Abstract
Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic cause of acute coronary syndrome, characterized by the development of a false lumen within the coronary arterial wall, leading to narrowing or complete occlusion of the true lumen. This underrecognized condition accounts for a substantial proportion of sudden cardiac death (SCD), particularly among young, otherwise healthy women. Macroscopically, SCAD is defined by intramural hematoma and focal thickening of the arterial wall, while histological examination demonstrates separation of the tunica media, elastic fiber degeneration, and variable inflammatory infiltrates. Proposed pathogenic mechanisms include primary intimal tear and primary intramural hematoma, frequently associated with predisposing conditions such as fibromuscular dysplasia, connective tissue disorders, and specific hormonal states. In cases of myocardial infarction, the myocardium exhibits acute ischemic necrosis and early hypoperfusion injury. Postmortem diagnosis requires meticulous coronary dissection, adjunctive histochemical and immunohistochemical staining, and, when indicated, molecular autopsy (MA). The purpose of this review is to provide an updated synthesis of current knowledge on SCAD as a cause of SCD, integrating pathogenetic, morphological, and genetic perspectives, and to emphasize the role of MA as both a diagnostic and preventive tool.