Prolonged QTc interval and its relationship to autonomic cardiovascular reflexes in patients with cirrhosis.

BACKGROUND/AIMS: We have previously shown that an abnormality in cardiac autonomic reflexes (AN) is an independent predictor of mortality in patients with chronic liver disease. Aim of this study was to determine whether there was an association between prolonged QTc interval and cardiac AN. METHODS: Cardiac AN and QTc interval were determined in 130 patients (Child A 42, B 53, C 35) with alcoholic and non-alcoholic liver disease. RESULTS: Prolonged QTc (>440ms) was seen in 58 (Child A 30%, B 46%, C 60%, P=0.04) patients. Autonomic tests were normal in 21%, borderline abnormal in 36% and definitely abnormal in 43%. QTc correlated with albumin (P<0.001), prothrombin time (P=0.003) and Child-Pugh score (P<0.001), but not with Valsalva ratio, heart rate variation with 6 breath/min breathing, tilt table or isometric exercise. By logistic regression analysis, QTc correlated only with Child-Pugh score (P<0.001). Mean QTc of 34 who died during the follow up was higher than survivors. Cox regression analysis showed that only Child-Pugh score and AN were independent predictors of mortality. CONCLUSIONS: Prolonged QTc seen in liver disease is independent of their cardiac autonomic function, but is related to the severity of the liver disease.

Autonomic dysfunction and cholelithiasis in patients with cirrhosis.

Gallstones are seen in 33-46% of patients with cirrhosis, and their prevalence is known to increase with the duration and severity of liver disease. We hypothesized that autonomic neuropathy may contribute to the formation of gallstones or gallbladder disease, as in diabetics with autonomic neuropathy, due to impaired gallbladder emptying. The objective of our study was to determine the prevalence of gallstones or gallbladder disease in cirrhotic patients with and without autonomic neuropathy. We determined autonomic function tests, gallstones, and other gallbladder disease in 123 (male 71) with varying severity of liver disease (Child classes: A, 40; B, 45; C, 35). In all, 54 patients had gallstones and an additional 22 patients had other gallbladder disease (cholecystitis, common bile duct stones, or debris). Autonomic neuropathy was seen in 97 patients (one abnormal test in 48 and two or more in 49). The prevalence of gallstones was similar in Child A (57%), Child B (64%), and Child C (63%) cirrhosis. The gallstones or gallbladder disease was not increased in women, blacks, diabetics, or alcoholic cirrhotics. The prevalence of gallbladder disease was increased in patients with autonomic neuropathy (51% vs 35%, P = 0.08); in patients with Child C cirrhosis, gallstones (P = 0.018) and gallbladder disease (P = 0.03) were seen more commonly in patients with autonomic neuropathy. Our findings suggest that autonomic neuropathy may contribute to the formation of gallstones in patients with advanced cirrhosis, perhaps by impairing gallbladder and sphincter of Oddi dysmotility.