BACKGROUND: We attempted to identify the physiologic circumstances associated with the portal Doppler waveform. METHOD: The subjects were 98 patients: 42 had cirrhosis; 23, hepatitis; and 33, no liver disorder. We measured right portal venous peak velocity, minimum velocity, and hepatic arterial peak systolic velocity. Portal venous pulsatility was calculated as portal venous minimum velocity divided by portal venous peak velocity. We analyzed portal waveforms both qualitatively and quantitatively. RESULTS: Portal Doppler waveforms were classified as nonphasic, monophasic, biphasic, biphasic including spike wave, and triphasic. Portal waveforms were phasic in 84 subjects who had a mild systolic dip during the arterial systolic period. Markedly portal pulsatility (portal venous pulsatility<0.6) was present in only 7 subjects. A systolic spike wave corresponding to a hepatic arterial peak systolic wave was detected in 48 subjects. Hepatic arterial peak systolic velocity was significantly higher in the group with spike wave than in the group without it. CONCLUSION: Although portal pulsatility is generally attributed to multiple factors, the present study has pointed out a new factor; transmission via the hepatic artery through the portal vein vasa vasorum. Hepatic venous drainage and hepatic arterial blood flow influence portal waveform.
BACKGROUND: We attempted to identify the physiologic circumstances associated with the portal Doppler waveform. METHOD: The subjects were 98 patients: 42 had cirrhosis; 23, hepatitis; and 33, no liver disorder. We measured right portal venous peak velocity, minimum velocity, and hepatic arterial peak systolic velocity. Portal venous pulsatility was calculated as portal venous minimum velocity divided by portal venous peak velocity. We analyzed portal waveforms both qualitatively and quantitatively. RESULTS: Portal Doppler waveforms were classified as nonphasic, monophasic, biphasic, biphasic including spike wave, and triphasic. Portal waveforms were phasic in 84 subjects who had a mild systolic dip during the arterial systolic period. Markedly portal pulsatility (portal venous pulsatility<0.6) was present in only 7 subjects. A systolic spike wave corresponding to a hepatic arterial peak systolic wave was detected in 48 subjects. Hepatic arterial peak systolic velocity was significantly higher in the group with spike wave than in the group without it. CONCLUSION: Although portal pulsatility is generally attributed to multiple factors, the present study has pointed out a new factor; transmission via the hepatic artery through the portal vein vasa vasorum. Hepatic venous drainage and hepatic arterial blood flow influence portal waveform.