OBJECTIVES: To investigate intrahepatic arteriovenous shunt rate due to cirrhosis and hepatocellular carcinoma (HCC), complicated by cirrhosis, and its change after transcatheter arterial embolization. METHODS: The shunt rate was measured by hepatic artery infusion of labeled macroaggregated albumin. Counts were taken over the liver and both lungs for calculation of the shunt rate: cpm in lungs divided by (cpm in liver and lungs) x 100%. RESULTS: The intrahepatic arteriovenous shunt rate of cirrhosis ranged from 6.8% to 16.6% (12.6% +/- 3.4%, mean +/- SD). In HCC, it ranged from 7.2% to 27.1% (16.0% +/- 4.9%, mean +/- SD). The difference between the groups was statistically significant (p < 0.05). When the liver was more than 20% replaced by tumor, the intrahepatic arteriovenous shunt rate was higher than when less than 20% occupied (n = 6, 20.1% +/- 4.8% vs. n = 15, 14.4% +/- 4.0%; p < 0.05). Although the former was significantly different from liver cirrhosis, the latter was not significantly different from the shunt rate observed in liver cirrhosis without HCC. After transcatheter arterial embolization, excluding one patient who developed a visible hepatofugal arterioportal shunt, the mean change in shunt rate between the effective treatment group (n = 9, -2.1% +/- 2.8%, mean +/- SD) and the ineffective treatment group (n = 5, 3.0% +/- 3.3%, mean +/- SD) was statistically significant (p < 0.05). CONCLUSIONS: We found that intrahepatic arteriovenous shunt rate more sensitively detects intrahepatic arteriovenous shunting due to HCC than does angiography alone. Measuring intrahepatic arteriovenous stunt rate may provide useful information regarding response to treatment.
OBJECTIVES: To investigate intrahepatic arteriovenous shunt rate due to cirrhosis and hepatocellular carcinoma (HCC), complicated by cirrhosis, and its change after transcatheter arterial embolization. METHODS: The shunt rate was measured by hepatic artery infusion of labeled macroaggregated albumin. Counts were taken over the liver and both lungs for calculation of the shunt rate: cpm in lungs divided by (cpm in liver and lungs) x 100%. RESULTS: The intrahepatic arteriovenous shunt rate of cirrhosis ranged from 6.8% to 16.6% (12.6% +/- 3.4%, mean +/- SD). In HCC, it ranged from 7.2% to 27.1% (16.0% +/- 4.9%, mean +/- SD). The difference between the groups was statistically significant (p < 0.05). When the liver was more than 20% replaced by tumor, the intrahepatic arteriovenous shunt rate was higher than when less than 20% occupied (n = 6, 20.1% +/- 4.8% vs. n = 15, 14.4% +/- 4.0%; p < 0.05). Although the former was significantly different from liver cirrhosis, the latter was not significantly different from the shunt rate observed in liver cirrhosis without HCC. After transcatheter arterial embolization, excluding one patient who developed a visible hepatofugal arterioportal shunt, the mean change in shunt rate between the effective treatment group (n = 9, -2.1% +/- 2.8%, mean +/- SD) and the ineffective treatment group (n = 5, 3.0% +/- 3.3%, mean +/- SD) was statistically significant (p < 0.05). CONCLUSIONS: We found that intrahepatic arteriovenous shunt rate more sensitively detects intrahepatic arteriovenous shunting due to HCC than does angiography alone. Measuring intrahepatic arteriovenous stunt rate may provide useful information regarding response to treatment.