I‐123 metaiodobenzylguanidine—thallium‐201 mismatch following myocardial infarction

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Abstract
Experimental data show that myocardial infarction (MI) results in regional depletion of myocardial cathecholamines more extensively than necrosis. To investigate the extent of adrenergic denervation post MI in humans, we examined 16 patients, 59 ± 12 years old, with recent (7-12 days) MI. Resting thallium-201 (201Tl) single photon emission computerized tomography (SPECT) imaging was performed to assess necrosis; metaiodobenzylguanidine I123 (MIBG) SPECT was used to evaluate adrenergic denervation. 201Tl and I123 MIBG defects were evaluated quantitatively using polar maps, and differences in defects were expressed as percent of total polar map. in all patients, I123 MIBG defect was larger than 201Tl defect, and difference ranged from 19 to 61 % (39.5 ± 13.2%). Thrombolysis and age > 60 did not influence the difference. Anterior MI showed larger differences (44± 13 vs. 32± 11 %, p < 0.05); patients with ischemic electrocardiographic (ECG) changes in leads without abnormal Q waves had larger differences (45 ± 9 vs. 33 ± 14%, p< 0.05). It was concluded that (a) patients with recent MI present denervation larger than 201Tl perfusion defect, and (b) patients with anterior MI and ischemic ECG changes present a larger area of denervation.