The Use of E/A Ratio as a Predictor of Outcome in Cirrhotic Patients Treated With Transjugular Intrahepatic Portosystemic Shunt


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Abstract

OBJECTIVES:The clinical significance of diastolic dysfunction in cirrhosis, a feature of cirrhotic cardiomyopathy, is unclear. The aim of this study was to assess the utility of E/A ratio, an indicator of diastolic dysfunction, to predict ascites clearance and mortality after transjugular intrahepatic portosystemic stent shunt (TIPS) insertion.METHODS:A total of 101 cirrhotic patients who received TIPS had pre-TIPS assessments of demographics, severity of liver dysfunction (Child-Pugh and Model for End-Stage Liver Disease (MELD) scores), renal function, hemodynamics, and cardiac function (two-dimensional echocardiography). An E/A ratio of ≤1 was used to indicate diastolic dysfunction. Patients were followed-up for a mean period of 24.6±2.4 months post TIPS.RESULTS:A total of 41 patients with an E/A ratio of ≤1 (group A), and 60 patients with an E/A ratio of >1 (group B) were studied. Group A had significantly higher MELD scores (14.0±1.0 vs. 11.4±0.8;P=0.03), because of higher serum creatinine levels (107±5 vs. 86±6 μmol/l;P<0.01). There was no difference in pre-TIPS systemic hemodynamics, systolic function, or portal pressure between the two groups. After TIPS, more patients in group B had ascites clearance (log rank,P=0.038), and the same patients had a higher probability of survival (log rank,P=0.046). There were three post-TIPS cardiac deaths in group A only. A multivariate analysis showed that an E/A of ratio ≤1 was predictive of slow ascites clearance (hazard ratio = 7.3, 95% confidence interval = 1.3-40.7,P=0.021) and death after TIPS (hazard ratio=4.7, 95% confidence interval = 1.1-20.2,P=0.035).CONCLUSIONS:Diastolic dysfunction, indicated by reduced E/A ratio, is prevalent in advanced cirrhosis and is associated with reduced ascites clearance and increased mortality post TIPS, possibly related to worsening of hemodynamic dysfunction in the post-TIPS period.Am J Gastroenterol 2009; 104:2458-2466; doi: 10.1038/ajg.2009.321; published online 16 June 2009

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