A 46-year-old woman without a history of cardiovascular disease and no coronary risk factor was urgently admitted to our hospital with rest crushing chest pain, which had started 3 hours before. The ECG demonstrated minimal anterior STsegment elevation in leads V 1 to V 4 (Figure 1). In the first sample cardiac troponin T was 0.08 ng/mL. Coronary angiography was urgently performed and demonstrated a 50% smooth stenosis in the proximal left anterior descending (LAD) coronary (Figure 2) with a faint dye staining just proximal to the first diagonal branch. Because initial differential diagnosis included variant angina, intracoronary ergonovine (32 g) was given. Diffuse LAD coronary vasoconstriction, more severe on the LAD coronary ostium, was seen. Because there was still no clear indication of a culprit lesion, intravascular ultrasound (IVUS) examination was performed, which surprisingly showed an intramural hematoma starting from the mid-LAD up to its ostium, with mild lumen compromise, and the presence of nonobstructive atheroma (Figure 2). Echo-free material, consistent with contrast medium or saline, was seen mixing with echogenic blood within the hematoma (Figure 3), indirectly indicating that the hematoma was the result of a spontaneous coronary dissection (SCAD), with an occult entry flap. Stenting was considered, but because of the stable hemodynamic condition, medical management with aspirin, clopidrogel, nitrates, and -blockers was chosen. After 12 hours, repeat ECG demonstrated deep, negative T waves in the anterior leads. (Figure 1). The cardiac troponin T peak was 0.2 ng/dL at 24 hours. Angiography and IVUS were repeated at 48 hours and showed persisting intramural hematoma, although with reduced lumen compression (Figure 4). Because of the absence of what we considered to be "high-risk" IVUS features, the patient was discharged home on medical therapy. At 3 months, IVUS control showed an almost complete disappearance of intramural hematoma, and echocardiography was normal ( Figure 5). Oneyear clinical follow-up was uneventful.SCAD is an uncommon cause of acute coronary syndrome and sudden death. 1 Its etiology and pathogenesis have not been fully elucidated, and prognosis and treatment are not clearly defined. Connective tissue disease, immune system alterations, pregnancy, oral contraceptive use, intense physical activity, and illicit drug consumption are known to be involved in SCAD etiology, 1 and yet in a relevant percentage of SCAD, as in our case, none of these conditions is overtly present.The initial presentation is frequently an acute coronary syndrome, and SCAD should be taken into consideration in patients without known cardiovascular risk factors presenting with acute coronary syndrome. 1 Because there is lack of consensus concerning SCAD treatment, management decisions are generally made on a case-by-case basis, integrating the clinical scenario with angiographic assessment of dissection location and the extent and degree of flow compromise. 1 Treatment options include medical therapy, ...