The data on the 161 patients with takotsubo syndrome (TTS), by Stiermaier et al published ahead of print in the journal on July 30, 2014, have put to rest the issue of “bridging” of the left anterior descending coronary artery (LAD) as a plausible pathophysiologic mechanism for TTS. However, the LAD “wraparound” issue remains alive although one wonders why half of the authors’ patients with TTS had such LAD morphologic feature and half did not (55.6% vs 44.4%). It is not clear whether the reported information about left ventricular (LV) wall motion abnormalities and the LV ejection fraction were derived from contrast ventriculography or echocardiography; but if the former is the case, the authors have the opportunity to correlate the extent of the LV wall motion abnormalities (by superimposing LV end-diastolic and LV end-systolic angiographic frames and measuring the circumferential percentages of akinesia and/or dyskinesia) and the reduction of LV ejection fraction in the subgroups with and without LAD “wraparound” features. Perhaps, LAD “wraparound” appearance may not be related to the cause of TTS (primary role) but to the LV extent of dysfunction (secondary role).