Thanks to Dr. Madias [ ] for his valuable and encouraging comments on the case of a 76-years-old woman who presented with acute coronary syndrome (ACS) with severe 3-vessel disease triggering post-ischemic myocardial stunning (PIMS) with features typical for that of mid-apical takotsubo syndrome (TS) recently published in Cardiovascular Revascularization Medicine [ ]. During the last years, the concept of coexistence of ACS and TS is also accepted by other researchers in the field of TS [ , ]. In this context, I would like to remind that the two most important features of TS, which are the myocardial stunning extending beyond the coronary artery supply territory and the histo-pathological feature of contraction band necrosis (coagulative myocytolysis) also extending beyond the coronary artery supply territory, were first described in patients presenting with ACS [ , ]. ACS is an extreme physical stressor and is probably one of the common trigger factors for TS. The association of ACS and TS may, with justifiable reasons, explain the increased mortality in women suffering ACS during the first days of presentation [ ]. The myocardial stunning in the above-mentioned case presentation caused reversible systo-diastolic compression of a segment of the left anterior descending artery (LAD) with myocardial bridging during the acute and sub-acute stages of the disease. In addition to the other evidences mentioned in the case presentation, the most convincing proof for the notion that the myocardial stunning in TS is in a “cramp state” is the histo-pathological findings of hyper-contracted sarcomeres. This myocardial cramp may compress the coronary artery segments with myocardial bridging as in the case mentioned above. Cato et al. reported a case of mid-ventricular TS with septal occlusion causing myocardial infarction in the corresponding territory. It will be insightful to believe that the myocardial stunning was compressing the septal branch in that case. Follow up coronary angiography in such a case will be invaluable to reveal the recovery of the septal branch patency during the resolution of the left ventricular dysfunction. Recently, Sabra et al. [ ] reported on a case of focal anterior mid-ventricular TS confirmed by cardiac magnetic resonance (CMR) imaging where there was myocardial edema but no delayed gadolinium enhancement in the hypo-/akinetic segments; however, myocardial perfusion scintigraphy revealed reduced to absent perfusion in the “anterior and antero-septal segments”. Myocardial edema may have contributed in compressing the micro-vascular circulation causing perfusion defects but not severe enough to cause myocardial infarction. Myocardial edema, as suggested by Dr. Madias [ ], may also have contributed in compression of larger coronary arteries with myocardial bridging or septal branches in addition to myocardial muscle cramp. Under physiological conditions, there may be only systolic compression of the coronary arteries with myocardial bridging. However, with continual myocardial cramp, there may be systo-diastolic compression of the coronary segments with myocardial bridging. I believe that the myocardial cramp, which results in hypo-/akinesis and continues for minute, hours, days, or weeks, is a pathological condition and not a functional process even if it recovers after minutes or hours. TS is most probably a broad continuum of clinical manifestation ranging from mild disease with only neurogenic (sympathetic)-induced myocardial cramp recovering within minutes or hours to more severe disease with cardiac sympathetic disruption and norepinephrine spillover inducing chemical myocarditis [ ] with myocardial edema, which may take days or weeks to recover. However, the slingshot-like hyper-contractility of the apical segments in apical sparing patterns of TS and the valve-like motion of the basal segments in mid-apical or midventricular patterns of TS may be functional. Consequently, in the myocardial “muscle cramp”, the myocardium is in a pathological cramp state during both systole and diastole and causes myocardial hypo-/akinesia continuing for a varying periods of time depending on the severity of the disease.