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Evidence of functional and structural cardiac abnormalities in cirrhotic patients with and without ascites
1Cattedra di Medicina Interna, Università degli Studi di Milano, Divisione di Medicina 1, Monza, Italy.
Insights
Advanced cirrhosis causes heart abnormalities, including diastolic dysfunction and increased left ventricle wall thickness. Treating ascites improves diastolic function by reducing neurohumoral overactivity.
Area of Science:
- Cardiology
- Hepatology
- Internal Medicine
Background:
- Cirrhosis is linked to cardiovascular issues, but data on diastolic dysfunction and wall thickness is limited.
- Understanding these cardiac changes is crucial for managing advanced liver disease.
Purpose of the Study:
- To investigate left ventricle diastolic and systolic function, and wall thickness in cirrhotic patients.
- To assess the impact of ascites and its resolution on these cardiac parameters.
Main Methods:
- Echocardiography and echocolor Doppler were used to evaluate cardiac function in 27 cirrhotic patients with ascites, 17 without ascites, and 11 controls.
- Measurements were repeated after ascites removal (paracentesis) in affected patients.
- Neurohumoral variables were also assessed.
Main Results:
- Cirrhotic patients, with or without ascites, showed reduced E/A ratio (diastolic dysfunction) and increased left ventricle wall thickness compared to controls.
- Ascites removal improved diastolic function and reduced plasma renin activity, aldosterone, norepinephrine, and epinephrine.
- Systolic function was only slightly reduced in patients with ascites and unaffected by paracentesis.
Conclusions:
- Advanced cirrhosis is associated with left ventricle diastolic dysfunction and increased wall thickness, regardless of ascites or liver disease cause.
- Neurohumoral overactivity may contribute to cardiac fibrosis and impaired relaxation in cirrhotic patients, particularly those with ascites.
Abstract:
Cirrhosis is associated with cardiovascular abnormalities. Scanty information is available as to whether these include left ventricle diastolic dysfunction and wall thickness increase. To this aim in 27 cirrhotic patients with tense ascites, 17 cirrhotic patients with previous episodes of ascites (not actual), and 11 controls we investigated by echocardiography and echocolor Doppler left ventricle diastolic function (E wave, A wave, E/A ratio, deceleration time of E wave), systolic function (ejection fraction), and wall thickness (left ventricle posterior wall thickness + interventricular septum thickness) along with neurohumoral variables. All measurements (supine position) were repeated after total paracentesis (10.7 +/- 0.6 L of ascites) in ascitic patients. Both in patients with and without ascites E/A ratio was reduced as compared with controls (0.93 +/- 0.07 and 0.97 +/- 0.06 vs. 1.18 +/- 0.08, P < .05) while left ventricle wall thickness was increased (18.6 +/- 0.6 and 20.1 +/- 0.8 vs. 17.2 +/- 0.7, P < .05 and P < .01, respectively), irrespective of the postviral or alcoholic cause of liver disease. In all cirrhotics both right and left atrial and right ventricle diameters were significantly greater. Ejection fraction was slightly but significantly (P < .01) reduced in ascitic patients. Paracentesis induced a reduction of the highly increased basal plasma renin activity, aldosterone, norepinephrine (P < .01), and epinephrine (P < .05) and improved diastolic function (E/A, P < .05). Systolic function was unaffected. Thus, irrespective of ascites and cause, advanced cirrhosis is associated with left ventricle diastolic dysfunction and wall thickness increase. We can speculate that neurohumoral overactivity, known to stimulate cardiac tissue growth, may challenge the heart, promoting fibrosis and exerting a further hindrance to ventricular relaxation in patients with cirrhosis experiencing episodes of ascites.