Objective: The objective of this experimental study was to investigate a possible myocardial involvement in acute liver failure.
Materials and methods: A porcine model of acute liver failure induced by hepatic devascularization was used. Twenty animals were allocated to the Acute Liver Failure (ALF) or Control Group (CG). Serum cardiac troponin I (cTnI), MB isoenzyme of creatine kinase (CK-MB), and also hemodynamic variables were measured and compared before surgery (T1), at 4 hr (T2), and at 7 hr (T3) after the end of surgery.
Results: Data from 10 pigs in the ALF and 7 in the CG were analyzed. In the ALF group, cTnI increased from 0.3 ± 0.055 to 0.35 ± 0.696 and 0.39 ± 0.06 ng/ml at T1, T2, and T3 time points, respectively (p < .001). In the CG, cTnI was not significantly changed from 0.29 ± 0.07, to 0.31 ± 0.01, and 0.31 ± 0.11 ng/ml at T1, T2, and T3 time points, respectively (p = .895). A statistically significant difference was found in cTnI between the groups at T3 (z = -2.93, p = .002). CK-MB increased significantly in both groups: in ALF group, CK-MB changed from 3.43 ± 0.53 to 4.33 ± 0.73 and 7.14 ± 1.12 ng/ml at T1, T2, and T3 time points, respectively (p < .001). In the CG, CK-MB changed from 3.6 ± 0.597 to 4.6 ± 1.07 and 6.2 ± 1.17 ng/ml at T1, T2, and T3 time points, respectively, (p = .001). Mean arterial pressure (MAP) was significantly reduced in the ALF group.
Conclusions: In a porcine model of acute liver failure, a significant increase of cTnI serum levels was found, indicating that a subclinical myocardial damage may occur as a result of heart involvement in the multiple organ dysfunction.