Key result
Elevated high-sensitivity cardiac troponin I immediately after living donor liver transplantation was associated with increased in-hospital death or graft failure (7.6% vs 1.9%; HR 4.15; P=0.049).
Why the study?
Does elevated hs-cTnI immediately after living donor liver transplantation predict death or graft failure in adult recipients?
Cohort (n=313)
Does elevated hs-cTnI immediately after living donor liver transplantation predict death or graft failure in adult recipients?
Hazard Ratio: 4.15 (95% CI 1.01–17.14)
Absolute Event Rate: 7.6% vs 1.9%
p-value: p=0.049
Myocardial injury detected by elevated hs-cTnI immediately after living donor liver transplantation is an independent predictor of death or graft failure during the hospital stay.
Elevated post-transplant hs-cTnI may flag higher in-hospital risk; hypothesis-generating for routine monitoring in liver recipients.
BACKGROUND: This study aimed to evaluate risk factors and postoperative clinical outcome associated with myocardial injury detected by an elevated high-sensitivity cardiac troponin I (hs-cTnI) immediately after living donor liver transplantation (LDLT). METHODS: Between January 2011 and December 2016, 313 adult recipients undergoing LDLT, with normal preoperative hs-cTnI were selected. Hs-cTnI level above 0.04 ng/mL according to 99th percentile reference limit was defined as myocardial injury. The recipients were divided into 2 groups according to postoperative hs-cTnI measured immediately after LDLT and postoperative clinical outcome was compared. RESULTS: The primary outcome was composite of death or graft failure during hospital stay. Risk factors associated with myocardial injury during LDLT was also evaluated. Of the 313 recipients with normal preoperative hs-cTnI level, 159 (50.8%) had elevated hs-cTnI level and 154 (49.2%) had normal level after LDLT. The incidence of all-cause death or graft failure during hospital stay was significantly higher in recipients with myocardial injury (1.9% vs 7.6%; hazard ratio, 4.15; 95% confidence interval, 1.01-17.14; P = 0.049). The same result was shown in propensity-matched population (0.9% vs 9.0%; hazard ratio, 9.08; 95% confidence interval, 1.16-71.01; P = 0.04). The results during 1-year follow-up were not consistent. Female sex, ischemia time, and presence of postreperfusion syndrome were independent predictors of myocardial injury during LDLT. CONCLUSIONS: Myocardial injury detected by elevation of hs-cTnI level immediately after LDLT was independently associated with adverse outcome during hospital stay.
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Park et al. (2018) conducted a cohort in Living donor liver transplantation (n=313). Elevated high-sensitivity cardiac troponin I (hs-cTnI > 0.04 ng/mL) vs. Normal postoperative hs-cTnI was evaluated on Composite of death or graft failure during hospital stay (HR 4.15, 95% CI 1.01-17.14, p=0.049). Elevated high-sensitivity cardiac troponin I immediately after living donor liver transplantation was associated with increased in-hospital death or graft failure (7.6% vs 1.9%; HR 4.15; P=0.049).
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