room visit and early detection of escalation to HH can be beneficial in cardiogenic shock patients. Further study regarding the management of such acute hypoxic liver damage resulting from cardiogenic shock is warranted.
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Choi et al. (2026) conducted a cohort in Cardiogenic shock (n=1,274). Hypoxic liver injury with hypoxic hepatitis (HLI+/HH+) vs. No hypoxic liver injury or hypoxic hepatitis (HLI-/HH-) was evaluated on In-hospital mortality (HR 1.44, 95% CI 1.001-2.070, p=0.049). Concomitant hypoxic liver injury and hypoxic hepatitis in cardiogenic shock increased in-hospital mortality risk (HR 1.44; 95% CI 1.001-2.070; p=0.049).
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