title: Abnormal glucose tolerance contributes to the progression of chronic heart failure in patients with dilated cardiomyopathy.
abstract: Since 1) dilated cardiomyopathy (DCM) causes chronic heart failure (CHF), and 2) augmentation of neurohumoral factors such as angiotensin II impairs glucose metabolism, we examined the rate of abnormal glucose metabolism in patients having both DCM and CHF and whether correction of the impairment of glucose metabolism would improve the pathophysiology of CHF in DCM patients. A 75-g oral glucose tolerance test (OGTT) was performed in 56 patients with DCM-induced CHF and 168 age- and sex-matched control subjects. Among the CHF patients, 26.8% and 50.0% suffered from diabetes mellitus (DM) and impaired glucose tolerance (IGT), respectively, showing that abnormal glucose tolerance was more prevalent in DCM patients than in the control subjects (7.7% and 14.3%, respectively). In the patients with DCM-induced CHF, a correlation was observed between the brain natriuretic peptide (BNP) levels and the difference between the plasma glucose levels at the time of fasting and at 2 h of OGTT. Since neither DM nor IGT are thought to cause DCM, the abnormalities of glucose metabolism may be attributed to the progression of CHF. Furthermore, we tested whether correction of the abnormal glucose tolerance using voglibose (an alpha-glucosidase inhibitor) would improve the severity of CHF in another group of 30 patients with DCM-induced CHF and IGT. The patients treated with voglibose for 24 weeks showed decreases in left ventricular dimension, NYHA functional classification values, and plasma BNP levels, and an improvement in cardiac function. In conclusion, abnormal glucose tolerance was more prevalent among patients with DCM-induced CHF than controls, and the correction of IGT improved the pathophysiology of CHF.
authors.affiliation: Cardiovascular Division, National Cardiovascular Center, Suita, Japan.
authors.forename: Jiyoong
authors.initials: J
authors.lastname: Kim
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nakatani
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Hashimura
authors.forename: Kazuo
authors.initials: K
authors.lastname: Komamura
authors.forename: Hideaki
authors.initials: H
authors.lastname: Kanzaki
authors.forename: Masanori
authors.initials: M
authors.lastname: Asakura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Asanuma
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Kokubo
authors.forename: Hitonobu
authors.initials: H
authors.lastname: Tomoike
authors.forename: Masafumi
authors.initials: M
authors.lastname: Kitakaze
mesh_terms: D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000503:physiopathology; D002908:Chronic Disease; D018450:Disease Progression; D004452:Echocardiography; D005260:Female; D018149:Glucose Intolerance / Q000188:drug therapy / Q000453:epidemiology* / Q000503:physiopathology; D005951:Glucose Tolerance Test; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000503:physiopathology; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007294:Inositol / Q000031:analogs & derivatives / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D015995:Prevalence; D012720:Severity of Illness Index
chemical_list: D007004:Hypoglycemic Agents; D020097:Natriuretic Peptide, Brain; D007294:Inositol; C102817:voglibose