No description available.

No description available.

No description available.

No description available.

No description available.

Patients with portal hypertension who have bled from oesophageal varices have a mortality of approximately 30&37 . It is a therapeutic paradox that life-saving resuscitation following haemorrhagic shock may be detrimental by causing variceal rebleeding or continued haemorrhage and by inducing gastric erosions. This thesis addresses the hypotheses: i) secondary bleeding from varices in portal hypertension (PHT) is precipitated by blood volume restitution resulting from increased portal pressure, an increase which can be prevented by the somatostatin analogue, SMS 201-995 (Octreotide); ii) erosive gastritis found in patients with varices results from increased susceptibility to mucosal injury, is exacerbated by reperfusion, and is mediated by oxygen-derived free radicals. The three principal approaches employed were initially to establish prehepatic portal hypertension in a rat model by graded portal vein ligation (PVL). Acute PHT (3 days post-PVL) was characterised by high portal pressure and little portasystemic shunting, while chronic PHT (14 days post-PVL) was characterised by lower portal pressure and increased shunting. In anaesthetised hypovolaemic animals, arterial pressure was reduced below 35mmHg for 30 minutes. Following reperfusion, portal pressure increased by up to 34&37 above baseline values. In acute PHT, this was mediated by increased portal venous inflow, whereas in chronic PHT, outflow resistance increased. The rise in portal pressure was prevented by SMS 201-995 (dose-related). Secondly, studies of the gastric mucosa in PHT demonstrated that; it was not more susceptible to injury; injury was dependent on gastric luminal acidity; a gradient of injury existed, and there was no correlation between injury and portal pressure or shunting.

No description available.

There are limited data on the outcomes of chronic liver disease (CLD) patients admitted for percutaneous coronary intervention (PCI). All PCI hospitalizations from the Nationwide Inpatient Sample (2004 to 2015) were analyzed and stratified by the presence, cause and severity of CLD, as well as the indication for PCI. Multivariable logistic regression analysis was performed to determine the adjusted odds ratios (aOR) of in-hospital adverse outcomes in patients with CLD compared with those without CLD. Among 7,296,679 PCI admissions, 54,368 (0.7%) had a CLD diagnosis. Among patients with CLD, 36,853 (67.8%) had severe CLD. Patients with CLD had higher likelihood of adverse outcomes including major adverse cardiovascular and cerebrovascular events (MACCE) (aOR 1.25, 95%CI 1.20 to 1.30), mortality (aOR 1.43, 95%CI 1.35 to 1.51), major bleeding (aOR 2.22, 95%CI 2.12 to 2.32). When accounting for severity, only severe CLD subgroup was more likely to have MACCE and all-cause mortality compared to no-CLD patients (p <0.001). Among CLD etiologic subgroups, those with ‘alcohol-related liver disease’ and ‘other CLD’ were consistently more likely to develop MACCE, all-cause mortality and major bleeding in comparison to no-CLD patients, while ‘chronic viral hepatitis’ subgroup had only increased odds of major bleeding (p <0.001). In conclusion, CLD patients admitted for PCI are more likely to have worse in-hospital outcomes, particularly in the severe CLD subgroup and ‘alcohol-related liver disease’ and ‘other CLD’ etiologic subgroups.

No description available.

No description available.