M. Galli et al., ECG-MANIFEST AND ECG-SILENT DIPYRIDAMOLE TC-99M SESTAMIBI SPET PERFUSION DEFECTS IN PATIENTS WITH ISCHEMIC-HEART-DISEASE, European journal of nuclear medicine, 24(2), 1997, pp. 160-169
At dipyridamole myocardial scintigraphy, perfusion defects are seldom
backed up by significant ECG changes. This would suggest myocardial bl
ood flow heterogeneity, rather than true ischaemia, as the cause of th
e scintigraphic abnormalities. Electrocardiographic surface mapping ha
s been documented to be more accurate than standard 12-lead ECG in the
detection of provoked ischaemia. Thus, to investigate the relationshi
p between ECG changes and perfusion abnormalities, body surface maps w
ere recorded during dipyridamole infusion in 55 subjects (11 normals a
nd 44 patients with ischaemic heart disease) undergoing dipyridamole t
echnetium-99m sestamibi single-photon emission tomography (SPET). All
had a normal resting ECG. The extent and severity of the sestamibi def
ect were quantified. New negative areas in the isointegral maps and re
st-dipyridamole map differences >2 SD from normal limits were consider
ed abnormal. After dipyridamole in normals, neither perfusion defects
nor greater than or equal to 1 mm ST segment depression on 12-lead ECG
nor new negative areas in isointegral maps occurred. In patients, dip
yridamole induced new perfusion defects in 35 (80%) but ST segment dep
ression in only 18 (41%, P<0.001). Of the 35 patients with perfusion d
efects, 17 (49%, group 1) showed ST segment depression, while the othe
r 18 (51%, group 2) did not. Abnormal body surface maps were found in
100% of group 1 and 88% of group 2 patients (NS). In group 1, the prov
oked hypoperfusion was of greater extent (P=0.007) and severity (P=0.0
1) and the onset of map abnormalities was significantly earlier (P<0.0
01) than in group 2; time to map abnormalities was also significantly
shorter than time to ST segment depression (P=0.01). In the 35 patient
s with complete scintigraphic, body map and angiographic data, the sev
erity of reversible perfusion defect proved to be the strongest correl
ate of ST segment depression upon logistic regression analysis. Thus,
sestamibi SPET abnormalities after dipyridamole are almost always asso
ciated with electrical changes on body surface maps, suggesting myocar
dial ischaemia as their cause. The much less common 12-lead ECG change
s sire slower to appear and reflect a more severe hypoperfusion.