ECG-MANIFEST AND ECG-SILENT DIPYRIDAMOLE TC-99M SESTAMIBI SPET PERFUSION DEFECTS IN PATIENTS WITH ISCHEMIC-HEART-DISEASE

Citation
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
Citations number
29
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging
ISSN journal
03406997
Volume
24
Issue
2
Year of publication
1997
Pages
160 - 169
Database
ISI
SICI code
0340-6997(1997)24:2<160:EAEDTS>2.0.ZU;2-P
Abstract
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.