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Byoung Ho Sin  (Sin BH) 3 Articles
Association Between QTc Dispersion and Cardiovascular Autonomic Dysfuction in Non-insulin Dependent Dabetes Mellitus.
Jung Guk Kim, Hun Sik Park, Jick Hwa Nam, Byoung Ho Sin, Seong Mo Koo, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 1998;22(2):173-181.   Published online January 1, 2001
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BACKGROUND
Diabetic patients with autonomic dysfunction have worse prognosis, including an increased incidence, of sudden death, than those without autonomic dysfunction. This event may be due to sympathetic imbalance causing disturbances of ventricular repolarization. QT dispersion have recently been demonstrated to reflect dispersion of ventricular refractoriness and is a marker of arrhythmogenic potential. METHODS: Sixty diabetic patients and 31 normal subjects were studied. All patients had clinical test for cardiovascular autonomic dysfunction by Ewings method and defined as normal, early involved, definitely involved, severely involved and atypical group for 5 validated tests. Resting standard 12-lead electrocardiograms were recorded for measurement of QT dispersion, defined as the difference of longest QT interval and shortest QT interval, and corrected for heart rate using Bazetts formula. RESULTS: Twenty-seven dIiabetic patient were abnormal in cardiovascular autonomic function tests. In these patients corrected QT dispersion (QTc) were significantly longer compared to that 33 patients without autonomic dysfunction(47.4+14.7 vs 22.6+ 8.1msec p<0.001). And also there was significant difference of QTc dispersion between normal subject and diabetic patients with autonomic neuropathy group(20.5+9.2 vs 47.4+14.7msec p<0.001). But there was no difference between normal control and diabetic patients without autonomic neuropathy group. And QTc dispersion was not related to the presence ot nephropathy, retinopathy or peripheral polyneuropathy. We also found that there was no relationship between the severity of autonomic neuropathy and degree of Q7c dispersion. CONCLUSION: We concluded that QTc dispersion may be a good method for evaluation of cardiovascular autonomic neuropathy and increased QTc dispersion may be one of the markers of arrhythmia in diabetic patients with autonomic neuropathy.
Relationship between Peripheral Neuropathy and Cardiovascular Autonomic Neuropathy in Non-Insulin Dependent Diabetics.
Sung Woo Ha, Hyun Jeong Lee, Jeung Hun Han, Sang Won Jung, Jick Hwa Nam, Byoung Ho Sin, Seong Mo Koo, Jung Guk Kim, Sam Kwon, Bo Wan Kim
Korean Diabetes J. 1997;21(4):476-483.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Autonomic neuropathy was detected in some diabetics with symmetric peripheral neuropathy, a common complication of diabetes mellitus that may be associated with considerable morbidity. There has been known to be similarity of pathogenic mechanism in two neuropathies. Then we examined nerve conduction velocity and cardiovascular autonomic function tests. We studied relationship between peripheral and cardiovascular autonomic neuropathy in non-insulin dependent diabetics. METHODS: We studied 166 patients with or witbout peripheral neuropathy who had been diagnosed as non-insulin dependent diabetes mellitus. We examined nerve conduction tests to assess diabetic peripheral neuropathy and classified them into 4 groups aecording to neuropathic symptoms and results of nerve conduction tests. We examined five cardiovascular autonomic function tests by Ewing's methods. RESULTS: 1. The duration of diabetes mellitus was significantly longer in the group of cliabetics with neuropathic symptoms and abnormal findings in the nerve conduction velocity tests than the other groups. The level of blood glucose was significantly higher in the group of diabetics with neuropathic symptoms and findings than the other groups. 2. In the 5 cardiovascular autonomic function tests, heart rate response to deep breathing and Valsalva maneuver had significant differences between the diabetic group with peripheral neuropathy and the other groups. 3. The frequency and severity of autonomic neuropathy were higher in the group with peripheral neuro-pathic symptoms and findings than the other groups without neuropathic syrnptoms and findings. There was an overall significant relationship between sensorirnotor neural function and autonomic function. 4. There was no association between peripheral neuropathy and nephropathy although peripheral neuropathy was related with retinopathy. CONCLUSION: Diabetic peripheral neuropathy accompanies autonomic neuropathy. Then, this result suggests that there is the relationship between peripheral and cardiovascular autonomic neuropathy.
Lipopolysaccharide-Induced Changes in Vascular Reactivity of Diabetic Rat Aorta.
Ye Kyung Seo, Sang Won Chung, Jik Hwa Nam, Byoung Ho Sin, Dong Hee Kim, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 1997;21(3):280-288.   Published online January 1, 2001
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Backgound: Hemodynamic deteriorations in diabetes mellitus may be mediated by increased contractile response to catecholamines and/or by decreased relaxative response to vasodilators such as acetylcholine(Ach). Decrease in peripheral vascular reactivity to vasoconstrictor was known to be an ominous sign that happens during sepsis or after injection of bacterial lipopolysaccharides(LPS). In this study, we compared the effects of LPS on function of diabetic rat aorta with impaired vascular reactivity with those of control rat aorta. METHODS: Contractile responses to cumulative concentrations(10'M to 3X10'M) of norepinephrine (NE) were measured in aorta isolated ftom the control and 4 to 5-week streptozotocin-induced diabetic rat at 6 hours after LPS treatment to compare with contractile responses of untreated group. We measured relaxative responses to cumulative concentrations(10'M to 10M) of Ach and nitroprusside (NTP) in these aortas contracted submaximally by NE. RESULTS: Diabetic rat aortas showed significantly more impairment in relaxative responses to Ach than control rat aortas before LPS treatment(p0.05 = 0.0l). LPS treatment in those diabetic rat aortas decreased contractile responses to NE by 26.6%(p < 0.01); the changes were sirnilar to those of control (30.9%, p0.01). Relaxative responses to Ach were also significantly decreased by 25.0%(p 0.01) after L.PS treatment; the changes were similar to those of control(34.1%, p0.01). However relaxative responses to NTP were not changed in control and d.iabetic rat aortas by LPS treatment. CONCLUSION: These results suggest that diabetes may induce impairment in endothelium-dependent vascular relaxation and there rnay be no difference of L,P,S-induced effects on hemodynamic deterioration between 4 to 5-week diabetic and control rats.

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