Shimonagata T, Ishida Y, Hayashida K, Takamiya M, Uehara T, Nishimura T
Department of Radiology, National Cardiovascular Centre, Osaka, Japan.
Nucl Med Commun. 1995 Nov;16(11):893-900. doi: 10.1097/00006231-199511000-00003.
To test the hypothesis that myocardial sympathetic denervation reflects silent myocardial ischaemia early after infarction, 12 patients with myocardial infarction but without post-infarction angina pectoris underwent single photon emission tomography (SPET) at rest with 201Tl and 123I-metaiodobenzylguanidine (MIBG) shortly after and 3 months after infarction. Short-axis SPET images at the basal, mid-ventricular and apical portions of the left ventricle were selected, and each short-axis image was divided into eight segments. Tracer uptake in each of the 24 segments was scored using a 4-point scale. The total score in each segment was calculated as the defect score for each image, and the difference between the total defect score for the 201Tl and 123I-MIBG images was calculated as the delta defect score. All 12 patients underwent exercise stress 201Tl scintigraphy 1 month after infarction, and they were divided into two groups: those patients with (Group A, n = 7) and those patients without (Group B, n = 5) transient perfusion defects in the peri-infarcted region without chest pain. For the 123I-MIBG defect score, a marked reduction at 3 months was observed in Group A (24 +/- 12 vs 13 +/- 6; P < 0.01), whereas the defect score remained unchanged in Group B (25 +/- 7 vs 23 +/- 8; N.S.). The delta defect score was significantly reduced in Group A (10 +/- 5 vs 6 +/- 4; P < 0.05), whereas it remained unchanged in Group B. The 123I-MIBG defect score early after infarction was higher than the exercise-induced 201Tl defect score (24 +/- 12 vs 20 +/- 9; P < 0.01), whereas at 3 months post-infarction it was lower than the exercise-induced 201Tl defect score (13 +/- 6 vs 20 +/- 9; P < 0.05). Moreover, effort chest pain during daily activities was noted in 5 of the 7 (71%) patients in Group A within 3 months post-infarction. The results of this study suggest that viable but denervated myocardium (mismatched 123I-MIBG defects) is present in peri-infarcted regions, and that myocardial sensory nervous disturbance, which may co-exist with sympathetic nervous denervation, may induce silent myocardial ischaemia in patients with myocardial infarction.
为验证心肌交感神经去神经支配反映梗死早期无症状性心肌缺血这一假说，12例心肌梗死但无梗死后心绞痛的患者在梗死后不久及3个月时接受了静息状态下的单光子发射断层扫描（SPET），分别使用201Tl和123I - 间碘苄胍（MIBG）。选取左心室基底、心室中部和心尖部的短轴SPET图像，每张短轴图像分为8个节段。使用4分制对24个节段中的每个节段的示踪剂摄取进行评分。计算每个图像中每个节段的总分作为缺损分数，计算201Tl和123I - MIBG图像的总缺损分数之差作为差值缺损分数。所有12例患者在梗死后1个月接受运动负荷201Tl心肌显像，并分为两组：梗死周边区域有（A组，n = 7）和无（B组，n = 5）无胸痛的短暂灌注缺损的患者。对于123I - MIBG缺损分数，A组在3个月时观察到明显降低（24±12对13±6；P < 0.01），而B组缺损分数保持不变（25±7对23±8；无统计学意义）。A组的差值缺损分数显著降低（10±5对6±4；P < 0.05），而B组保持不变。梗死后早期的123I - MIBG缺损分数高于运动诱发的201Tl缺损分数（24±12对20±9；P < 0.01），而在梗死后3个月时低于运动诱发的201Tl缺损分数（13±6对20±9；P < 0.05）。此外，A组7例患者中有5例（71%）在梗死后3个月内日常活动时有劳力性胸痛。本研究结果提示梗死周边区域存在存活但去神经支配的心肌（123I - MIBG不匹配缺损），并且心肌感觉神经紊乱可能与交感神经去神经支配并存，可诱发心肌梗死患者的无症状性心肌缺血。
