Sandbox: SCAD

Spontaneous coronary artery dissection

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Arzu Kalayci, M.D. [2]

Synonyms and keywords: SCAD

Overview

Spontaneous coronary artery dissection (SCAD) is becoming recognised as an important cause of myocardial infarction (MI) particularly among young women.

Spontaneous coronary artery dissection (SCAD) is an infrequent cause of coronary artery disease. Whilst a recognized disease entity since 1930s, its pathogenesis remains unclear and various hypotheses have been postulated from clinical and clinic-pathological association. Whilst angiography alone has traditionally been perceived to significantly under diagnose this condition, recent development in intravascular imaging, particularly optical coherence tomography (OCT), have seen significant advances in the understanding of SCAD. From a histopathological perspective, OCT has shown that there may be distinct pathological subsets in SCAD in reference to a dissection flap and an intramural hematoma. Early data also suggests that OCT may be important in optimizing PCI results in SCAD. The future is particularly promising if a collaborative approach is undertaken to utilize OCT as an in vivo microscope to shed more light in this poorly understood disease entity.

PATHOLOGY AND PATHOPHYSIOLOGY

The underlying mechanism of non-atherosclerotic spontaneous coronary artery dissection (NA-SCAD) is not fully understood, but an intimal tear or bleeding of vasa vasorum with intramedial hemorrhage has been proposed [1]. Both result in creation of a false lumen filled with intramural hematoma [2]. Pressure-driven expansion of the false lumen by an enlarging hematoma may lead to luminal encroachment and subsequent myocardial ischemia and infarction. Atherosclerotic SCAD is a mechanistically distinct variant of SCAD and is typically limited in extent by medial atrophy and scarring [3]. NA-SCAD, on the other hand, can result in extensive dissection lengths, especially in the presence of arterial fragility from predisposing arteriopathies, and intracoronary imaging studies clearly show the absence of atherosclerosis in these cases [4,5].

In pregnant or early postpartum women, dissection may be a consequence of increased physiological hemodynamic stresses or from hormonal effects weakening the coronary arterial wall [6,7]. The exposure to recurrent and chronic hormonal pregnancy changes can further increase SCAD risks in women with multiple previous births (multiparity), and dissection in all arterial beds are more common during pregnancy [7].

Although intimal tear or bleeding of vasa vasorum with intramedial hemorrhage seems to be most probable reason, the underlying mechanism of non-atherosclerotic spontaneous coronary artery dissection (NA-SCAD) is still unknown [1]. Consequently intramural hematoma creates a false lumen [2]. Progressive expansion of the false lumen may cause subsequent myocardial ischemia and infarction.

In pregnancy or early postpartum period, dissection may be occur because of the physiological responses to the increased hemodynamic stresses and having more fragile coronary arterial wall due to the hormonal effects.