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The present study was designed to determine the systemic haemodynamic effects of obliterating oesophageal varices by endoscopic sclerotherapy. We evaluated systemic and splanchnic haemodynamics before and after the first course of sclerotherapy in cirrhotic patients. The baseline cardiac index was significantly correlated with baseline azygos vein blood flow (r = 0.64; P < 0.01) and the azygos vein blood flow and cardiac index significantly decreased (-33% and -16%, respectively; P < 0.01) following sclerotherapy. The systemic vascular resistance index was also increased significantly (+ 20%; P < 0.01) in these patients. Moreover, the per cent change in azygos vein blood flow was directly correlated with that of the cardiac index (r = 0.51; P < 0.03). We conclude from these findings that the obliteration of portosystemic collaterals by sclerotherapy significantly reverses hyperdynamic circulation in such patients via a decrease in cardiac preload. The blood flow of the portosystemic shunt per se is a leading contributor to the hyperdynamic circulation observed in patients with well-developed portal systemic collateral vessels.

The effects of endoscopic variceal ligation (EVL) on systemic hemodynamics are unknown. This study was conducted to determine whether the obliteration of portal-systemic collaterals by EVL affects systemic hemodynamics and serum nitrate concentrations in patients with compensated cirrhosis. We measured systemic and hepatic hemodynamics, azygos vein blood flow (AzBF), and serum nitrate concentrations before and immediately following EVL. A prompt decrease in left ventricular end-diastolic volume (LVEDV), stroke volume, cardiac index (CI), and an increase in systemic vascular resistance index (SVRI) were observed following variceal ligation. The reduction in LVEDV was associated with a decline in CI with a rise in SVRI. There was also a prompt reduction in serum nitrate concentration following variceal ligation. AzBF also significantly decreased following variceal ligation. These findings indicate that EVL decreased cardiac output via a reduction in cardiac preload (central venous return). Blood flow through portal-systemic collaterals has an important role in the enhanced cardiac preload of cirrhotic patients. The sudden decrease in serum nitrate concentrations suggests that endogenous nitric oxide may be involved in the regulation of systemic hemodynamics in patients with compensated cirrhosis.

The aim of this study was to determine whether endoscopic variceal sclerotherapy affects systemic or splanchnic hemodynamics. We measured hemodynamic parameters before and after the first course of sclerotherapy in 35 patients with cirrhosis. Following sclerotherapy, there was a significant decrease in cardiac index and a significant increase in systemic vascular resistance. Changes in hepatic venous pressure gradient varied from patient to patient with no statistically significant change in the group overall. However, all 20 patients with a decline in the hepatic venous pressure gradient had a concomitant decrease in cardiac index and/or a large extravariceal shunt. The multivariate analysis disclosed that the decrease in cardiac index was a statistically significant contributor for the decline in hepatic venous pressure gradient. We conclude that the obliteration of esophageal varices by sclerotherapy significantly reverses the hyperdynamic circulatory state in patients with cirrhosis. Spontaneous changes in systemic hemodynamics and the interaction with hepatic hemodynamics must be taken into account when evaluating hepatic hemodynamics in patients undergoing variceal sclerotherapy.