A 66-year-old woman with hypertension, hyperlipidaemia, migraines, and no known CAD presented to the Emergency Department (ED) with chest pain. She awoke from sleep on the day of presentation with headache and pain in her left jaw that evolved to central chest pressure with left arm numbness. She denied associated nausea or diaphoresis and had never experienced these symptoms. She lived alone in a two-story home, and while she was usually independent in her activities of daily living, on the morning of symptom onset even ambulation of stairs resulted in complete exhaustion. The patient was proud of her self-care and boasted intake of daily vitamins, a strict organic diet, and minimal stress in her daily life as a retired public school teacher; she had never smoked. She denied recent respiratory infections and had not travelled in the past year. Her family history was negative for premature cardiovascular disease. Despite a trial of her aspirin analogue, White Willow, persistent symptoms led her to present to the ED. Initial evaluation revealed an anxious woman with stable vital signs (temperature 97°F, heart rate 90 b.p.m., blood pressure 133/81 mmHg, respiratory rate 18/min with an oxygen saturation of 98% on ambient air). Physical examination was unremarkable. Cardiovascular exam revealed a regular rate and rhythm with clear S1 and S2 and no murmurs or gallops. Lungs were clear to auscultation and lower extremities were warm without oedema. Labs were notable for a normal D-dimer 394 ng/mL (<500) and a Troponin-T elevation to 0.33 ng/mL (<0.01). ECG revealed normal sinus rhythm with 1 mm anterior ST-segment elevations in V1, V2, and aVR. Initial treatment in the ED included 325 mg of Aspirin, 80 mg of Atorvastatin, two doses of 0.4 mg of sublingual nitroglycerine, and an unfractionated heparin drip. Nitroglycerine allowed for complete resolution of chest pain but given persistent ECG changes and troponin elevation, P2Y12 inhibition was deferred with management focused on urgent transfer to the cardiac catheterization lab. Angiogram revealed only minimal luminal irregularities though coronary arteries were noted to be tortuous (see, Video S1A and B). Takotsubo cardiomyopathy was then considered for which ventriculography was attempted. During catheter insertion, however, the patient sustained transient ventricular fibrillation requiring defibrillation after which further invasive diagnostic imaging was deferred. To further guide diagnosis, a TTE was obtained. TTE revealed impaired systolic function (ejection fraction of 41%) and regional wall motion abnormalities at the mid anteroseptum, mid inferoseptum, and apical septum but basal wall motion was preserved (see, Video S2). While Takotsubo seemed most likely given the apical wall motion abnormalities with basal sparing and lack of obstructive CAD on angiography, several features remained atypical: (i) history revealed no antecedent stressor, (ii) angiogram revealed coronary tortuosity, (iii) apical wall motion abnormalities on TTE were asymmetric, and (iv) chest pain was not only recrudescent but nitrate-responsive. These features raised suspicion for SCAD not evident on luminal assessment by coronary angiography. A CCTA was then obtained. CCTA not only confirmed absence of calcified coronary artery plaques but additionally noted abrupt caliber changes in the left anterior descending artery (LAD) and its septal branches consistent with SCAD. The patient was started on low dose beta blockade (Metoprolol 50 mg daily) and continued on a low dose Aspirin (81 mg daily). Given her untreated hyperlipidaemia (total cholesterol 296 mg/dL, LDL cholesterol 192 mg/dL), she was additionally discharged on a high dose statin (Atorvastatin 80 mg daily). At 1 month follow-up after discharge, a repeat TTE revealed improvement in her ejection fraction to 78% but with persistent anteroseptal dyskinesis. A repeat CCTA is planned. The patient subsequently completed cardiac rehabilitation and has not had additional medical events.