Patients with a normal findings on gated SPECT scans have a low event rate and low mortality.1–5 A gated SPECT scan is a perfusion study and only detects major obstructions causing a significant reduction in coronary flow. In the setting of nonobstructive coronary artery disease, gated SPECT scan findings should be normal. On the other hand, most acute ST-elevation myocardial infarctions occur in the setting of nonobstructive plaque rupture of the coronary artery, evading detection by gated perfusion studies.6–8 The question remains, why, after a normal finding on a gated SPECT scan, is the event rate too low, despite the fact that a gated SPECT scan should, 100% of the time, not be able to detect nonobstructive coronary plaque, which is a major cause of acute ST-elevation myocardial infarction? There is no adequate explanation for this paradox in the literature. This is the first case report describing this dilemma, and the fact that gated a SPECT scan failed to detect an imminent nonobstructive plaque rupture causing acute myocardial infarction. There are many imaging modalities for detection of vulnerable plaque that are being tested in animal and clinical trials; however, none of these modalities have met the requirements of the ideal diagnostic method. Although ultrasound,9computed tomography scan,10–11 and MRI12can identify the atherosclerotic plaque composition, they cannot image inflammation, which is a key component of vulnerable plaque. On the other hand, 18F-fluorodeoxyglucose positron emission tomography scans can identify the metabolic activity of macrophages and other hypermetabolic cells in lesions with inflammation.15 Other markers, such as 99mTc-labeled annexin V, which is a marker of apoptosis, have also been studied.17 At this point, there are no sufficient data available for the clinical usage of these tracers. Furthermore, it is not unusual to detect in the same patient multiple vulnerable plaques simultaneously in different locations,18–19 and there is no accurate way to predict the timing and location of a future plaque rupture.20However, aggressive therapy with lipid-lowering medications has been shown21–24 to cause the regression of atherosclerosis, to improve endothelial dysfunction, and to reduce the number of coronary events. Therefore, the early detection of nonobstructive plaque, particularly vulnerable plaque, could lead to early aggressive treatment and the prevention of atherosclerosis-related morbidity and mortality.