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.
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 diabeticpatients. RESEARCH DESIGN AND METHODS: We evaluated cardiac sympathetic innervation in a population-based group of 10 asymptomatic diabeticpatients with angiographically proven CAD and in an age- and sex-matched group of 10 diabeticpatients 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 diabeticpatients with CAD are complex and are not solely explained by autonomic neuropathy.
Authors: Marie Louise M Ghorbani; Chao Qin; Mingyuan Wu; Jay P Farber; Majid Sheykhzade; Bjarne Fjalland; Niels C B Nyborg; Robert D Foreman Journal: Auton Neurosci Date: 2011-09-08 Impact factor: 3.145