A little less than a century ago, in their classical work, Tennant and Wiggers 1 observed in open-chest dogs that within 60 seconds of coronary occlusion myocardial contractions in the ischemic zone change from active shortening to passive systolic lengthening. After restoration of myocardial blood flow, contractile dysfunction was reversed. In later animal work, Heyndrickx and colleagues 2 demonstrated that while regional electrocardiograms normalize within seconds, contractile dysfunction lasts for up to 2 hours after a 5-minute occlusion and for up to 24 hours after a 15-minute occlusion. The functional effects in the ischemic myocardium were shown to persist longer than one could have been predicted by the rapid normalization of coronary flow. The concept of myocardial stunning was born-and defined as a state of prolonged contractile dysfunction of post-ischemic myocardium in which myocardial function is gradually restored over time.Post-ischemic stunning can be quantified on single photon emission computed tomography (SPECT)-myocardial perfusion imaging (MPI) from regional wall motion abnormalities or more globally as a reduction in left ventricular ejection fraction (LVEF).Another marker for myocardial stunning is the increase in LV volumes after stress, namely transient ischemic dilatation (TID) that is considered indicative of severe and extensive coronary artery disease and a poor prognostic sign.3,4 These parameters have been investigated by a staggering number of studies and their added diagnostic and prognostic value is undisputed.
5-8Reliable assessment and quantification of myocardial stunning by SPECT-MPI pose however a series of challenges on the applied imaging protocols. First, the timing of the image acquisition is key. The time elapsed between stress testing and image acquisition determines the severity of post-stress LVEF decrease. Further, if the delay between stress and rest image acquisition is too short to allow for recovery of myocardial contractility, the post-stress EF decrease may be underestimated.10 Second, the type of stress agent may influence the severity of stress. Although the initial investigations on TID were performed by physical stress, 4 more recent studies have confirmed these results by vasodilator stress.7 Last but not least, measurement of LVEF and LV volumes might be limited by SPECT-MPI given its spatial resolution. The pathophysiological mechanism of these phenomena is also a highly debated subject. Some authors see it as true increase in LV volume due to post-ischemic stunning and offer several potential mechanisms for the increased contractility (i.e., enhanced venous return via Frank-Starling, increased myocardial blood flow via Gregg mechanism and/or by higher heart rate). 11,12 Others explain it by a stress-induced subendocardial hypoperfusion giving the visual impression of dilatation on ungated SPECT. 13,14 Nonetheless, the severity of post-ischemic stunning differs between the different stress agents: it seems that myocardial dysfunction persists much longe...