摘要
Background/Aims: The Q-Tc interval is prolonged in a substantial fraction of patients with cirrhosis, thus indicating delayed repolarisation. However, no information is available in mild portal hypertensive patients. We therefore determined the Q-Tc interval in cirrhotic patients with hepatic venous pressure gradient (HVPG) < 12 mmHg. Methods: Forty-four patients with cirrhosis and HVPG < 12 mmHg underwent a haemodynamic study. They were compared with 36 cirrhotic patients with clinically significant portal hypertension (HVPG ≥ 12 mmHg) and controls without liver disease. Results: The fraction with prolonged Q-Tc interval ( > 0.440 s1/2) was similar in the two cirrhotic groups (49 vs 50% , ns) and significantly above that of the controls (5% , P < 0.005). Q-Tc was normal in patients with normal HVPG. Likewise, mean Q-Tc was 0.449 and 0.447 s1/2 in the two cirrhotic groups (ns), values which are significantly above that of the controls (0.410 s1/2, P < 0.01). In the mild portal hypertensive group, the Q-Tc interval was inversely related to indicators of liver function, such as indocyanine green clearance (r = -0.34, P < 0.02). Conclusions: Delayed repolarisation of the myocardium already occurs in a substantial fraction of patients with cirrhosis with only a mild increase in portal pressure. The prolonged Q-Tc interval may be related to liver dysfunction and to the presence of portal hypertension.
Background/Aims: The Q-Tc interval is prolonged in a substantial fraction of patients with cirrhosis, thus indicating delayed repolarisation. However, no information is available in mild portal hypertensive patients. We therefore determined the Q-Tc interval in cirrhotic patients with hepatic venous pressure gradient (HVPG) < 12 mmHg. Methods: Forty-four patients with cirrhosis and HVPG < 12 mmHg underwent a haemodynamic study. They were compared with 36 cirrhotic patients with clinically significant portal hypertension (HVPG ≥ 12 mmHg) and controls without liver disease. Results: The fraction with prolonged Q-Tc interval ( > 0.440 s1/2) was similar in the two cirrhotic groups (49 vs 50% , ns) and significantly above that of the controls (5% , P < 0.005). Q-Tc was normal in patients with normal HVPG. Likewise, mean Q-Tc was 0.449 and 0.447 s1/2 in the two cirrhotic groups (ns), values which are significantly above that of the controls (0.410 s1/2, P < 0.01). In the mild portal hypertensive group, the Q-Tc interval was inversely related to indicators of liver function, such as indocyanine green clearance (r = -0.34, P < 0.02). Conclusions: Delayed repolarisation of the myocardium already occurs in a substantial fraction of patients with cirrhosis with only a mild increase in portal pressure. The prolonged Q-Tc interval may be related to liver dysfunction and to the presence of portal hypertension.
