About this Research Topic
Cirrhosis and its complications are responsible for a large number of deaths worldwide annually. Almost 90% of the patients with cirrhosis eventually develop portal hypertension (PHT) and this condition is a prequel to the majority of deaths in these patients. In cirrhosis, PHT is initiated by increased intrahepatic vascular resistance due to tissue fibrosis, architectural distortion and vasoactivity of contractile cells. It is also associated with a hyperdynamic circulatory state characterized by a high cardiac output and splanchnic vasodilatation, resulting in increased mesenteric blood flow. A major life-threatening complication of PHT is the formation of varices and variceal bleeding.
Current ‘gold standard’ clinical treatment to prevent variceal bleeding and improve patient survival by reducing portal pressure is non-selective beta blockade which works by reducing cardiac output and splanchnic vasodilatation. However, the efficacy and tolerability of non-selective beta-blockers is suboptimal as approximately 15% of patients are intolerant to these drugs and up to 60% of patients fail to achieve the treatment response required to prevent variceal bleeding defined as a fall in estimated portal pressure of greater than 20% of baseline values or a fall in the hepatic venous pressure gradient (HVPG) to <12 mmHg.
The goal of this Research Topic is to provide a platform for potential authors to highlight recent advances in PHT research utilizing basic laboratory techniques and/or clinical research. We therefore invite authors to contribute with highly innovative original papers or critical reviews in the field of PHT.
Since there have been very few new therapies introduced for the long-term management of PHT over the last 30 years, we encourage researchers and clinicians in the area of hepatology and liver transplantation to present cutting-edge research on novel aspects of PHT, including novel mechanisms of splanchnic vasodilatation and intrahepatic vascular resistance in cirrhotic PHT, and on new therapies that have the potential to reduce portal pressure.
Current ‘gold standard’ clinical treatment to prevent variceal bleeding and improve patient survival by reducing portal pressure is non-selective beta blockade which works by reducing cardiac output and splanchnic vasodilatation. However, the efficacy and tolerability of non-selective beta-blockers is suboptimal as approximately 15% of patients are intolerant to these drugs and up to 60% of patients fail to achieve the treatment response required to prevent variceal bleeding defined as a fall in estimated portal pressure of greater than 20% of baseline values or a fall in the hepatic venous pressure gradient (HVPG) to <12 mmHg.
The goal of this Research Topic is to provide a platform for potential authors to highlight recent advances in PHT research utilizing basic laboratory techniques and/or clinical research. We therefore invite authors to contribute with highly innovative original papers or critical reviews in the field of PHT.
Since there have been very few new therapies introduced for the long-term management of PHT over the last 30 years, we encourage researchers and clinicians in the area of hepatology and liver transplantation to present cutting-edge research on novel aspects of PHT, including novel mechanisms of splanchnic vasodilatation and intrahepatic vascular resistance in cirrhotic PHT, and on new therapies that have the potential to reduce portal pressure.
Keywords: Portal hypertension, liver cirrhosis, hyperdynamic circulation, intrahepatic resistance, splanchnic vasodilation
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