ANP but not BNP reflects early left diastolic dysfunction in type 1 diabetics with myocardial dysinnervation.
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.
Bayerle-Eder
M
M
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
Zangeneh
M
M
Kreiner
G
G
Raffesberg
W
W
Nowotny
P
P
Vierhapper
H
H
Waldhäusl
W
W
Wolzt
M
M
Pleiner
H
H
Gasic
S
S
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*
D000806:Angiotensin-Converting Enzyme Inhibitors; D009320:Atrial Natriuretic Factor; D015415:Biomarkers; D001786:Blood Glucose; D017328:Fosinopril; D006442:Glycated Hemoglobin; D020097:Natriuretic Peptide, Brain