Cardiac dysfunction in portal hypertension among patients with cirrhosis and non-cirrhotic portal fibrosis

Background/Aims: In cirrhosis, diastolic dysfunction of heart is well documented. Contribution of portal hypertension towards cardiac changes in cirrhosis is difficult to assess. We examined the patients of non-cirrhotic portal fibrosis who have portal hypertension without liver insufficiency to und...

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Veröffentlicht in:Journal of hepatology 2003-09, Vol.39 (3), p.315-319
Hauptverfasser: De, Binay K, Majumdar, Debabrata, Das, Debasish, Biswas, Pranab K, Mandal, Sanjay K, Ray, Sujay, Bandopadhyay, Kausik, Das, Tapas K, Dasgupta, Sanjay, Guru, Supriya
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Sprache:eng
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Zusammenfassung:Background/Aims: In cirrhosis, diastolic dysfunction of heart is well documented. Contribution of portal hypertension towards cardiac changes in cirrhosis is difficult to assess. We examined the patients of non-cirrhotic portal fibrosis who have portal hypertension without liver insufficiency to understand the contribution of portal hypertension in causing cardiac changes. Methods: Cardiac function was studied in four groups of patients: normal controls, patients with non-cirrhotic portal fibrosis (having portal hypertension without liver dysfunction) and cirrhotics with and without ascites. Cardiac function was evaluated by echocardiography. Additional measurements of plasma renin activity and aldosterone levels were performed. Results: Diastolic function as assessed by the ratio between E wave and A wave (E/A ratio), was significantly lower in patients with non-cirrhotic portal fibrosis (median 1.3) compared to normal controls (median 1.52). However, even lower values were observed in cirrhotics without ascites (median 1.05) and with ascites (median 0.94). There was a significant correlation ( r=−0.75) between plasma aldosterone levels and the E/A ratio in cirrhotics. Conclusions: Diastolic dysfunction is not only present in cirrhosis but also in non-cirrhotic portal fibrosis. It indicates that portal hypertension is an important factor in the genesis of cardiac dysfunction.
ISSN:0168-8278
1600-0641
DOI:10.1016/S0168-8278(03)00271-X