title: ANP but not BNP reflects early left diastolic dysfunction in type 1 diabetics with myocardial dysinnervation.
abstract: OBJECTIVE
  We investigated whether plasma concentrations of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) reflect impaired diastolic relaxation or its improvement after ACE inhibition.
  
  
  METHODS
  7 long-term Type 1 diabetic patients with normal systolic but impaired diastolic function and with sympathetic myocardial dysinnervation and 10 controls were included. Exercise tolerance and maximal O 2 uptake were evaluated by bicycle exercise prior to the study. ANP, BNP and norepinephrine/epinephrine (NE/E) were determined at baseline and at 80 % .VO2 max workload and after recovery, before and following 12 weeks of treatment with fosinopril (10 mg/d).
  
  
  RESULTS
  Isovolumetric relaxation time (IVRT) and A/E wave ratio were increased by 26.7 +/- 11.5 % and 54.4 +/- 26.1 % in diabetic patients as compared to controls, respectively (p < 0.02). After 12 weeks of fosinopril treatment, no differences in IVRT or A/E wave ratio were detectable between groups. ANP was enhanced in Type 1 diabetes as compared to controls (baseline: 9.2 +/- 3.0 vs. 4.5 +/- 1.1; exercise: 22.4 +/- 7.7 vs. 7.9 +/- 1.2; recovery: 20.3. +/- 4.6 vs. 9.5 +/- 2.0 fmol/ml, p < 0.02). Fosinopril treatment abolished any differences between groups. BNP plasma levels did not differ between groups and no exercise dependent changes were observed. NE- and E-increase was greater at 80 % .VO2 max work load in Type 1 diabetes than in controls (p < 0.05). Again, fosinopril abolished differences between groups.
  
  
  CONCLUSIONS
  In Type 1 diabetes, impaired diastolic function is associated with elevated ANP and catecholamine plasma levels that are normalized after ACE inhibition. Thus, ANP but not BNP appears to be a sensitive biochemical marker for early diastolic dysfunction in Type 1 diabetes.
authors.affiliation: Department of Internal Medicine III, Division of Endocrinology and Metabolism, University Hospital Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. Michaela.Bayerle-Eder@akh-wien.ac.at
authors.forename: M
authors.initials: M
authors.lastname: Bayerle-Eder
authors.forename: M
authors.initials: M
authors.lastname: Zangeneh
authors.forename: G
authors.initials: G
authors.lastname: Kreiner
authors.forename: W
authors.initials: W
authors.lastname: Raffesberg
authors.forename: P
authors.initials: P
authors.lastname: Nowotny
authors.forename: H
authors.initials: H
authors.lastname: Vierhapper
authors.forename: W
authors.initials: W
authors.lastname: Waldhäusl
authors.forename: M
authors.initials: M
authors.lastname: Wolzt
authors.forename: H
authors.initials: H
authors.lastname: Pleiner
authors.forename: S
authors.initials: S
authors.lastname: Gasic
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000097:blood*; D015415:Biomarkers; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D015992:Body Mass Index; D009202:Cardiomyopathies / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000097:blood* / Q000503:physiopathology; D003971:Diastole / Q000502:physiology; D005260:Female; D017328:Fosinopril / Q000494:pharmacology; D006442:Glycated Hemoglobin / Q000378:metabolism; D006321:Heart / Q000294:innervation*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D009320:Atrial Natriuretic Factor; D015415:Biomarkers; D001786:Blood Glucose; D017328:Fosinopril; D006442:Glycated Hemoglobin; D020097:Natriuretic Peptide, Brain