## 4 Discussion  
### Liver Elastography  
Liver disease is a known side-effect of the Fontan operation for functional uninventricular hearts. Fibrosis is universally present in patients 10 years after surgery [4]. Hepatic \begin{table}
\begin{tabular}{c c c c c c} \hline \hline
**Investigation** & **Mean—[PERSON] + [PERSON]** & **n** & **Mean—Control** & **n** & \(p\)** \\ \hline E\({}_{\rm median}\)-SWE (kPa) & 4.33 \(\pm\) 0.93 & 33 & 3.91 \(\pm\) 0.39 & 32 & 0.12 \\ \hline V\({}_{\rm median}\)-SWE (m/s) & 1.2 \(\pm\) 0.1 & 30 & 1.12 \(\pm\) 0.16 & 32 & 0.08 \\ \hline Fibrotest & 0.29 \(\pm\) 0.19 & 30 & 0.14 \(\pm\) 0.07 & 30 & **0.0018** \\ \hline Actitest & 0.1 \(\pm\) 0.05 & 30 & 0.05 \(\pm\) 0.03 & 30 & **<0.0001** \\ \hline AST (U/L) & 33.62 \(\pm\) 12.1 & 33 & 26.68 \(\pm\) 11.9 & 28 & **0.0076** \\ \hline ALT (U/L) & 23.06 \(\pm\) 9 & 34 & 17.35 \(\pm\) 7.54 & 30 & **0.0049** \\ \hline Fib-4 & 0.19 \(\pm\) 0.13 & 33 & 0.19 \(\pm\) 0.13 & 26 & 0.92 \\ \hline GCT (U/L) & 23.57 \(\pm\) 15.75 & 33 & 16 \(\pm\) 18 & 30 & **0.0045** \\ \hline TB (mg/dL) & 0.49 \(\pm\) 0.29 & 28 & 0.9 \(\pm\) 2.48 & 30 & 0.98 \\ \hline A2 MG (g/L) & 3.31 \(\pm\) 0.65 & 30 & 3.14 \(\pm\) 0.58 & 30 & 0.32 \\ \hline Haptoglobin (g/L) & 0.77 \(\pm\) 0.54 & 30 & 1.03 \(\pm\) 0.58 & 30 & **0.05** \\ \hline ApoA1 (g/L) & 1.21 \(\pm\) 0.2 & 30 & 1.41 \(\pm\) 0.27 & 30 & **0.0053** \\ \hline Right liver lobe (mm) & 102.06 \(\pm\) 25.4 & 32 & 101.83 \(\pm\) 20.3 & 31 & 0.57 \\ \hline Left liver lobe (mm) & 41.6 \(\pm\) 8.8 & 31 & 42.8 \(\pm\) 9.5 & 31 & 0.68 \\ \hline APRI & 0.35 \(\pm\) 0.2 & 32 & 0.21 \(\pm\) 0.13 & 32 & **0.0001** \\ \hline Thrombocyte count (\(\times 10^{3}\)/uL) & 260.5 \(\pm\) 65 & 33 & 290.72 \(\pm\) 64.4 & 34 & **0.02** \\ \hline \hline \end{tabular} Legend: n = number, \(p\) = \(p\) value, E: elasticity, V: velocity, SWE: Sheavrave elastography, TE: transient elastography, GGT: Gamma glutlymlymseptidase, TB: total bilirubin, A2 MG: alpha 2 macroglobulin, ApoA1: Apolipoprotein A1, APRI: AST-to-Platelet ratio index. In bold- values with statistical significance (\(p\) < 0.05).  
\end{table} 
Table 3: Operated patients ([PERSON] + [PERSON]) vs. controls—elastography and biomarker results. damage seems to precede the operation as shown in the study by [PERSON] et al., which showed fibrosis being present in patients who died immediately after surgery [27]. Nevertheless, few studies have been performed documenting the liver alterations in patients with univentricular hearts before the [PERSON] palliation and the majority lack the validation with liver biopsy. Recently, [PERSON] and co. published a study on 30 Fontan patients and found that liver stiffness values determined by SWE correlated significantly to liver fibrosis scores measured on biopsy specimens [28]. [PERSON] and co-workers used SWE as well and found significantly higher levels of liver stiffness compared to controls in a study of patients with Fontan surgery (15.6 vs. 5.5 kPa) [29]. For the patients who had liver biopsies, increased hepatic stiffness correlated with greater degrees of hepatic fibrotic changes. Another study of the same team on liver disease in patients with the Glenn procedure, showed that patients had slightly increased liver stiffness compared to healthy subjects (7.2 vs. 5.7 kPa) and that liver stiffness was correlated with increased right atrial pressure before surgery [30]. Interestingly, [PERSON] et al. [31] using 2D-SWE obtained normal liver stiffness values in children with Glenn palliation which immediately increased after the Fontan procedure, probably due to the sharp pressure increase in the inferior vena cava [32]. Furthermore, high liver stiffness values immediately after the Fontan procedure might indicate inappropriate circulation. This could explain why liver stiffness determined by TE was found to be much higher after Fontan surgery compared to patients with heart failure due to right ventricle decompensation and secondary liver congestion [33].