Abstract 19961: Factors Associated with Glucose Intolerance and Abnormal Lipid Metabolism in Fontan Patients
Background: Multi-organs dysfunctions including glucose intolerance has been reported in young adults after the Fontan operation.
We investigated factors associated with abnormalities in glucose tolerance and lipid metabolism in the chronic phase after the Fontan operation.
Methods: We studied 51 patients (mean 25.0, range 16-51 years old) after the Fontan operation who were hospitalized for catheter examination in our hospital. We excluded patients under 16 years of age.
HbA1c was used for the assessment of glucose tolerance, and total cholesterol (T-Cho) and triglyceride (TG) for the assessment of lipid metabolism.
Results: Mean HbA1c value was 5.8± 4.5%, and 77% of patients had abnormal HbA1c value higher than the normal upper value of 5.6%. In addition, high TG and T-Cho were recognized in 11% and 15% of patients, respectively. HbA1c had a negative correlation with cardiac index(CI)(P<0.05 ,r=-0.52), and a positive correlation with BNP(P<0.05, r=0.55). Serum Von Willebrand (vW) factor levels, which increase with endothelial dysfunction, also correlated with increased HbA1c (P <0.001). Multivariate analysis including age and BMI showed that CI was an independent determinant of HbA1c(P=0.05). Increased levels of TG and T-Cho had a positive correlation with serum levels of dopamine and noradrenaline (P <0.01), suggesting the importance of the sympathetic nervous activation for abnormal lipid metabolism in patients after the Fontan operation. There was no correlation between glucose tolerance and lipid metabolism.
Discussions: There is a high incidence of impaired glucose tolerance and abnormal lipid metabolism in patients after the Fontan operation. Both were closely associated with the severity of heart failure status of Fontan circulation. In addition, impaired glucose tolerance may be an important pathophysiology underlying vascular endothelial dysfunction often observed in Fontan patients, and may be an important therapeutic target to improve Fontan physiology.
Author Disclosures: C. Kurishima: None. K. Inai: None. S. Asagai: None. H. Senzaki: None. T. Nakanishi: None.
- © 2014 by American Heart Association, Inc.