FUNCTIONAL AND STRUCTURAL CARDIAC ABNORMALITIES IN CIRRHOTIC PATIENTS WITH AND WITHOUT ASCITES
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This study was done to clarify the nature of cardiac involvement in liver cirrhosis, the study comprised 40 patients with liver cirrhosis and 10 healthy control subjects. These patients were categorized under 3 groups :- Patients with liver cirrhosis and tense ascites : This group comprised 20 patients (7 females (3596) and .13 males (65%) with age range from 40 to 70 years (mean = 55+8) (Group 1). Patients with liver cirrhosis with no evidence of actual ascites at clinical and abdominal ultrasound examination but with history of clinically previous episodes of ascites. This group comprised 20 patients (5 females (25%) and 15 males (75%) with age range from 46 to 70 years (mean 55+5) (Group 2). 10 healthy subjects (3 females (30%) and 7 males (70%)) with age range from 45 to 70 years (mean= 56+7), served as normal control for comparison (Group 3). All patients were subjected to fill history taking, fi.ill clinical examination, laboratory investigation (assessment of liver function, hepatitis marker, indirect haemaglutirtation (1HA) for bilharziasis, arterial blood gases), abdominal ultrasound, X ray chest and heart, electrocardiography, doppler echocardiography. the results showed that patients with liver cirrhosis with and without ascites showed increased prevalence of g-Tc interval prolongation that correlate positively with the severity of liver cirrhosis and Child Pugh Score and was attributed to autonomic dysfunction, adrenergic hypertone, electrolyte imbalance and female gender. The study showed also irrespective of the ascites and the cause, patients with advanced liver cirrhosis had left ventricular diastolic ..dysfunction and wall thickness increase while the left ventricular systolic function still normal and impairment of left ventricular diastolic function correlates positively with the severity of liver disease and Child Pugh Score. The possible mechanisms responsible for the cardiac changes in liver cirrhosis inch irlp left ventricular overload induced by hyperdynamic circulation, impairment of B adrertergic receptors and its signal transudation pathway, abnormalities of circulating humoral factors and changes of cardiac plasma membrane physical properties.