Hepatic Veins ; physiopathology ; Humans ; Hypertension, Portal ; physiopathology ; Portal Pressure

Pathologic increase in portal pressure can be caused by increased resistance to blood flow at the level of the portal vein (pre-hepatic), hepatic sinusoids (hepatic) or hepatovenous outflow (post-hepatic). This results in recruitment and dilatation of tiny portosystemic collateral pathways, diverting portal venous blood flow to low pressure systemic veins. Based on the location of the causative factor of portal venous resistance, different collateral pathways and shunts may develop, resulting in unique syndromes of portal hypertension and in-turn requiring unique treatment options. Knowledge of the common and less-common portosystemic collateral pathways have important implication for clinicians and interventionalists. The objective of this pictorial review is to illustrate the various collateral pathways using diagrammatic and conventional non-invasive and invasive radiologic examples. Additionally, we will briefly address minimally invasive interventional techniques used to treat the sequelae of portal hypertension.
Dilatation ; Hypertension, Portal ; Portal Pressure ; Portal Vein ; Radiology, Interventional ; Varicose Veins ; Veins

Splenoportography has been proved as a useful method for the evaluation of circulatory distrubances in portalhypertension. Authors analyzed the various aspects of these disturbances on splenoportography in 22 cases thatwere performed under the clinical suspicion of portal hypertension during recent 6 years, from May, 1976 to July,1982 at the Department of Radiology, National Medical Center. The results were as follows; 1. Liver cirrhosis wasthe most frequent cause of intrahepatic obstruction type in portal hypertenstion (86%). 2. The portal pressure wasmore than 400 mmH2O in 67% of the cases (range; 300-540 mmH2O). 3. In the majority of the cses, the higher theportal pressure was, the more dilated splenic and portal veins were. The diameter of portal vein was more than15mm in 79%, more than 21 mm in 47% of the cases (range; 10-26mm). The diameter of splenic vein was more than 15mmin 48% of the cases (range; 7-23mm). Especially the diameter of splenic vein was larger than that of portal veinin 20% of the cases. 4. There was no definite correlation between the development of collateral circulation andthe diameter of splenic and portal veins. 5. The filling of collateral circulation was definite sign of portalhypertenstion, though not regular. In portal hypertension, the collateral circulation was formed via coronary vein(91%), short gastric vein (64%), inferior mesenteric vein(36%). 6. Splenic-hilum time was delayed in 64% of thecases. Intrahepatic portal vein emptying time was more than 6 seconds in all the cases. 7. Most of the cases (91%)could be diagnosed as portal hypertension with vasculogram and hepatogram.
Collateral Circulation ; Hypertension, Portal ; Liver Cirrhosis ; Methods ; Portal Pressure ; Portal Vein ; Portography ; Splenic Vein ; Veins

Gastroesophageal varices are the most common lethal complication of cirrhosis that result most directly from portal hypertension. Patients with cirrhosis and gastroesophageal varices have an hepatic venous pressure gradient (HVPG) of at least 10~12 mmHg. An increased portal pressure gradient results from both an increase in resistance to portal flow and an increase in portal blood inflow. Patients whose HVPG decreased to < 12 mmHg or at least 20% from baseline levels have a lower probability of developing recurrent variceal hemorrhage. Therefore, a reduction in HVPG is most important. Nonselective beta-blockers are the gold standard in the prevention of first variceal hemorrhage in pateints with medium/large varices. Endoscopic variceal ligation (EVL) has been established as an alternative to nonselective beta-blockers for the prevention of initial variceal hemorrhage. The combination of vasoconstrictive pharmacological therapy and variceal ligation is the preferred approach to the management of acute variceal hemorrhage. Prophylactic antibiotic therapy is considered standard of care as adjunctive treatment of the acute bleeding episode. Both combination pharmacological therapy and EVL have been proven effective for the prevention of recurrent variceal hemorrhage. For failures of medical therapy, TIPS or surgically created shunts are excellent salvage procedures.
Fibrosis ; Hemorrhage ; Humans ; Hypertension, Portal ; Ligation ; Portal Pressure ; Standard of Care ; Varicose Veins ; Venous Pressure

Portal hypertension is responsible for most of the complications associated with liver cirrhosis, including variceal hemorrhage, ascites, and hepatic encephalopathy. It has become clear that a decrease in portal pressure can prevent or manage these serious complications. Until now, the pharmacotherapy of portal hypertension has focused on agents that reduce splanchnic blood flow, such as non-selective beta blockers and splanchnic vasoconstrictors. However, recent advances in the knowledge of the pathophysiology of portal hypertension have directed future treatment towards modulating the increased intrahepatic vascular resistance, in addition to managing the splanchnic circulation. Consequently, agents that modulate either the hyperdynamic circulation or angiogenesis are new therapeutic targets for managing portal hypertension. Several have been developed or are under investigation. To incorporate these pharmacologic approaches into clinical practice, data on patient-oriented outcomes are needed.
Ascites ; Hemorrhage ; Hepatic Encephalopathy ; Hypertension, Portal ; Liver Cirrhosis ; Portal Pressure ; Splanchnic Circulation ; Vascular Resistance ; Vasoconstrictor Agents

OBJECTIVETo evaluate the agreement and correlation between hepatic vein pressure gradient (HVPG) and portal vein pressure (PVP) in patients with portal hypertension,and explore their clinical value.

METHODSA total of 46 patients with portal hypertension were directly measured the free hepatic pressure, wedged hepatic pressure, portal vein pressure before and after TIPS therapy. The agreement and correlation of HVPG and PVP were analyzed, and explore their clinical value.

RESULTSThere is no significant agreement or correlation between HVPG and PVP in 5 patients, whose third hilar have large communicating branches between portal vein and Inferior vena cava, or with obvious umbilical vein opened. The HVPGs were significantly agreed with portal vein pressure in other 41 patients. There is no significant difference of HVPG or PVP between earlyTIPS and not early-TIPS groups. In addition, the portal vein pressures after TIPS were significantly decreased compared with that before TIPS.

CONCLUSIONThe HVPG can well show the PVP except these with obvious communicating branches between portal vein and Inferior vena cava in third hilar, and TIPS can effectively decrease the portal vein pressure in patients with portal hypertension.

A growing number of studies have explored endoscopic ultrasound (EUS)-guided vascular catheterization. Potential clinical applications of EUS-guided portal venous access include angiography, measurement of the portosystemic pressure gradient, EUS-guided transhepatic intrahepatic portosystemic shunt creation and portal vein sampling for the evaluation in gastrointestinal cancer. The following article reviews the different devices and techniques employed in these applications.
Angiography ; Endosonography ; Gastrointestinal Neoplasms ; Portal Pressure* ; Portal Vein ; Portasystemic Shunt, Surgical ; Ultrasonography ; Vascular Access Devices

The Baveno VII workshop held in October 2021 was featured by the subject of personalized care in portal hypertension. The workshop focused on the following 9 topics including: the relevance and indications for measuring the hepatic venous pressure gradient as a gold standard; the use of non-invasive tools for the diagnosis of compensated advanced chronic liver disease and clinically significant portal hypertension; the impact of etiological and of non-etiological therapies in the course of cirrhosis; the prevention of the first episode of decompensation; the management of the acute bleeding episode; the prevention of further decompensation; as well as the diagnosis and management of splanchnic vein thrombosis and other vascular disorders of the liver. This essay provides a compilation and summary of recommendations regarding the abovementioned topics, and presents the most recent research proceedings and the corresponding consensus to our readers.
Consensus ; Esophageal and Gastric Varices ; Humans ; Hypertension, Portal/therapy* ; Liver Cirrhosis/therapy* ; Portal Pressure

The liver is abundant in blood supply and receives 25% of the cardiac output via the hepatic artery and portal vein. Circulatory disorders may cause hepatic injury, resulting in congestive hepatopathy(CH) and ischemic hepatitis(IH). Hepatic congestion arising from increased hepatic venous pressure and decreased cardiac output is the common pathophysiological basis of both CH and IH. In addition, extensive arteriovenous shunts affect portal pressure and cardiac function, leading to alterations of hepatic blood supply. The current review summarizes the pathophysiology, clinical manifestations and therapeutic interventions of the above diseases, in order to provide reference for clinical practice.
Cardiovascular Diseases ; Hepatic Artery ; Humans ; Liver ; Liver Diseases ; Portal Pressure ; Portal Vein

BACKGROUND/AIMS: Non-selective beta blockers (NSBBs) are currently the only accepted regimen for preventing portal hypertension (PHT)-related complications. However, the effect of NSBBs is insufficient in many cases. Bacterial translocation (BT) is one of the aggravating factors of PHT in cirrhosis; therefore, selective intestinal decontamination by rifaximin is a possible therapeutic option for improving PHT. We investigated whether the addition of rifaximin to propranolol therapy can improve hepatic venous pressure gradient (HVPG) response. METHODS: Sixty-four cirrhosis patients were randomly assigned to propranolol monotherapy (n=48) versus rifaximin and propranolol combination therapy (n=16). Baseline and post-treatment HVPG values, BT-related markers (lipopolysaccharide [LPS], LPS-binding protein [LBP], interleukin-6 [IL-6], and tumor necrosis factor α [TNF-α]), serological data, and adverse event data were collected. HVPG response rate was the primary endpoint. RESULTS: Combination therapy was associated with better HVPG response rates than monotherapy (56.2% vs 87.5%, p=0.034). In combination therapy, posttreatment BT-related markers were significantly decreased (LPS, p=0.005; LBP, p=0.005; IL-6, p=0.005; TNF-α, p=0.047). CONCLUSIONS: Rifaximin combination therapy showed an additive effect in improving PHT compared to propranolol monotherapy. These pilot data suggest that the addition of rifaximin to NSBBs could be a good therapeutic option for overcoming the limited effectiveness of NSBBs.
Bacterial Translocation ; Decontamination ; Fibrosis ; Humans ; Hypertension, Portal ; Interleukin-6 ; Pilot Projects* ; Portal Pressure* ; Propranolol* ; Tumor Necrosis Factor-alpha ; Venous Pressure