No difference in cardiac innervation of diabetic patients with painful and asymptomatic coronary artery disease
No difference in cardiac innervation of diabetic patients with painful and asymptomatic coronary artery disease. M J Koistinen , K E Airaksinen , H V Huikuri , M M Linnaluoto , J Heikkila , P Torniainen and A Ahonen Department of Internal Medicine, University of Oulu, Finland. Abstract OBJECTIVE: To...
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Published in: | Diabetes care Vol. 19; no. 3; pp. 231 - 235 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Alexandria, VA
American Diabetes Association
01-03-1996
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Subjects: | |
Online Access: | Get full text |
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Summary: | No difference in cardiac innervation of diabetic patients with painful and asymptomatic coronary artery disease.
M J Koistinen ,
K E Airaksinen ,
H V Huikuri ,
M M Linnaluoto ,
J Heikkila ,
P Torniainen and
A Ahonen
Department of Internal Medicine, University of Oulu, Finland.
Abstract
OBJECTIVE: To test the hypothesis that diabetic autonomic neuropathy interfering with sensory impulses from the heart by sympathetic
denervation is the major cause of the high prevalence of asymptomatic coronary artery disease (CAD) in diabetic patients.
RESEARCH DESIGN AND METHODS: We evaluated cardiac sympathetic innervation in a population-based group of 10 asymptomatic diabetic
patients with angiographically proven CAD and in an age- and sex-matched group of 10 diabetic patients with symptomatic CAD
using [123I]metaiodobenzylguanide (MIBG) scintigraphy. Exercise electrocardiography and myocardial perfusion imaging by 201Tl
were used to detect myocardial ischemia, and standard cardiovascular tests were used to diagnose autonomic nervous dysfunction.
RESULTS: Thallium scintigraphy revealed perfusion defects in all 10 symptomatic patients and in 9 of the asymptomatic patients.
MIBG accumulation defects were found in all cases with painless and with painful disease. In the asymptomatic group, the denervation
area exceeded the ischemic area in six cases and areas with total MIBG accumulation defects were seen in four cases. In one
case, the MIBG defect was not in the ischemic region. In the symptomatic group, the denervation area exceeded the area of
the ischemic region in all cases and areas of total denervation were seen in six cases. The autonomic nervous function tests
were abnormal in two asymptomatic and three symptomatic patients with CAD. CONCLUSIONS: Cardiac sympathetic denervation is
common in both patients with painful CAD and patients with asymptomatic CAD regardless of diabetic autonomic neuropathy. This
finding supports the view that sympathetic innervation of the heart is highly sensitive to ischemia and this profound effect
of ischemia masks the potential effects of autonomic neuropathy on sympathetic innervation. Mechanisms leading to the lack
of ischemic pain in diabetic patients with CAD are complex and are not solely explained by autonomic neuropathy. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0149-5992 1935-5548 |
DOI: | 10.2337/diacare.19.3.231 |