A 33-year-old Caucasian woman with no cardiovascular history was admitted to the gynecology department
due to a threat of preterm birth. During hospitalization, the patient experienced chest pain complicated by
ventricular fibrillation. Resuscitation maneuvers were performed, followed by an emergency cesarean
section with fetal extraction and DC shock, resulting in return of spontaneous circulation. Coronary
angiography revealed spontaneous dissection of the first marginal branch, treated with conservative
strategy. After 3 days, another episode of chest pain occurred with evidence of inferolateral STEMI.
Emergency coronary angiography showed severe stenosis in the proximal segment of the circumflex branch
and the mid-segment of the anterior descending branch;OCT confirmed spontaneous coronary dissection
(SCAD) in these vessels. A conservative strategy was adopted, with medical therapy including DAPT for a
year, ACE inhibitor and beta-blocker. After 1 month, a follow-up OCT of the coronary arteries showed
almost complete resolution of the previously observed dissections. 7 years later, the patient presented to
the emergency room with chest pain similar to the previous episode. A diagnosis of NSTEMI was made and
the patient was admitted to the cardiac intensive care unit. Coronary angiography revealed spontaneous
dissection of the right coronary artery causing occlusion in the mid-segment. Coronary angioplasty guided
by IVUS was performed with a drug-coated balloon achieving TIMI 3 flow. Given the patient ‘s medical
history and suspicion of fibromuscular dysplasia, further diagnostic evaluation was conducted with CT
angiography of the intracranial circulation, revealing double focal dissections in the both carotid arteries,
asymptomatic and without flow obstruction. The patient was discharged, prescribed SAPT and scheduled
for follow-up with coronary and intracranial circulation CT angiography. SCAD is defined as an epicardial
coronary artery dissection that is not associated with atherosclerosis. It commonly occurs in patients with
few traditional cardiovascular risk factors. Its cause is hypothesized to be multifactorial with contributions
from underlying arteriopathies, hormonal influences or systemic inflammatory diseases, often compounded
by environmental precipitants or stressors. The abstract emphasizes the challenges of diagnosis, limited
understanding of pathophysiology and the absence of well-defined guidelines regarding the treatment of
SCAD.
