ECG-manifest and ECG-silent dipyridamole technetium-99m sestamibi SPET perfusion defects in patients with ischaemic
M Galli1, C Marcassa, E Bosimini
1Cardiology Division, "Salvatore Maugeri" Foundation IRCCS, Veruno (No), Italy.
Insights
Body surface mapping detects myocardial ischemia during dipyridamole stress tests more effectively than standard ECG. These electrical changes correlate with perfusion defects, indicating ischemia, while ECG changes appear later and signify more severe hypoperfusion.
Area of Science:
- Cardiology
- Nuclear Medicine
- Diagnostic Imaging
Background:
- Dipyridamole myocardial scintigraphy often shows perfusion defects without significant ECG changes.
- This discrepancy suggests heterogeneity in myocardial blood flow rather than true ischemia.
- Electrocardiographic surface mapping (BSM) is more sensitive than standard 12-lead ECG for detecting provoked ischemia.
Purpose of the Study:
- To investigate the relationship between ECG changes and perfusion abnormalities during dipyridamole infusion.
- To compare the diagnostic accuracy of BSM with standard ECG in identifying ischemia.
Main Methods:
- 55 subjects (11 normal, 44 ischemic heart disease) underwent dipyridamole technetium-99m sestamibi SPET with simultaneous BSM.
- Perfusion defects and BSM abnormalities were quantified and compared to 12-lead ECG changes.
- Logistic regression analyzed correlations between perfusion defect severity and ECG changes.
Main Results:
- Dipyridamole induced perfusion defects in 80% of patients, but ST depression in only 41%.
- Abnormal BSMs were detected in 100% of patients with ECG changes and 88% without.
- BSM abnormalities appeared earlier and correlated with less severe perfusion defects than ST depression.
Conclusions:
- Sestamibi SPET abnormalities after dipyridamole are consistently linked to electrical changes on BSM, indicating myocardial ischemia.
- BSM is a more sensitive tool for detecting dipyridamole-induced ischemia than standard 12-lead ECG.
- Delayed and less frequent ECG changes reflect more severe myocardial hypoperfusion.
Abstract:
At dipyridamole myocardial scintigraphy, perfusion defects are seldom backed up by significant ECG changes. This would suggest myocardial blood flow heterogeneity, rather than true ischaemia, as the cause of the scintigraphic abnormalities. Electrocardiographic surface mapping has been documented to be more accurate than standard 12-lead ECG in the detection of provoked ischaemia. Thus, to investigate the relationship between ECG changes and perfusion abnormalities, body surface maps were recorded during dipyridamole infusion in 55 subjects (11 normals and 44 patients with ischaemic heart disease) undergoing dipyridamole technetium-99m sestamibi single-photon emission tomography (SPET). All had a normal resting ECG. The extent and severity of the sestamibi defect were quantified. New negative areas in the isointegral maps and rest-dipyridamole map differences >2 SD from normal limits were considered abnormal. After dipyridamole in normals, neither perfusion defects nor >/=1 mm ST segment depression on 12-lead ECG nor new negative areas in isointegral maps occurred. In patients, dipyridamole induced new perfusion defects in 35 (80%) but ST segment depression in only 18 (41%, P<0.001). Of the 35 patients with perfusion defects, 17 (49%, group 1) showed ST segment depression, while the other 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 provoked hypoperfusion was of greater extent (P=0.007) and severity (P=0.01) and the onset of map abnormalities was significantly earlier (P<0. 001) than in group 2; time to map abnormalities was also significantly shorter than time to ST segment depression (P=0.01). In the 35 patients with complete scintigraphic, body map and angiographic data, the severity of reversible perfusion defect proved to be the strongest correlate of ST segment depression upon logistic regression analysis. Thus, sestamibi SPET abnormalities after dipyridamole are almost always associated with electrical changes on body surface maps, suggesting myocardial ischaemia as their cause. The much less common 12-lead ECG changes are slower to appear and reflect a more severe hypoperfusion.
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