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MINERVA GASTROENTEROLOGICA E DIETOLOGICA
A Journal on Gastroenterology, Nutrition and Dietetics
Indexed/Abstracted in: CAB, EMBASE, PubMed/MEDLINE, Scopus, Emerging Sources Citation Index
Minerva Gastroenterologica e Dietologica 2005 June;51(2):179-86
Time-course of diastolic dysfunction in different stages of chronic HCV related liver diseases
Pozzi M., Redaelli E., Ratti L., Poli G., Guidi C., Milanese M., Calchera I., Mancia G.
Aim. A hyperdynamic circulatory pattern in advanced liver disease is known since a long time. The first studies evaluating cardiac function in cirrhosis were performed in patients with alcoholic liver disease and thus this condition was attributed to the toxic effects of ethanol. A reduced performance of the left ventricle after physical and pharmacological strains along with an altered diastolic function has been demonstrated also in postviral cirrhosis. Many factors are involved in advanced cirrhosis whereas little is known in the earlier stages of disease.
Methods. To this aim we have investigated patients with different stages of hepatitis C virus (HCV)-related liver disease to detect the time-course of diastolic dysfunction. An impaired relaxation and increased thickness of left ventricular walls along with an altered pattern of transmitral flow can be easily detected by means of echocardiography.
Results. In chronic hepatitis diastolic function is preserved but increased thickness of left ventricle parietal walls can be detected in patients with fibrosis on liver biopsy. The typical pattern of diastolic dysfunction is observed in Child A cirrhotic patients and in Child C ascitic patients but thickness of parietal walls is more relevant in the former group. Chronic aldosterone blockade could exert favourable effects in heart remodeling suggesting a potential role of these drugs in cirrhotic cardiomyopathy.
Conclusions. The presence of increased thickness of left ventricle parietal walls in chronic hepatitis C in the precirrhotic stage point to a putative role of HCV in this heart structural abnormality that can become a co-factor in the more advanced stages of cirrhosis when portal hypertension and its deleterious effects on systemic hemodynamics, cardiac function and structure become manifest.