Cardiac, Neuroadrenergic, and Portal Hemodynamic Effects of Prolonged Aldosterone Blockade in Postviral Child A Cirrhosis

Pozzi, Massimo; Grassı, Guıdo; Ratti, Laura; Favini, Giorgio; Dell’Oro, Raffaella; Redaelli, Elena; Calchera, Ivan; Boari, Giuseppe; Mancia, Giuseppe

doi:10.1111/j.1572-0241.2005.41060.x

Cited by 65 publications

(40 citation statements)

References 32 publications

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“…Recently Pozzi et al [28] confirmed these findings in a human study highlighting a potential protective role of chronic aldosterone blockade currently employed in decompensated cirrhosis. Nevertheless, autoptic findings notably are biased by the nature of the events that lead to death cirrhotic subjects: circumstances like sepsis, shock and hepatorenal syndrome may have a severe impact on cardiac function [22] besides post-mortem heart tissue changes.…”

Section: Discussionsupporting

confidence: 73%

“…Previous studies have identified structural change of the heart in cirrhotic subjects and postulated its role as the anatomic background of impaired transmitral flow [14,28]. Nevertheless in vivo studies of myocardial tissue characterization in compensated cirrhosis are substantially lacking so far.…”

Section: Discussionmentioning

confidence: 99%

“…In cirrhotic subjects with indirect signs of portal hypertension at ultrasound portal pressure measurement was obtained by hepatic vein catheterization as previously reported [28]. Briefly, a 8F venous introducer (Cordis Corporation, Miami, USA) was inserted in the right jugular vein under local anesthesia: then a 7F balloon catheter (Meditech, Boston Scientific Corporation, Waterton, USA) was used for measurements.…”

Section: Methodsmentioning

confidence: 99%

“…Diastolic dysfunction, characterized by an altered pattern of transmitral flow due to impaired diastolic relaxation of left ventricle, can be easily assessed by echocardiography and accordingly can be considered as a marker of this condition. As far as diastolic dysfunction is concerned, many etiological factors have been reliably advocated as potential pathogenic agents: notably substances as NO [18][19][20][21], TNF [22], reactive nitrogen species [23], neurohormones [24][25][26][27][28] may well affect heart structure and function along with circulatory overload [24,29] and overactivity of the SNS [30]. Thickening of heart parietal walls has been reported [12,14,17,31], nevertheless the nature of the structural changes underlying diastolic dysfunction has not been clarified so far.…”

Section: Introductionmentioning

confidence: 99%

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Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

Pozzi¹,

Pizzala²,

Ratti³

et al. 2007

TOGASJ

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Evidence of diastolic dysfunction in cirrhosis contributed to the definition of cirrhotic cardiomyopathy. In 109 patients with chronic HCV infection with or without cirrhosis E/A ratio, a Doppler marker of diastolic dysfunction, was decreased in cirrhotics (0.89 ± 0.03 vs controls 1.21 ± 0.07, p < 0.01) and to a lesser extent in patients with advanced liver fibrosis (1.17 ± 0.07, p < 0.01). Left ventricular parietal wall thickness was increased. The nature of this abnormality in human cirrhosis has not been clarified, animal studies reporting cardiac hypertrophy. To this aim we employed the echocardiographic integrated backscatter (IBS) technique to obtain an indirect estimate of tissue density (decreased when a higher percentage of muscle fibres is present and increased when fibrosis prevails) to provide myocardial tissue characterization in a subset of patients with compensated HCV cirrhosis. The average IBS signal was reduced in cirrhotics at the level of the posterior wall (21.72 ± 1.46 dB versus 30.85 ± 1.40 dB in controls, p < 0.01). Our results confirm diastolic dysfunction in postviral cirrhosis pointing to cardiac hypertrophy as the anatomopathological background in the compensated stage of disease.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

Pozzi¹,

Pizzala²,

Ratti³

et al. 2007

TOGASJ

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“…Pozzi and colleagues [94] recently demonstrated that the use of an aldosterone antagonist, k-canrenoate, for 6 months can reduce the parietal wall thickness of the left ventricle even in patients at an early stage of cirrhosis, the so-called preascitic cirrhosis. The rationale for using an aldosterone antagonist was to counteract the fibrotic effects of aldosterone and reduce the circulatory volume load, and this has the potential of reducing myocardial hypertrophy and stiffness, thereby improving diastolic dysfunction in cirrhosis.…”

Section: Treatment Of Cirrhotic Cardiomyopathymentioning

confidence: 99%

Cirrhotic cardiomyopathy

2008

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Cirrhotic cardiomyopathy is a recently recognized condition in cirrhosis consisting of systolic incompetence under condition of stress, diastolic dysfunction related to altered diastolic relaxation, and electrophysiological abnormalities in the absence of any known cardiac disease. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers such as brain natriuretic factor. The underlying pathogenetic mechanisms include abnormalities in the b-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects. Various compounds for which levels are elevated in cirrhosis such as nitric oxide and carbon monoxide can also exert a negative inotropic effect on the myocardium, whereas excess sodium and volume retention can lead to myocardial hypertrophy. Various toxins can also aggravate the ion channel defects, thereby widening the QRS complex causing prolonged QT intervals. Clinically, systolic incompetence is most evident when cirrhotic patients are placed under stress, whether physical or pharmacological, or when the extent of peripheral arterial vasodilatation demands an increased cardiac output as in the case of bacterial infections. Acute volume overload such as immediately after insertion of a transjugular intrahepatic portosystemic shunt or after liver transplantation can also tip these cirrhotic patients into cardiac failure. Treatment of cirrhotic cardiomyopathy is unsatisfactory. There is some evidence that b-blockade may help some cirrhotic patients with baseline prolonged QT interval. Long-term aldosterone antagonism may help reduce myocardial hypertrophy. Future studies should include further elucidation of pathogenetic mechanisms so as to develop effective treatment strategies.

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Primary prevention of variceal bleeding in people with oesophageal varices due to liver cirrhosis: a network meta-analysis

Roccarina

Best

Freeman

et al. 2021

Cochrane Database of Systematic Reviews

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Cardiac, Neuroadrenergic, and Portal Hemodynamic Effects of Prolonged Aldosterone Blockade in Postviral Child A Cirrhosis

Cited by 65 publications

References 32 publications

Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

Cirrhotic cardiomyopathy

Primary prevention of variceal bleeding in people with oesophageal varices due to liver cirrhosis: a network meta-analysis

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