Matsuo S, Takahashi M, Nakamura Y, Kinoshita M
First Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan.
J Nucl Med. 1996 May;37(5):712-7.
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.
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.
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.
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.
糖尿病性神经病变引起的自主神经系统异常是无症状性心肌缺血(SMI)的主要原因之一。本研究定量评估了糖尿病患者临床可检测到的SMI与心肌123I-间碘苄胍(MIBG)摄取之间的关联。
患有糖尿病的SMI患者、不患有糖尿病的SMI患者、患有糖尿病的心绞痛患者以及正常对照受试者参与了本研究。受试者在注射[123I]MIBG后即刻和3小时接受平面和SPECT成像,并进行运动铊闪烁显像。基于[123I]MIBG计数的心肌与纵隔比值(H/M)、下壁与前壁计数比值(I/A)、相对区域摄取(RRU)、洗脱率和校正后的[123I]MIBG缺损评分对MIBG进行定量分析。
糖尿病性SMI组(2.1±0.3)和非糖尿病性SMI组(2.3±0.3)的H/M比值显著低于对照组(2.6±0.3)。正常组左心室下壁的RRU最低(78±7)。与前壁节段相比,正常受试者下壁和心尖节段的[123I]MIBG摄取较低(p<0.05)。在糖尿病患者中,SMI组和心绞痛组之间左心室远端下节段的RRU存在显著差异(p<0.05)。糖尿病性SMI组的I/A比值最小(p<0.05)。然而,所有组校正后的[123I]MIBG缺损评分未见显著差异。
正常受试者的MIBG摄取存在异质性。下壁MIBG摄取降低可能是心脏交感神经功能障碍的重要标志,提示心脏神经系统异常在无症状性心肌缺血机制中起重要作用。