Tropical gastroenterology : official journal of the Digestive Diseases Foundation · 2014
QT interval prolongation: a risk factor for development of hepatorenal syndrome in cirrhotic patients with acute variceal bleeding.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Peter George, George Paul Cheruvathoor, Villyoth Mashhood Padincharepurathu, Sivaraman Sijil, Hamza Rooby Erachamveettil, Bahuleyan Suthanu, Srijith Kadavanoor, Haridas Abhilash, Abdul Sathar Shanid, Sreesh Srijaya, Narayanan Premalatha, Vinayakumar Kattoor Ramakrishnan
Аннотация
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.
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.