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PWE-060 Prolonged QT interval and serum brain natriuretic peptide in cirrhotic cardiomyopathy
  1. P Yap,
  2. D Das
  1. Department of Gastroenterology, Stepping Hill Hospital NHS Foundation Trust, Stockport, UK

Abstract

Introduction Cirrhotic cardiomyopathy is a recently recognised cardiac complication of liver cirrhosis,1 characterised by blunting of the cardiac responses to stresses secondary to liver disease. The heart is unable to increase its cardiac output despite increased cardiac stresses due to a combination of diastolic dysfunction, from increased myocardial fibrosis and cardiomyocyte hypertrophy causing abnormal relaxation of the left ventricle and impaired left ventricular filling, abnormalities in the β-adrenergic conduction pathway and alteration to the membrane fluidity of the cardiomyocytes. This was a prospective study to measure the BNP levels and QT interval in patients with liver disease and cirrhosis, of all aetiology.

Methods Prospective study over 6 months. 22 patients fulfilled inclusion criteria; acute decompensated liver disease of any cause with ascites. Patients excluded if they had a history of cardiac disease. All the patients had—ECGs on admission and serum BNP requested as in-patient. The QT interval was corrected using Bazetts formula.

Results Of the 22 patients recruited, 16 were due to alcohol, 1 PBC, 2 NASH, 1 Hepatitis C and 2 unclear diagnosis. 17 of the 22 patients had a positively raised serum BNP. (normal <300 ng/l) (min 13, max 4307; Mean 960). 18 of 22 patients had ECGs appropriate for analysis. The excluded patients had Atrial Fibrillation or ECG not done on latest admission. 14 of 18 patients ECG showed a prolonged QT interval, (normal QT interval >0.44 ms) min 0.404 ms, max 0.558 ms; Mean 0.465 ms.

Conclusion A large majority of the patients with cirrhosis had a raised BNP level and prolonged QT interval. This strongly suggests that they have underlying cardiac dysfunction in the form of cirrhotic cardiomyopathy and consequently lack the ability to increase their cardiac output in presence of stress, with the subsequent risk of developing acute heart failure and pulmonary oedema. Evidence shows that BNP levels and degree of QT interval prolongation are proportional to severity of cardiomyopathy in these patients1 and β-blockers have a beneficial role in normalising the QT interval.2 Given this background, we would advise routine assessment of all cirrhotics with electrocardiography and BNP estimations and a prospective trial be carried out to explore the protective role of β-blockers in these patients even in the absence of evidence of portal hypertension.

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