Myocardial sympathetic innervation in diabetic patients with symptomatic coronary artery disease.
OBJECTIVE
In non-diabetic patients, sympathetic innervation can be preserved even if there is major impairment of myocardial blood supply. Matters may be more complex in diabetic patients because denervation can be caused by cardiac autonomic neuropathy (CAN) or by ischemic injury. Our aim was to determine whether restrictions in myocardial blood supply have a pronounced influence on sympathetic innervation in diabetics and if this effect can be differentiated from CAN.


METHODS
We analyzed 20 diabetics with advanced coronary artery disease (CAD) and without known CAN. We determined quantitative myocardial blood flow using (13)N-ammonia-PET, myocardial viability with (18)F-FDG, and cardiac innervation with (11)C-HED. We investigated the relationship between regional HED retention, blood flow, and coronary flow reserve (CFR). Attenuated heart rate response to adenosine was taken as indicator for CAN (HR ratio).


RESULTS
There was minor correlation of segmental stress flow and HED retention (r(2)=0.063, p<0.0001). Correlation improved when stress flow as well as HED retention were normalized to the individual maximum (r(2)=0.162, p<0.0001). In nine patients, a HR ratio <1.2 implicated subclinical CAN. Duration of diabetic disease or glycaemic control (HbA1c) did not correlate with mean HED retention in the viable segments, but with its variation coefficient.


CONCLUSIONS
As in non-diabetic patients, a slight correlation exists between CFR and sympathetic innervation. The sensitivity of sympathetic nerves to reductions in CFR does not seem to be increased as compared to the results reported for non-diabetics. Besides impaired blood supply, long duration of diabetic disease and bad glycaemic control also seem to impair sympathetic innervation provoking higher heterogeneity.
Fricke
E
E
Institute of Radiology, Nuclear Medicine and Molecular Imaging, Heart and Diabetes Centre North Rhine-Westphalia, Bad Oeynhausen, Germany. efricke@hdz-nrw.de
Eckert
S
S
Fricke
H
H
Körfer
J
J
Weise
R
R
Lindner
O
O
Tschöpe
D
D
Horstkotte
D
D
Burchert
W
W
D017668:Age of Onset; D000368:Aged; D001692:Biological Transport; D003326:Coronary Circulation; D003327:Coronary Disease / Q000000981:diagnostic imaging*; D003925:Diabetic Angiopathies / Q000000981:diagnostic imaging*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics*; D015309:Glucose Clamp Technique; D006442:Glycated Hemoglobin / Q000378:metabolism; D006329:Heart Conduction System / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D012044:Regression Analysis
D019788:Fluorodeoxyglucose F18; D006442:Glycated Hemoglobin; D019275:Radiopharmaceuticals