BACKGROUND/AIMS: A prolonged QT interval is frequent in chronic liver disease and its aetiology remains unsettled. The study's aim was to assess the role of portal hypertension in the pathogenesis of QT prolongation. METHODS: We measured the QT interval in: (1) 10 patients with non-cirrhotic portal hypertension (NCPH) and preserved liver function; (2) 19 cirrhotic patients before, 1-3 and 6-9 months after transjugular intrahepatic porto-systemic shunt (TIPS) insertion. RESULTS: Baseline corrected maximum QT interval (QTcmax) was prolonged (>440 ms) in eight NCPH and 16 cirrhotic patients, and its value did not differ between the two groups (453+/-8 vs. 465+/-6 ms, P=NS). No patients showed an abnormal baseline QT dispersion. In cirrhotic individuals, QTcmax further increased 1-3 months after TIPS (P=0.042), thereafter remaining steadily elevated. QT dispersion only increased at the second post-TIPS determination (P=0.030). Such changes occurred despite no deterioration of liver function, plasma electrolytes and haemoglobin. CONCLUSIONS: QT interval is frequently prolonged in patient with both non-cirrhotic and cirrhotic portal hypertension and portal decompression by TIPS worsens this abnormality. These results suggest that the porto-systemic shunting is responsible for the altered ventricular repolarisation possibly through a dumping into the systemic circulation of splanchnic-derived cardioactive substances.
BACKGROUND/AIMS: A prolonged QT interval is frequent in chronic liver disease and its aetiology remains unsettled. The study's aim was to assess the role of portal hypertension in the pathogenesis of QT prolongation. METHODS: We measured the QT interval in: (1) 10 patients with non-cirrhotic portal hypertension (NCPH) and preserved liver function; (2) 19 cirrhotic patients before, 1-3 and 6-9 months after transjugular intrahepatic porto-systemic shunt (TIPS) insertion. RESULTS: Baseline corrected maximum QT interval (QTcmax) was prolonged (>440 ms) in eight NCPH and 16 cirrhotic patients, and its value did not differ between the two groups (453+/-8 vs. 465+/-6 ms, P=NS). No patients showed an abnormal baseline QT dispersion. In cirrhotic individuals, QTcmax further increased 1-3 months after TIPS (P=0.042), thereafter remaining steadily elevated. QT dispersion only increased at the second post-TIPS determination (P=0.030). Such changes occurred despite no deterioration of liver function, plasma electrolytes and haemoglobin. CONCLUSIONS: QT interval is frequently prolonged in patient with both non-cirrhotic and cirrhotic portal hypertension and portal decompression by TIPS worsens this abnormality. These results suggest that the porto-systemic shunting is responsible for the altered ventricular repolarisation possibly through a dumping into the systemic circulation of splanchnic-derived cardioactive substances.
Authors: Pierpaolo Pellicori; Concetta Torromeo; Angela Calicchia; Alessandra Ruffa; Martina Di Iorio; John G F Cleland; Manuela Merli Journal: Clin Res Cardiol Date: 2013-09-01 Impact factor: 5.460
Authors: Mohammed F Faramawi; Rachel P Wildman; Jeanette Gustat; Janet Rice; Mohammed Y Abdul Kareem Journal: Eur J Epidemiol Date: 2008-05-29 Impact factor: 8.082