Portal Vein Congestion Index Research Articles

Hepatic blood flow changes in chronic hepatitis C measured by duplex Doppler color sonography: relationship to histological features.

Our aim was to determine if portal vein and hepatic artery blood flow indices are a noninvasive index of severity of liver disease in chronic hepatitis C. The effect of interferon-alpha treatment on liver blood flow was also studied. Liver blood flow measurements were recorded by duplex Doppler color sonography in 39 patients with chronic hepatitis C, 50 healthy controls, and a single patient with hepatocellular carcinoma. Doppler perfusion index (DPI) (calculated as the ratio of hepatic artery flow to total hepatic flow) and the congestive index of the portal vein (area/velocity) were calculated. Liver biopsies were scored for hepatic inflammation and fibrosis. Hepatic arterial flow (415.7+/-329.1 ml/min vs 195.1+/-103.5 ml/min) and DPI (0.27+/-0.14 vs. 0.17+/-0.06) were elevated in chronic hepatitis C patients compared to controls (P = 0.0002 and 0.0003, respectively) while portal vein flow and total hepatic flow were similar. Portal vein congestive index was similar in chronic hepatitis C (0.106+/-0.05) compared to controls (0.125+/-0.08) P 0.52. Hepatic blood flow indices were not related to the grade of hepatic inflammation or the stage of hepatic fibrosis. Twelve weeks of treatment with interferon-alpha had no effect on liver blood flow. In conclusion, patients with chronic hepatitis C have elevated hepatic artery blood flow. Hepatic blood flow indices have no relationship to the severity of histological liver injury in chronic hepatitis C, and these flow indices are unaffected by a 12-week course of interferon-alpha.

Hepatic arterial resistance in cirrhosis with and without portal vein thrombosis: Relationships with portal hemodynamics

Background/Aims : Little information is available on hepatic arterial hemodynamics in cirrhosis because of the invasiveness of methods. Hepatic arterial resistance indexes were evaluated noninvasively by Doppler ultrasonography and were correlated with portal hemodynamics evaluated both noninvasively and invasively. Methods : Hepatic arterial resistance indexes, portal blood flow velocity and volume, and portal vein congestion index were evaluated in 31 controls and 171 cirrhotic patients with (n = 13) or without (n = 158) portal vein thrombosis. Resistance to portal blood flow was also calculated in 15 patients from hepatic venous pressure gradient, measured by hepatic vein catheterization, and portal blood flow. Results : Resistance indexes were significantly higher in cirrhotics without portal thrombosis than in controls (pulsatility index, 1.30 ± 0.29 vs. 0.89 ± 0.09; P < 0.001; resistive index, 0.71 ± 0.07 vs. 0.59 ± 0.04; P < 0.001). In patients with portal thrombosis, the pulsatility index (1.86 ± 0.39) and resistive index (0.81 ± 0.06) were significantly higher than in controls ( P < 0.001) and in patients without thrombosis ( P < 0.001). Resistance indexes directly correlated with portal resistance ( P < 0.01), the congestion index ( P < 0.01), and the degree of esophageal varices ( P < 0.01). Conclusions : Hepatic arterial resistance indexes increase in cirrhosis, particularly with portal vein thrombosis. The pathophysiology of the increase in hepatic arterial resistance seems to be parallel to that of portal resistance.