Effect of glycaemic control on myocardial sympathetic innervation assessed by [123I]metaiodobenzylguanidine scintigraphy: a 4-year prospective study in IDDM patients.
Diabetic cardiovascular autonomic neuropathy (CAN) has been directly characterized by reduced or absent myocardial [123I]metaiodobenzylguanidine (MIBG) uptake, but there is no information available on the relationship between the myocardial adrenergic innervation defects and long-term glycaemic control. In a prospective study over a mean of 4 years we examined myocardial sympathetic innervation in 12 Type 1 (insulin-dependent) diabetic patients using MIBG scintigraphy (absolute and relative global MIBG uptake at 2 h p.i.) in conjunction with cardiovascular autonomic function tests, QTc interval, and QT dispersion. Six healthy non-diabetic subjects served as controls for the MIBG scintigraphy at baseline. HbA1c was measured twice a year. One patient, in whom MIBG accumulation was reduced maximally, died during follow up. Among the remaining patients 5 had good or borderline glycaemic control (mean HbA1c < 7.6%; Group 1), whereas 6 patients were poorly controlled (mean HbA1c > or = 7.6%; Group 2). Absolute global MIBG uptake increased from baseline to follow-up by 260 (-190-540) [median (range)] cpm/g in Group 1 and decreased by -150 (-450-224) cpm/g in Group 2 (p < 0.05 vs Group 1). Relative global MIBG uptake decreased by -1.7 (-3.4-9.4) % in Group 1 and by -4.7 (-17.4-1.3) % in Group 2 (p < 0.05 vs Group 1). No differences between the groups were noted for the changes in the automatic function tests, QTc interval, and QT dispersion. In conclusion, long-term poor glycaemic control constitutes an essential determinant in the progression of left ventricular adrenergic dysinnervation which may be prevented by near-normoglycaemia. Evaluation of susceptibility to metabolic intervention may be superior when CAN is characterized directly by MIBG scintigraphy rather than by indirect autonomic function testing.
Ziegler
D
D
Diabetes Research Institute at the Heinrich Heine University, Düsseldorf, Germany.
Weise
F
F
Langen
K J
KJ
Piolot
R
R
Boy
C
C
Hübinger
A
A
Müller-Gärtner
H W
HW
Gries
F A
FA
D019797:3-Iodobenzylguanidine / Q000493:pharmacokinetics; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure; D003922:Diabetes Mellitus, Type 1 / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000503:physiopathology; D003930:Diabetic Retinopathy / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis*; D006321:Heart / Q000000981:diagnostic imaging / Q000294:innervation*; D006339:Heart Rate; D006801:Humans; D008133:Long QT Syndrome; D008297:Male; D008875:Middle Aged; D010525:Peripheral Nerves / Q000503:physiopathology; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D012016:Reference Values; D013564:Sympathetic Nervous System; D016277:Ventricular Function, Left
D019797:3-Iodobenzylguanidine; D015415:Biomarkers; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D019275:Radiopharmaceuticals