UNLABELLED: An abnormality of the autonomic nervous system caused by diabetic neuropathy is one of the major causes of silent myocardial ischemia (SMI). This study evaluated quantitatively the association between clinically detectable SMI and myocardial 123I-metaiodobenzylguanidine (MIBG) uptake in patients with diabetes. METHODS: Patients with SMI with diabetes, with SMI without diabetes, with angina pectoris with diabetes and normal control subjects participated in this study. Subjects underwent planar and SPECT imaging immediately and 3 hr after injection of [123I]MIBG, and exercise thallium scintigraphy. MIBG was quantified based on the myocardial-to-mediastinal ratio (H/M) of [123I]MIBG count, the inferior wall to anterior wall count ratio (I/A), the relative regional uptake (RRU), washout rate and corrected [123I]MIBG defect score. RESULTS: H/M ratio was significantly lower in diabetic SMI (2.1 +/- 0.3) and nondiabetic SMI (2.3 +/- 0.3) than in control subjects (2.6 +/- 0.3). RRU was the lowest in inferior wall of the left ventricle in the normal group (78 +/- 7). Compared with anterior segments, the uptake of [123I]MIBG was lower in inferior and apex segments in normal subjects (p < 0.05). A significant difference was observed in RRU in the inferior segment of the distal left ventricle between SMI and angina groups (p < 0.05) among patients with diabetes mellitus. I/A ratio in the diabetic SMI group was the smallest (p < 0.05). However, no significant difference was observed in the corrected [123I]MIBG defect score among all groups. CONCLUSION: The MIBG uptake was heterogeneous in normal subjects. Decreased MIBG uptake in the inferior wall may be an important sign of cardiac sympathetic dysfunction, suggesting that the abnormalities in cardiac nervous system play an important role in the mechanism of silent myocardial ischemia.
UNLABELLED: An abnormality of the autonomic nervous system caused by diabetic neuropathy is one of the major causes of silent myocardial ischemia (SMI). This study evaluated quantitatively the association between clinically detectable SMI and myocardial 123I-metaiodobenzylguanidine (MIBG) uptake in patients with diabetes. METHODS:Patients with SMI with diabetes, with SMI without diabetes, with angina pectoris with diabetes and normal control subjects participated in this study. Subjects underwent planar and SPECT imaging immediately and 3 hr after injection of [123I]MIBG, and exercise thallium scintigraphy. MIBG was quantified based on the myocardial-to-mediastinal ratio (H/M) of [123I]MIBG count, the inferior wall to anterior wall count ratio (I/A), the relative regional uptake (RRU), washout rate and corrected [123I]MIBG defect score. RESULTS: H/M ratio was significantly lower in diabeticSMI (2.1 +/- 0.3) and nondiabetic SMI (2.3 +/- 0.3) than in control subjects (2.6 +/- 0.3). RRU was the lowest in inferior wall of the left ventricle in the normal group (78 +/- 7). Compared with anterior segments, the uptake of [123I]MIBG was lower in inferior and apex segments in normal subjects (p < 0.05). A significant difference was observed in RRU in the inferior segment of the distal left ventricle between SMI and angina groups (p < 0.05) among patients with diabetes mellitus. I/A ratio in the diabeticSMI group was the smallest (p < 0.05). However, no significant difference was observed in the corrected [123I]MIBG defect score among all groups. CONCLUSION: The MIBG uptake was heterogeneous in normal subjects. Decreased MIBG uptake in the inferior wall may be an important sign of cardiac sympathetic dysfunction, suggesting that the abnormalities in cardiac nervous system play an important role in the mechanism of silent myocardial ischemia.