T. Shimonagata et al., SCINTIGRAPHIC ASSESSMENT OF SILENT-MYOCARDIAL-ISCHEMIA AFTER EARLY INFARCTION USING MYOCARDIAL SPET IMAGING WITH TL-201 AND I-123 MIBG, Nuclear medicine communications, 16(11), 1995, pp. 893-900
To test the hypothesis that myocardial sympathetic denervation reflect
s silent myocardial ischaemia early after infarction, 12 patients with
myocardial infarction but without post-infarction angina pectoris und
er-went single photon emission tomography (SPET) at rest with Tl-201 a
nd I-123-metaiodobenzylguanidine (MIBG) shortly after and 3 months aft
er infarction. Short-axis SPET images at the basal, mid-ventricular an
d apical portions of the left ventricle were selected, and each short-
axis image was divided into eight segments. Tracer uptake in each of t
he 24 segments was scored using a 4-point scale. The total score in ea
ch segment was calculated as the defect score for each image, and the
difference between the total defect score for the Tl-201 and I-123-MIB
G images was calculated as the Delta defect score. All 12 patients und
erwent exercise stress Tl-201 scintigraphy 1 month after infarction, a
nd they were divided into two groups: those patients with (Group A, n
= 7) and those patients without (Group B, n = 5) transient perfusion d
efects in the peri-infarcted region without chest pain. For the I-123-
MIBG defect score, a marked reduction at 3 months was observed in Grou
p A (24 +/- 12 vs 13 +/- 6; P < 0.01), whereas the defect score remain
ed 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 I-123-MIBG defect
score early after infarction was higher than the exercise-induced Tl-
201 defect score (24 +/- 12 vs 20 +/- 9; P < 0.01), whereas at 3 month
s post-infarction it was lower than the exercise-induced Tl-201 defect
score (13 +/- 6 vs 20 +/- 9; P < 0.05). Moreover, effort chest pain d
uring 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 I-123-MIBG defects)
is present in peri-infarcted regions, and that myocardial sensory nerv
ous disturbance, which may co-exist with sympathetic nervous denervati
on, may induce silent myocardial ischaemia in patients with myocardial
infarction.