Open AccessI‐123 metaiodobenzylguanidine—thallium‐201 mismatch following myocardial infarction
Author(s) -
Lekakis John,
Antoniou Anna,
Vassilopoulos Nicos,
Tsinikas Dimitrios,
Palaistides Christos,
Kostamis Panos,
Moulopoulos Spyridon
Publication year - 1994
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960170105
Subject(s) - medicine , denervation , thallium , perfusion , cardiology , myocardial infarction , thrombolysis , nuclear medicine , infarction , sympathetic denervation , necrosis , ischemia , inorganic chemistry , chemistry
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 ( 201 Tl) single photon emission computerized tomography (SPECT) imaging was performed to assess necrosis; metaiodobenzylguanidine I 123 (MIBG) SPECT was used to evaluate adrenergic denervation. 201 Tl and I 123 MIBG defects were evaluated quantitatively using polar maps, and differences in defects were expressed as percent of total polar map. in all patients, I 123 MIBG defect was larger than 201 Tl 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 201 Tl perfusion defect, and (b) patients with anterior MI and ischemic ECG changes present a larger area of denervation.