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Left ventricular diastolic function in liver cirrhosis
G Finucci1, A Desideri, D Sacerdoti
1Dept. of Clinical Medicine, University of Padua, Italy.
Insights
Liver cirrhosis (LC) patients show impaired left ventricular diastolic function, with abnormalities in relaxation and filling patterns. Ascites severity influences these diastolic changes, potentially masking underlying myocardial issues.
Area of Science:
- Cardiology
- Hepatology
- Echocardiography
Background:
- Left ventricular systolic dysfunction is documented in liver cirrhosis (LC).
- Diastolic function in LC patients has not been extensively studied.
Purpose of the Study:
- To investigate left ventricular diastolic function in patients with liver cirrhosis.
- To compare diastolic parameters between cirrhotic patients and healthy controls.
Main Methods:
- Doppler echocardiography was used to assess diastolic function.
- 42 patients with liver cirrhosis and 16 healthy controls were included.
Main Results:
- Cirrhotic patients exhibited increased left ventricular volumes and stroke volume.
- Key diastolic parameters including peak A velocity, time E, and deceleration time (DT) were significantly altered.
- The ratio of peak E to peak A filling velocities was decreased in cirrhotics.
Conclusions:
- Impaired left ventricular relaxation suggests myocardial involvement in liver cirrhosis.
- Tense ascites may lead to pseudo-normalization of diastolic parameters, masking underlying abnormalities.
Background:
Left ventricular systolic abnormalities have been reported in liver cirrhosis (LC). Diastolic function in cirrhotics, on the contrary, does not seem to have been studied so far.
Methods:
Diastolic function was evaluated in 42 cirrhotic patients and in 16 controls by means of Doppler echocardiography.
Results:
Compared with the controls, cirrhotics had increased left ventricular end-diastolic and left atrial volume, stroke volume, late diastolic flow velocity (peak A) (71 + or - 17 cm/sec versus 56 +/- 18; p <0.01), time from onset of mitral inflow to the early peak (time E) (86 + or - 11 msec versus 72 +/- 14; p < 0.003), and deceleration time (DT) (194 +/- 40 msec versus 159 +/- 27; p < 0.001) and decreased ratio of peak E to peak A filling velocities (1.02 +/ - 0.35 versus 1.22 +/- 0.25; p < 0.02). Patients with tense ascites had a higher E/A ratio (p < 0.03) and a shorter DT (p < 0.03) than patients with mild or no ascites.
Conclusions:
The impaired left ventricular relaxation in the presence of high stroke volume suggests a myocardial involvement in LC. The pseudo normalization of the E/A ratio and DT in patients with tense ascites could reflect loading conditions masking the relaxation abnormality.