BACKGROUND: Liver dysfunction increases post-surgical morbidity and mortality. The Model of End-stage Liver Disease (MELD) estimates liver function but can be inaccurate in patients receiving oral anti-coagulation. We evaluated the effect of liver dysfunction on outcomes after ventricular assist device (VAD) implantation and the dynamic changes in liver dysfunction that occur during VAD support. METHODS: We retrospectively analyzed 255 patients (147 with pulsatile devices and 108 with continuous-flow devices) who received a long-term VAD between 2000 and 2010. Liver dysfunction was estimated by MELD and MELD-eXcluding INR (MELD-XI), with patients grouped by a score of ≥ 17 or < 17. Primary outcomes were on-VAD, after transplant, and overall survival. RESULTS: MELD and MELD-XI correlated highly (R ≥ 0.901, p < 0.0001) in patients not on oral anti-coagulation. Patients with MELD or MELD-XI < 17 had improved on-VAD and overall survival (p < 0.05) with a higher predictive power for MELD-XI. During VAD support, cholestasis initially worsened but eventually improved. Patients with pre-VAD liver dysfunction who survived to transplant had lower post-transplant survival (p = 0.0193). However, if MELD-XI normalized during VAD support, post-transplant survival improved and was similar to that of patients with low MELD-XI scores. CONCLUSIONS: MELD-XI is a viable alternative for assessing liver dysfunction in heart failure patients on oral anti-coagulation. Liver dysfunction is associated with worse survival. However, if MELD-XI improves during VAD support, post-transplant survival is similar to those without prior liver dysfunction, suggesting an important prognostic role. We also found evidence of a transient cholestatic state after LVAD implantation that deserves further examination.
BACKGROUND:Liver dysfunction increases post-surgical morbidity and mortality. The Model of End-stage Liver Disease (MELD) estimates liver function but can be inaccurate in patients receiving oral anti-coagulation. We evaluated the effect of liver dysfunction on outcomes after ventricular assist device (VAD) implantation and the dynamic changes in liver dysfunction that occur during VAD support. METHODS: We retrospectively analyzed 255 patients (147 with pulsatile devices and 108 with continuous-flow devices) who received a long-term VAD between 2000 and 2010. Liver dysfunction was estimated by MELD and MELD-eXcluding INR (MELD-XI), with patients grouped by a score of ≥ 17 or < 17. Primary outcomes were on-VAD, after transplant, and overall survival. RESULTS: MELD and MELD-XI correlated highly (R ≥ 0.901, p < 0.0001) in patients not on oral anti-coagulation. Patients with MELD or MELD-XI < 17 had improved on-VAD and overall survival (p < 0.05) with a higher predictive power for MELD-XI. During VAD support, cholestasis initially worsened but eventually improved. Patients with pre-VAD liver dysfunction who survived to transplant had lower post-transplant survival (p = 0.0193). However, if MELD-XI normalized during VAD support, post-transplant survival improved and was similar to that of patients with low MELD-XI scores. CONCLUSIONS: MELD-XI is a viable alternative for assessing liver dysfunction in heart failurepatients on oral anti-coagulation. Liver dysfunction is associated with worse survival. However, if MELD-XI improves during VAD support, post-transplant survival is similar to those without prior liver dysfunction, suggesting an important prognostic role. We also found evidence of a transient cholestatic state after LVAD implantation that deserves further examination.
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