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.
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.
Authors: Samil Hizli; A Koçyigit; N Arslan; S A Tuncel; F Demircioglu; H Cakmakçi; B Büyükgebiz Journal: Indian J Pediatr Date: 2010-03-19 Impact factor: 1.967
Authors: S Gaiani; A Avogaro; G C Bombonato; M Bolognesi; F Amor; S Vigili de Kreutzenberg; G Guarneri; D Sacerdoti Journal: J Ultrasound Date: 2009-01-20