Abstract Male, 59 years old with no significant pathological history or cardiovascular risk factors. Access to the ER ( 12.30 AM ) with infero–lateral STEMI (Killip I, 2 hours of symptom onset; haemodynamic and electrical stability): chest pain associated with profuse sweating and transient arterial hypotension, ST elevation in V3–V6 and inferior leads on the ECG and apical hypokinesia with slight reduction of LVEF (50%) on the Trans–Thoracic Echocardiography. Urgent coronary angiography: non–obstructive coronary arteries stenosis, short intramyocardial tract of DA with moderate systolic compression with ‘milking effect‘. Blood sampling: mild elevation of cardiac troponin hs value (479 pg / ml), mild anemia and thrombocytopenia; normal value of markes of liver and kidney function. Hospitalization in Cardiac ICU with standard antithrombotic and anti–ischemic therapy. 12 hours after admission (01.00 PM) acute low–flow heart failure with pulmonary edema treated with inotropic agent and need of endotracheal intubation and ventilatory support (ineffective attempt of NIV); ECG unchanged from the previous one and appearance of LVEF 25% for akinesia of septum, apex and lateral wall. Peak of troponin 2083 pg / ml III day: effective extubation with successive cycles of NIV and weaning from noradrenaline. Progressive recovery of LVEF with appearance of SAM with LVOT dynamic obstruction (v max> 4m / s at pulsed doppler) and moderate mitral regurgitation: stop inotropic agent and start beta–blocker therapy (atenolol) not tolerated for hypokinetic arrhythmias (also total BAV) and then successful replaced in the following days with low doses of bisoprolol. Post–Iintubation pneumonia treated with antibiotic therapy. X day: hemodynamic and electrical stability, disappearance of the SAM with complete recovery of the left ventricle contractile function, mild mitral regurgitation(minimal valve prolapse) Cardiac MRI: normal LVEF, absence of myocardial LGE with the exception of small areas of the papillary muscles due to traction of the mitral flaps. In the patient‘s medical history: stressful last months related to smart working and family problems; absence of a specific identifiable trigger. Conclusions Stress cardiomyopathy in man patient complicated by progressive acute heart failure and SAM with rapid restitutio ad integrum. Presence of DA myocardial bridge with absence of myocardial LGE on MRI.