The aim of this study was to assess the relationship between subtle cardiovascular abnormalities and abnormal sodium handling in cirrhosis. A total of 35 biopsy-proven patients with cirrhosis with or without ascites and 14 age-matched controls underwent two-dimensional echocardiography and radionuclide angiography for assessment of cardiac volumes, structural changes and systolic and diastolic functions under strict metabolic conditions of a sodium intake of 22 mmol/day. Cardiac output, systemic vascular resistance and pressure/volume relationship (an index of cardiac contractility) were calculated. Eight controls and 14 patients with non-ascitic cirrhosis underwent repeat volume measurements and the pressure/volume relationship was re-evaluated after consuming a diet containing 200 mmol of sodium/day for 7 days. Ascitic cirrhotic patients had significant reductions in (i) cardiac pre-load (end diastolic volume 106±9 ml; P < 0.05 compared with controls), due to relatively thicker left ventricular wall and septum (P < 0.05); (ii) afterload (systemic vascular resistance 992±84 dyn·s·cm-5; P < 0.05 compared with controls) due to systemic arterial vasodilatation; and (iii) reversal of the pressure/volume relationship, indicating contractility dysfunction. Increased cardiac output (6.12±0.45 litres/min; P < 0.05 compared with controls) was due to a significantly increased heart rate. Pre-ascitic cirrhotic patients had contractile dysfunction, which was accentuated when challenged with a dietary sodium load, associated with renal sodium retention (urinary sodium excretion 162±12 mmol/day, compared with 197±12 mmol/day in controls; P < 0.05). Cardiac output was maintained, since the pre-load was normal or increased, despite a mild degree of ventricular thickening, indicating some diastolic dysfunction. We conclude that: (i) contractile dysfunction is present in cirrhosis and is aggravated by a sodium load; (ii) an increased pre-load in the pre-ascitic patients compensates for the cardiac dysfunction; and (iii) in ascitic patients, a reduced afterload, manifested as systemic arterial vasodilatation, compensates for a reduced pre-load and contractile dysfunction. Cirrhotic cardiomyopathy may well play a pathogenic role in the complications of cirrhosis.
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Research Article|
July 15 1999
Role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis
Florence WONG;
*Division of Gastroenterology, The Toronto Hospital, University of Toronto, Toronto, Ontario, Canada
Correspondence: Dr Florence Wong, Room 220, 9th Floor, Eaton Wing, Toronto Hospital, 200 Elizabeth Street, Toronto M5G 2C4, Ontario, Canada.
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Peter LIU;
Peter LIU
†Divisionof Cardiology, The Toronto Hospital, University of Toronto, Toronto, Ontario, Canada
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Lesley LILLY;
Lesley LILLY
*Division of Gastroenterology, The Toronto Hospital, University of Toronto, Toronto, Ontario, Canada
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Arieh BOMZON;
Arieh BOMZON
‡Department of Pharmacology, Technion Medical School, Haifa, Israel
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Laurence BLENDIS
Laurence BLENDIS
*Division of Gastroenterology, The Toronto Hospital, University of Toronto, Toronto, Ontario, Canada
§Institute of Gastroenterology, Ichilov Hospital, Tel Aviv, Israel
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Publisher: Portland Press Ltd
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 1999
1999
Clin Sci (Lond) (1999) 97 (3): 259–267.
Citation
Florence WONG, Peter LIU, Lesley LILLY, Arieh BOMZON, Laurence BLENDIS; Role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis. Clin Sci (Lond) 1 September 1999; 97 (3): 259–267. doi: https://doi.org/10.1042/cs0970259
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