Spontaneous Coronary Artery Dissection: A Distinct Disease Repeatedly Managed as an Atherosclerotic One

Abstract

Spontaneous coronary artery dissection (SCAD) causes up to 4% of all acute coronary syndromes overall and as much as a
third of myocardial infarctions in women under 50, yet it is mechanistically unrelated to atherosclerosis: an epicardial
coronary artery tears or forms an intramural haematoma without any underlying plaque. Roughly 70% of cases lack the
angiographic hallmarks that make the disease easy to recognise, and case reports describe patients nearly discharged with a
panic-attack diagnosis before troponin results revealed infarction. Once recognised, SCAD is usually managed conservatively
-- roughly 86% of cases in a recent cohort, with only 2.3% of those needing subsequent invasive treatment -- because
percutaneous intervention on a dissected, non-atherosclerotic artery carries its own procedural risk. Fibromuscular
dysplasia, a systemic arteriopathy, co-occurs in a substantial but highly inconsistently reported fraction of SCAD patients
across studies (21.8% to 86%), and short-term outcomes look favourable relative to conventional acute coronary syndrome,
while three-year major adverse cardiac event rates and recurrence remain a real, if variably estimated, ongoing risk. This
review sets out that evidence and closes with a complication distinct from the diagnostic one that opens it: SCAD survivors,
overwhelmingly young and previously healthy women, show psychological symptom burden estimates that differ three- to
four-fold between studies, and no standardised post-SCAD psychological screening pathway yet exists in routine cardiology
follow-up.