Preoperative hemihepatic portal vein embolization (PVE) has been introduced in an attempt to extend the indications for major hepatic resections and increase the safety of this procedure.
PVE was first developed by Makuuchi et al. in 1990 (29) for the treatment of hilar cholangiocar-cinoma. PVE induces homolateral atrophy of the portion of the liver scheduled for resection and contralateral compensatory hypertrophy in the remnant liver, thereby decreasing the risk of postoperative liver failure. In 1986, Kinoshita began applying this technique in HCC patients scheduled to undergo hepatic resection (30).
Generally, PVE is indicated when the remnant liver is expected to be less than 40% of the preoperative liver volume in patients with normal liver function [no jaundice, 15-min retention rate of indocyanine green (ICG-R15) <10%], or less than 50% in patients with liver dysfunction (obstructive jaundice or an ICG-R15 of 10-19%) (31). PVE is not recommended for patients with moderate or severe liver dysfunction (ICG-R15 > 20%) because the hypertrophy of the unembo-lized lobe may be retarded, placing the patient at risk for hepatic failure after the PVE.
Tanaka et al. (32) compared the long-term outcomes of HCC patients who underwent a right hepatectomy with or without preoperative PVE. Although the tumor-free survival rates were similar in the two groups, the cumulative survival rate was significantly higher in the PVE group. They speculated that the improved survival rate in the PVE group was attributable to the better residual hepatic function in this group, which enhanced the patients' tolerance to further treatment, including second hepatic resections. Azoulay et al. (33) and Wakabayashi et al. (34) reported comparable long-term results in PVE and non-PVE groups (evidence Level 2b).
The indications for PVE in patients with HCC are controversial for several reasons: (1) the livers of most HCC patients are compromised by an underlying liver disease, and the capacity for liver regeneration after hepatic resection is thought to be impaired under such conditions, making it difficult to predict whether sufficient hypertrophy of the future remnant liver segments can be achieved after PVE; (2) most HCCs are hypervascular tumors fed mainly by arterial blood flow, and the cessation of the portal flow induces a compensatory increase in arterial flow in the embolized segments (35), resulting in the rapid progress of the tumors after PVE (34); and (3) arterioportal shunts are frequently found in cirrhotic livers and HCC tumors, and these shunts may attenuate the effect of PVE (36) (evidence Level 4). To overcome the above concerns, Aoki et al. combined selective TACE with PVE before performing major hepatic resections in HCC patients. This double preparation was aimed at (1) using TACE to prevent tumor progression during the period between the PVE and the planned hepatectomy and (2) strengthening the effect of the PVE by first embolizing any arterioportal shunt that may exist using TACE. They applied sequential TACE and PVE in 17 patients with HCC, and 16 of these patients (94%) actually underwent a subsequent major hepatectomy; no postoperative mortalities were experienced in this series, and the five-year overall survival rate was 55.6% (Fig. 7).
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