Early effects of total paracentesis and albumin infusion on muscle sympathetic nerve activity in cirrhotic patients with tense ascites

Pozzi, Massimo; Pecci, Valeria; Turri, C; Boari, Giuseppe; Bolla, G.; Massironi, Sara; Roffi, Luigi; Mancia, Giuseppe

doi:10.1016/s0168-8278(99)80012-9

Cited by 10 publications

(3 citation statements)

References 42 publications

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“…In the present study we have found that HRV, which reflects the balance between the parasympathetic and the sympathetic tone to the heart, progressively decreased with the increase of portal pressure, independently of the basal HR. Patients with advanced cirrhosis have increased levels of plasma catecholamines [31,32] and of muscle sympathetic nervous traffic, a direct index of autonomic nervous system activity [33,34]. Cirrhotic patients with oesophageal varices are currently treated with β-blockers to decrease portal pressure and the bleeding risk.…”

Section: Clinical Relevance Of Electrocardiographic Abnormalitiesmentioning

confidence: 99%

QT interval prolongation and decreased heart rate variability in cirrhotic patients: relevance of hepatic venous pressure gradient and serum calcium

et al. 2009

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A prolongation of QT interval has been shown in patients with cirrhosis and it is considered as part of the definition of the so-called 'cirrhotic cardiomyopathy'. The aim of the present study was to assess the determinants of QT interval prolongation in cirrhotic patients. Forty-eight male patients with different stages of liver disease were divided into three subgroups according to the Child-Pugh classification. All patients underwent a 24-h ECG Holter recording. The 24-h mean of QT intervals corrected for heart rate (termed QTc) and the slope of the regression line QT/RR were calculated. HRV (heart rate variability), plasma calcium and potassium concentration and HVPG (hepatic venous pressure gradient) were measured. QTc was progressively prolonged from Child A to Child C patients (P=0.001). A significant correlation between QTc and HVPG was found (P=0.003). Patients with alcohol-related cirrhosis presented QTc prolongation more frequently than patients with post-viral cirrhosis (P<0.001). The QT/RR slope was steeper in subjects with alcoholic aetiology as compared with viral aetiology (P=0.02), suggesting that these patients have a further QTc prolongation when heart rate decreases. The plasma calcium concentration was inversely correlated with QTc (P<0.001). The presence of severe portal hypertension was associated with decreased HRV (P<0.001). Cirrhotic patients with a more severe disease, especially of alcoholic aetiology, who have greater HVPG and lower calcium plasma levels, have an altered ventricular repolarization and a reduced vagal activity to the heart, which may predispose to life-threatening arrhythmias.

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Section: Clinical Relevance Of Electrocardiographic Abnormalitiesmentioning

confidence: 99%

QT interval prolongation and decreased heart rate variability in cirrhotic patients: relevance of hepatic venous pressure gradient and serum calcium

et al. 2009

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“…Splanchnic arterial vasodilatation, central blood volume displacement to splanchnic vascular territories and central hypovolaemia have been described (3). This condition is associated with an impaired autonomic function (4), characterized by reduced baroreceptor activity (5–7) and sympathetic overactivity (8–10). Baroreflex sensitivity (BRS) has been increasingly used as an index of cardiac autonomic control.…”

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Baroreceptor sensitivity and baroreceptor effectiveness index in cirrhosis: the relevance of hepatic venous pressure gradient

Genovesi¹,

Pizzala²,

Pozzi³

et al. 2010

Liver International

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These data support the hypothesis that liver disease severity and particularly portal hypertension have an important role in the derangement of baroreceptor function. The aetiology of cirrhosis seems to be related to baroreceptor impairment as well. Mortality rate is higher in subjects with a more damaged autonomic system, strengthening the idea of a worse prognosis in cirrhotic patients with autonomic neuropathy.

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“…neuroeffector junctions, 6 and muscle sympathetic nerve traffic as directly quantified by microneurography [7][8][9] are all increased. The sympathoactivation accompanying cirrhosis has not yet been thoroughly characterized, however.…”

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Patterns of regional sympathetic nerve traffic in preascitic and ascitic cirrhosis

et al. 2001

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Overactivity of the sympathetic nervous system and portal hypertension are key factors in the development of ascites in cirrhosis. The sympathoexcitation that characterizes the more advanced stages of liver diseases is less clearly defined in preascitic cirrhosis. We measured sympathetic nerve traffic to skeletal muscle (peroneal nerve) and to skin districts by microneurography in (1) 12 Child class A cirrhotic patients with clinically significant portal hypertension (portal pressure gradient > 10 mm Hg, 14.8 ؎ 1.2 mm Hg, mean ؎ SEM) but without actual or previous ascites, (2) 16 Child class C cirrhotic patients with tense ascites, and (3) 10 patients with mild congestive heart failure, a condition paradigmatic of a marked sympathetic activation. Muscle sympathetic nerve traffic was markedly increased in Child class C subjects as compared with controls (23.9 ؎ 1.6 bursts/min, P < .01) and superimposable to that recorded in heart failure patients (52.9 ؎ 4.7 vs. 60.3 ؎ 2 bursts/min, P ‫؍‬ not significant). Muscle sympathetic nerve traffic was also increased in Child class A subjects (41.6 ؎ 2 bursts/min, P < .01 vs. controls) although to a lesser extent (P < .05 vs. Child class C patients). Skin sympathetic nerve traffic was within the normal range in all patients. Neurohormones were all markedly increased in Child class C subjects. Only norepinephrine was increased in Child class A patients. Our data show that sympathetic nerve traffic activation (1) is already detectable in Child class A cirrhosis when clinically significant portal hypertension is present but ascites never developed and (2) Cirrhosis is accompanied by an increase in sympathetic activity 1 as shown by the observation that in this condition plasma norepinephrine, 2-5 norepinephrine spillover from neuroeffector junctions, 6 and muscle sympathetic nerve traffic as directly quantified by microneurography 7-9 are all increased. The sympathoactivation accompanying cirrhosis has not yet been thoroughly characterized, however. For example, it is not yet clear whether the sympathoactivation is a pathophysiologic feature of cirrhosis throughout its course or if it just appears when fluid retention, ascites, or the hepatorenal syndrome dramatically alter circulating blood volume. 10 It is also not clear whether the sympathoactivation is generalized to the entire cardiovascular system or if it involves some vascular beds but not others.The aim of the present study has been to provide information on these two issues; that is, whether sympathetic activity is increased in earlier stages of cirrhosis in which portal pressure is increased but ascites has never developed and whether in either preascitic and more advanced cirrhosis the sympathetic activation has a generalized or more regional distribution. PATIENTS AND METHODSStudy Population. This study was performed on a total of 48 subjects. Twenty-eight patients had cirrhosis and portal hypertension with different degrees of liver impairment as assessed by the ChildPugh classification. Twelve patients were Ch...

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Early effects of total paracentesis and albumin infusion on muscle sympathetic nerve activity in cirrhotic patients with tense ascites

Cited by 10 publications

References 42 publications

QT interval prolongation and decreased heart rate variability in cirrhotic patients: relevance of hepatic venous pressure gradient and serum calcium

QT interval prolongation and decreased heart rate variability in cirrhotic patients: relevance of hepatic venous pressure gradient and serum calcium

Baroreceptor sensitivity and baroreceptor effectiveness index in cirrhosis: the relevance of hepatic venous pressure gradient

Patterns of regional sympathetic nerve traffic in preascitic and ascitic cirrhosis

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