593 Spontaneous coronary artery dissection in young

Abstract Aims We present the case of a 25 years-old patient, presented to the Emergency Department for chest pain and epigastralgia complicated by vomiting. Symptoms started about 30 h before, afterwards an effort. The patient did not have any known cardiovascular risk factors (except for sporadic consumption of cannabis) and family medical history was negative for premature cardiovascular disease or sudden cardiac death. His past medical history was unremarkable. Methods and results Clinical examination was normal. ECG was suggestive for subacute anterior ST-elevation myocardial infarction (QS in V1–V4 leads with ST segment elevation and biphasic T-waves in V4–V6) and was accompanied by significant elevation of myocardial necrosis biomarkers (hsTnT 3416 ng/l, n.v. <15). Echocardiography revealed a severely reduced left ventricular ejection fraction (LVEF = 30%) with regional wall motion abnormalities (apical and septal akinesia, and anterior mid-ventricular segment hypokinesia). Coronary angiography was suggestive for a dissection of the proximal-to-mid left anterior descending artery. Dissection flap, subocclusion of the first septal branch, and intramural thrombosis were noted. Direct stenting with drug-eluting stent was successful, with thrombolysis in myocardial infarction (TIMI) flow grade 3. The patient was started on dual antiplatelet treatment (aspirin and ticagrelor), ACE-inhibitors, beta blockers, and spironolactone. Further testing ruled out other conditions that may be associated with spontaneous coronary artery dissection (autoimmune diseases, including vasculitis, connective tissue disease, coagulative disorders). The clinical course was complicated by pericarditis and the development of LV apical thrombus. So, patient was started on anticoagulation (warfarin) with subsequently downgrading from ticagrelor to clopidogrel. Echocardiographic follow-up documented a progressive improvement of LVEF (50%), and global longitudinal strain (GLS −15%) with persistence of wall motion abnormalities in the apical and septal segments. Partial resolution of intracavitary thrombi was documented. CMR revealed LV apical aneurysm. Moreover, the use of dedicated sequences showed transmural late gadolinium enhancement in akinetic segments, and fatty metaplasia of the apical portion of the anterior wall and anterior septal wall. Finally, early gadolinium enhancement imaging, confirmed the persistence of LV stratified apical thrombus. Conclusions Spontaneous coronary artery dissection (SCAD) is an underdiagnosed and frequent cause of acute coronary syndrome (ACS) in young-to-middle aged patients, particularly women; therefore, even in young people, a chest pain episode suggestive for an ischaemic cause should never be underestimated. Cardiac magnetic resonance is the most accurate method to evaluate the sequelae of myocardial infarction (including LV size and function, presence of fatty metaplasia, extent and transmurality of ischaemic scar, presence of thrombi), to aid in differential diagnosis and to define prognosis and guide the therapeutic management.