Background: This study aimed to assess whether QT interval prolongation is an independent risk factor for development of hepatorenal syndrome (HRS) in cirrhotic patients with acute variceal bleeding.
Methods: 78 consecutive cirrhotic patients with acute variceal bleeding were included in the study. All patients were evaluated before bleeding (T0), during bleeding (T1) and 6 weeks later (T2).
Results: HRS developed in 14 (17.9%) patients. QT corrected by heart rate (QTc) prolonged at T1, returning towards baseline at T2 (mean ± SD; from 424.0±10.2 to 461.2±17.6 to 426.1±8.8ms, P<0.001). At T1, patients who developed HRS had longer QTc (P=0.017) and lower serum sodium (P=0.039). QTc and serum sodium independently predicted HRS; the best cut-off values were QTc > 468 ms and sodium <120 mEq/L. Patients on beta-blocker were found to have significant risk for developing HRS (p=0.040). Based on these three factors, the risk for HRS was nil for patients without risk factors; 6.1%, 11.1%, and 83.3% for those with one, two or three risk factors, respectively (p<0.001).
Conclusions: Acute variceal bleeding causes further prolongation of QTc in cirrhosis. The combination of beta-blocker, QTc interval and serum sodium can aid in early detection of patients at increased risk of developing bleed-precipitated HRS, thus improving their outcome.