There are many diagnostic and prognostic elements arising from myocardial perfusion imaging studies. The equipment improvements have reduced acquisition time while enhancing quality imaging. In line with technological developments, a greater understanding of coronary pathophysiology, especially microcirculation, has allowed the clinical cardiologist to understand coronary artery disease (CAD). In the past, many cases had no physiopathology correlation with the clinical setting, for example, angina with normal coronary arteries. Nowadays, we have a more clear view of such findings.From the very beginning, ventricular dilatation (VD) during stress has proven to be associated with adverse outcomes, considering secondary to extensive ischemia.The prognostic value of VD has been associated with the presence of severe and extensive coronary disease since Chouraqui et al. 1 and Weiss et al. 2 publications 30 years ago.Exploring further, Mazzanti et al. 3 correlated the ischemia severity with VD using cinecoronariography as the gold standard. They showed a 71 and 95% of sensibility and specificity, respectively, by semiquantitative analysis.Ventricular dilatation without ischemia and normal myocardial perfusion imaging (MPI) have a less clear clinical and prognostic value. Gated SPECT (gSPECT) imaging relies on detection of endocardial edge for measurements of left ventricle (LV) volumes and transient ischemic dilatation (TID) ratio. The TID threshold depends on the radioisotope used, stress methods, proper algorithm, the avoidance of artifact motion, incorrect slice alignment, and the clinical setting of the population studied. Different cutoffs have been validated for different radioisotope and stress protocols (Table 1). 4 There are two possible interpretations related to VD in the gSPECT. The classic understanding is that there is extensive subendocardial ischemia generating stunning. The second interpretation, which is more frequently seen with pharmacological stress than exercise, is that adenosine induces subendocardial hypoperfusion. In patients with limited coronary flow reserve (CFR), adenosine produces vasodilatation in the vascular bed of both, the epicardial and endocardial vessels. As a consequence, there is an increasing flow from the subendocardium to the epicardium. This is different from ischemia in CAD. We called it ''vertical steal'' and it is a marker of impaired subendocardial CFR rather than a true myocardial stunning. The ''vertical steal'' explains the increasing frequency of TID in patients with diseases such as diabetes and hypertension and could go along with a change in left ventricular remodeling, more significant with adenosine than with exercise.Emmett et al. 5 studied TID on myocardial perfusion imaging with pharmacological stress. The author evaluated if TID was due to actual LV cavity dilation and ventricular stunning or to relative subendocardial hypoperfusion. He studied 31 patients undergoing