Influence of the degree of liver failure on systemic and splanchnic haemodynamics and on response to propranolol in patients with cirrhosis.

Braillon, Alain; Calès, Paul; Valla, Dominique; Gaudy, Daniele; Geoffroy, Patrick; Lebrec, Didier

doi:10.1136/gut.27.10.1204

Cited by 198 publications

(68 citation statements)

References 24 publications

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“…Second, AD is commonly detected in patients with cirrhosis, [9][10][11][12][13]16,[18][19][20][21]35 and its prevalence increases in parallel with the severity of liver disease, 9,10 as does the hyperdynamic circulatory syndrome. 36 Moreover, the presence of both abnormalities heralds an adverse prognosis. 2,16,18 Disparate events may contribute to the development of AD, including factors affecting nerve integrity, such as alterations in lipid metabolism, vitamin E deficiency, alcohol intake, immunologic mechanisms, and retention of toxic metabolites.…”

Section: Discussionmentioning

confidence: 99%

Autonomic dysfunction and hyperdynamic circulation in cirrhosis with ascites

et al. 1999

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Patients with advanced cirrhosis frequently show hemodynamic abnormalities. Autonomic dysfunction (AD) is also common and, owing to the importance of autonomic function in cardiovascular homeostasis, it may be involved in the pathogenesis of the hyperdynamic circulation. We, therefore, evaluated the hemodynamic status and autonomic function in 30 patients with cirrhosis, most of them with an advanced stage of the disease. Autonomic function was assessed with 7 cardiovascular tests exploring the vagal or sympathetic function. Each test was scored from 1 to 3 (normal, borderline, altered). Cardiac index (CI) was measured by an echocardiogram. Twenty-four (80%) patients showed an AD, this being definite in 14 (47%) patients. A vagal dysfunction (VD) was found in 19 patients (63%), this being definite in 11 patients (37%), and a sympathetic dysfunction (SD) in 7 patients (definite in 3 [10%] patients). The patients with AD showed a faster heart rate (P ‫؍‬ .021), lower indicized peripheral vascular resistance (P ‫؍‬ .013), and increased CI (P ‫؍‬ .004) than patients without AD whereas mean arterial pressure did not differ. Similar results were seen by grouping patients according to the VD. AD score was directly correlated with heart rate (r ‫؍‬ 0.53; P ‫؍‬ .002) and CI (r ‫؍‬ 0.45; P ‫؍‬ .016), and inversely correlated with peripheral vascular resistance (r ‫؍‬ 0.46; P ‫؍‬ .013). Even closer correlations were found with vagal score. AD (mainly VD) may be involved in the pathogenesis of the hyperdynamic circulatory syndrome of patients with advanced cirrhosis. (HEPATOLOGY 1999;30:1387-1392.)Hyperdynamic circulation is a common and long-recognized feature of patients with advanced cirrhosis, 1 consisting of elevated cardiac rate and output and reduced peripheral vascular resistance, so that arterial pressure is tendentially or frankly reduced. The clinical importance of this disorder was shown by subsequent studies, showing that the alterations of systemic hemodynamics, renal function, and vasoactive systems are prognostic indicators even more accurate than the tests exploring liver function. 2 The setting of the hyperdynamic circulatory syndrome is the pathogenetic background of complications such as renal sodium and water retention and hepatorenal syndrome. 3 Splanchnic blood pooling, opening of portal-systemic collaterals, and arterial vasodilation, as well as a compensatory increase in blood volume, are the causative events of the hyperdynamic circulatory syndrome. 4,5 The pathogenesis of arterial vasodilation is still debated. It has been proposed that an overproduction of a variety of vasorelaxant agents, such as histamine, adenosine, gut-derived peptides and endothelial cell-derived vasodilators, and bile acid retention reduce the responsiveness of the vascular bed to endogenous vasoconstrictor stimuli. 4,6 The autonomic nervous system plays a central role in modulating cardiac performance and vasomotor activity. The presence of an autonomic dysfunction (AD) in cirrhosis has been clearly shown through different...

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Section: Discussionmentioning

confidence: 99%

Autonomic dysfunction and hyperdynamic circulation in cirrhosis with ascites

et al. 1999

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“…Compared with controls, cirrhotic patients had attenuated ET-1 responses (P < A hyperdynamic circulation characterized by low arterial pressure, high cardiac output, and low systemic vascular resistance is a feature of patients with advanced cirrhosis and portal hypertension. [1][2][3] This hyperdynamic circulation worsens with disease progression [4][5][6] and is accompanied by a reduced reactivity to vasopressor systems including the reninangiotensin and sympathetic nervous systems. These hemodynamic changes play a crucial role in the pathogenesis of portal hypertension and its complications, including variceal hemorrhage, ascites, and the hepatorenal syndrome.…”

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confidence: 99%

Altered peripheral vascular responses to exogenous and endogenous endothelin-1 in patients with well-compensated cirrhosis

Helmy¹,

Jalan²,

Newby

et al. 2001

Hepatology

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Plasma endothelin concentrations are elevated in cirrhosis and correlate with disease severity. This study assessed forearm vascular responses to exogenous endothelin-1 (ET-1), and evaluated the contribution of endogenous ET-1 to the maintenance of basal peripheral vascular tone in patients with well-compensated cirrhosis (n ‫؍‬ 11) and matched healthy controls (n ‫؍‬ 8). Bilateral forearm blood flow (FBF) was measured at baseline and following unilateral, subsystemic, intrabrachial artery infusions of ET-1 (2 and 6 pmol/min); BQ-123, a selective ET A receptor antagonist (3 and 10 nmol/min); and BQ-788, a selective ET B receptor antagonist (0.3 and 1 nmol/min) using venous occlusion plethysmography. Baseline systemic hemodynamics and plasma ET-1 and big ET-1 concentrations were measured using electrical bioimpedance and radioimmunoassay, respectively. Patients and controls had similar baseline FBF, systemic hemodynamics, and plasma ET-1 and big ET-1 concentrations. In both groups, ET-1 and BQ-788 caused significant vasoconstriction (P < .001) and BQ-123 caused significant vasodilatation (P < .001). Compared with controls, cirrhotic patients had attenuated ET-1 responses (P < A hyperdynamic circulation characterized by low arterial pressure, high cardiac output, and low systemic vascular resistance is a feature of patients with advanced cirrhosis and portal hypertension. [1][2][3] This hyperdynamic circulation worsens with disease progression [4][5][6] and is accompanied by a reduced reactivity to vasopressor systems including the reninangiotensin and sympathetic nervous systems. These hemodynamic changes play a crucial role in the pathogenesis of portal hypertension and its complications, including variceal hemorrhage, ascites, and the hepatorenal syndrome. 7,8 Endothelin-1 (ET-1) is the most potent vasoconstrictor known, belonging to a 21-amino acid peptide family with a range of biological effects. 9-11 ET-1 was originally identified in the culture medium of porcine aortic endothelial cells 9,10 and is derived from a larger pre-pro-endothelin-1 (212 amino acids), which is cleaved by endopeptidases to produce big ET-1 (38 amino acids), which is then converted to ET-1 by specific endothelin-converting enzymes. [9][10] Molecular studies have, so far, identified 2 endothelin receptor subtypes in mammalian species: endothelin-A (ET A ) and endothelin-B (ET B ). In vascular smooth muscle cells, both receptors are expressed 11,12 and mediate vasoconstriction. [11][12][13][14] Only the ET B receptors are found on endothelial cells, where these cause vasodilatation through the release of endothelium-derived vasodilators, such as nitric oxide (NO). 15 ET-1-induced vasoconstriction is predominantly mediated by the ET A receptor, but ET B receptors may contribute under some circumstances. 16 Since 1991, many studies have reported increased plasma concentrations of ET-1 in patients with cirrhosis. [17][18][19][20][21][22][23][24][25][26] The mechanisms underlying the elevated ET-1 concentrations are unclear and do not appe...

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“…The present findings correlate with the results from a retrospective study by Hashizume et al 7 The hypertension, and Child's status is associated with portal venous pressure. 25 It is well known that portal venous pressize of the esophageal varices is also an important risk factor for hemorrhage from esophageal varices. 8,19 The portal and sure is an important risk factor for a rupture of esophageal varices.…”

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confidence: 99%

Risk factors for hemorrhage from gastric fundal varices

1997

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prospective trials. 8,9 However, the incidence of hemorrhage The incidence and the risk factors of hemorrhage from from FV has not been fully investigated. 3,7 Although several gastric fundal varices (FV) have not been fully evaluauthors have mentioned the incidence of hemorrhage from ated. We therefore conducted a retrospective and pro-FV, 3,7 to our knowledge, there has been no prospective study spective study to define the incidence and risk factors documenting the cumulative risk for FV hemorrhage in a for such episodes. We investigated 132 patients with cirlarge number of patients. The aim of this study was to define rhosis and gastric FV. Of these 132 patients, 15 patients the incidence and the risk factors for hemorrhage from FV. had hemorrhagic FV at the time of enrollment. The clinical characteristics were compared between these pa-PATIENTS AND METHODS tients and those without a first hemorrhage from FV. In Baseline Clinical Assessment. From January 1985 through Decemthe patients who had never previously bled, the inciber 1995, a total of 1,392 cirrhotic patients consecutively underwent dence and risk factors were prospectively investigated.upper gastrointestinal endoscopy at our institute. Of these patients, The size of FV was greater and red-spot on the FV were 540 patients had esophageal varices, 96 patients had gastric varices, more prevalent in patients with hemorrhagic FV. Child's and 253 patients had both esophageal and gastric varices. In the status was also more severe in these patients. In the 117 patients with gastric varices, 143 patients had FV, while the repatients who had never bled, 34 hemorrhages from FV maining 206 patients had varices in the cardia. In the 143 patients occurred during the follow-up period. The cumulative with FV, 11 patients were subsequently excluded from further evaluation because of their refusal to participate in the study. We thus risk for such hemorrhage at 1, 3, and 5 years was 16%, investigated a total of 132 patients with FV in the current study. 36%, and 44%, respectively. A multiple regression analy-The subjects consisted of 89 men and 43 women ranging in age from 1 The blood flow of such collaterals is abundant, 2 and apy. All patients were informed of the scientific nature of the investihemorrhage from FV is more serious than that of esophageal gation and gave their informed consent. The study protocol was apvarices. [3][4][5][6] The treatment of hemorrhagic FV by endoscopic proved by the Hospital Ethics Committee. procedures sometimes fails to cease the bleeding, and surgiAssessment of Endoscopic Findings. The diagnosis of FV was made cal modalities are thus often required for hemostasis.3-6 As a based on endoscopy with the agreement of two experienced endoscoresult, the mortality rate is high in patients with hemor-pists when one or more distinct venous channels were found in the rhagic FV. [3][4][5][6] In addition, because hemorrhagic esophageal gastric fundus. In patients with hemorrhagic FV, the endoscopic findings were analyzed after the cessation o...

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Influence of the degree of liver failure on systemic and splanchnic haemodynamics and on response to propranolol in patients with cirrhosis.

Cited by 198 publications

References 24 publications

Autonomic dysfunction and hyperdynamic circulation in cirrhosis with ascites

Autonomic dysfunction and hyperdynamic circulation in cirrhosis with ascites

Altered peripheral vascular responses to exogenous and endogenous endothelin-1 in patients with well-compensated cirrhosis

Risk factors for hemorrhage from gastric fundal varices

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