Arterial vasodilation is not the cause of increased cardiac output in cirrhosis

Lewis, Frederick W.; Adair, Olivia V.; Rector, William G.

doi:10.1016/0016-5085(92)90192-2

Cited by 60 publications

(29 citation statements)

References 24 publications

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“…the increase in left ventricular end systolic diameters seems not to be related to the diminished afterload, but determined by increase in vascular volume. (16) Finding in accordance with the hypothesis favouring central hypovolemia and decreased effective arterial blood volume in cirrhosis have shown that a higher portal pressure and higher hepatic blood flow independently determine a higher cardiac output. (17) Previous publication have found left atrial, right atrial and right ventricular diastolic diameters to be significantly greater than controls, but parameters concerning left ventricular systolic dimension, septal wall and posterior wall thickness did not show significant differences.…”

Section: Discussionsupporting

confidence: 75%

Study of Cardiac Status in End Stage Chronic Liver Disease and Its Correlation With Meld

Dubey¹,

Panjwani²

2016

jemds

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Section: Discussionsupporting

confidence: 75%

Study of Cardiac Status in End Stage Chronic Liver Disease and Its Correlation With Meld

Dubey¹,

Panjwani²

2016

jemds

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“…An acceleration of heart rate would ensue and contribute to increase cardiac output along with an enhanced cardiac preload. 5,44 Moreover, in the subset of patients with defective sympathetic function, this may contribute to the blunted cardiovascular response to adrenergic vasoconstrictors and maneuvers enhancing the sympathoadrenergic drive, which have been described in cirrhosis. 15,45,46 In conclusion, our study shows that cardiovascular disturbances of advanced cirrhosis are more prominent in patients with evidence of AD and their severity is related to the degree of the autonomic alteration.…”

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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“…13,14 However, although an echocardiographic study described increased left ventricular (LV) wall thickness in patients with advanced cirrhosis, 15 there is no direct evi-dence of the induction of myocardial hypertrophy by portal hypertension. In patients with portal hypertension and/or cirrhosis, LV function has been documented to be normal or hyperdynamic at baseline, 16,17 whereas numerous studies demonstrate an altered function under conditions of physiologic 18,19 or pharmacologic stress induced by exercise or ␤-adrenergic agonist infusion. 20,21 The aim of this study was to investigate the consequences of portal hypertension on the structure and function of the heart.…”

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confidence: 99%

Left ventricular hypertrophy in rats with biliary cirrhosis

et al. 2003

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Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague-Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin-II and endothelin-1 (P < .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (P < .01), 87% increase in cardiac index and 30% increase in heart weight (P < .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% (P < .01) increase in cross-sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, P < .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes (P < .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK-B genes (P < .01). Isolated perfused CBDL hearts showed pressure/end-diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with N-nitro-L-arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis. (HEPATOLOGY 2003;38:589-598.) H yperdynamic circulation is a common feature in human and experimental portal hypertension, with or without cirrhosis. This is also called hyperdynamic circulatory syndrome and is the consequence of splanchnic and systemic vasodilatation, manifested by increased heart rate, cardiac output, and regional blood flow with decreased mean arterial pressure and systemic vascular resistance (SVR). 1 The mechanism of systemic and splanchnic vasodilatation is multifactorial. Many studies have suggested a prominent role for increased biosynthesis of nitric oxide (NO), 2 which is due to increased endothelial nitric oxide synthase (eNOS) activity. 3,4 It has been shown that NO inhibition attenuates the hyperdynamic circulation observed in portal hypertensive rats. 5,6 Other studies have shown an increased splanchnic production of carbon monoxide in portal hypertension 7 as well as an increased release of splanchnic vasodilatory peptides, such as glucagon. 8,9 Vasoconstrictor systems are also up-regulated, probably as a counter-regulatory response to the hyperdynamic state. 10 Sympathetic nervous and renin-angiotensin aldosterone systems are enhanced, and the plasma levels of vasopressin and endot...

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Arterial vasodilation is not the cause of increased cardiac output in cirrhosis

Cited by 60 publications

References 24 publications

Study of Cardiac Status in End Stage Chronic Liver Disease and Its Correlation With Meld

Study of Cardiac Status in End Stage Chronic Liver Disease and Its Correlation With Meld

Autonomic dysfunction and hyperdynamic circulation in cirrhosis with ascites

Left ventricular hypertrophy in rats with biliary cirrhosis

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