Role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis

The aim of this study was to assess the relationship between subtle cardiov ascular abnormalities and abnormal sodium handling in cirrhosis. A total of 35 biopsy-proven patients with cirrhosis with or without ascites and 14 ag e-matched controls underwent two-dimensional echocardiography and radionucl ide angiography for assessment of cardiac volumes, structural changes and s ystolic and diastolic functions under strict metabolic conditions of a sodi um intake of 22 mmol/day. Cardiac output, systemic vascular resistance and pressure/volume relationship (an index of cardiac contractility) were calcu lated. Eight controls and 14 patients with non-ascitic cirrhosis underwent repeat volume measurements and the pressure/volume relationship was reevalu ated after consuming a diet containing 200 mmol of sodium/day for 7 days. A scitic cirrhotic patients had significant reductions in (i) cardiac pre-loa d (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) a fterload (systemic vascular resistance 992 +/- 84 dyn.s.cm(-5); P < 0.05 co mpared with controls) due to systemic arterial vasodilatation; and (iii) re versal of the pressure/volume relationship, indicating contractility dysfun ction. Increased cardiac output (6.12 +/- 0.45 litres/min; P < 0.05 compare d with controls) was due to a significantly increased heart rate. Pre-ascit ic cirrhotic patients had contractile dysfunction, which was accentuated wh en challenged with a dietary sodium load, associated with renal sodium rete ntion (urinary sodium excretion 162 +/- 12 mmol/day, compared with 197 +/- 12 mmol/day in controls; P < 0.05). Cardiac output was maintained, since th e pre-load was normal or increased, despite a mild degree of ventricular th ickening, indicating some diastolic dysfunction. We conclude that: (i) cont ractile dysfunction is present in cirrhosis and is aggravated by a sodium l oad; (ii) an increased pre-load in the preascitic patients compensates for the cardiac dysfunction; and (iii) in ascitic patients, a reduced afterload , manifested as system ic arterial vasodilatation, compensates for a reduce d pre-load and contractile dysfunction. Cirrhotic cardiomyopathy may well p lay a pathogenic role in the complications of cirrhosis.