UNLABELLED
Gated SPECT using Tc-99m-labeled flow tracers provides simultaneous assessment of global and regional myocardial perfusion and function. The aim of this study was to evaluate whether regional wall thickening (WT) obtained after stress and at rest makes it possible to identify and analyze a subgroup of post-ischemic stunned patients.
METHODS
We studied 20 patients (18 males) who underwent conventional diagnostic dual-day stress/rest Gated SPECT following injection of 925 MBq of 99mTc-tetrofosmin using a dual-head SPECT camera (Vertex ADAC). The mean age of these patients was 59 years (38-71) and 10 of them had a history of previous acute myocardial infarction (AMI). Perfusion was analyzed on ungated images using 20 segments scored on a 5-point scale (0 = normal, 4 = no uptake), while WT and motion were assessed visually on stress/rest end-systolic images using a 4-point score (0 = normal, 3 = absence of WT/motion). Left ventricular ejection fraction (LVEF) and volumes were calculated. All patients underwent coronary angiography.
RESULTS
All patients showed at least one reversible defect with post-stress WT reduction and normal rest WT. The stunned group showed a significant post-stress reduction of LVEF and a statistically non-significant increase of end systolic volume (ESV). A good correlation was observed between global perfusion and WT score both at stress and rest conditions; LVEF showed a significant inverse correlation with global post-stress and rest perfusion and WT score. ESV and the global perfusion stress/rest score showed a good correlation, while end-diastolic volume did not correlate. In 44% of the segments with fixed defects, there was a normal WT and normal coronary-related vessel (false positives); 28% of reversible segments showed a post-stress pathological WT and five of them a rest pathological WT.
CONCLUSIONS
The gated SPECT myocardial perfusion evaluation allowed us to analyze a subgroup of post-stress stunned coronary artery disease patients. The post-stress LVEF reduction in this population seems to be due to the increase of end-systolic volume caused by endocardial ischemia. The stunned segments showed severe perfusion defects.