Spontaneous coronary artery dissection
- Pamela S Douglas, MD
Pamela S Douglas, MD
- Ursula Geller Professor of Research in Cardiovascular Diseases
- Duke University Medical Center
- Jacqueline Saw, MD, FRCPC, FACC
Jacqueline Saw, MD, FRCPC, FACC
- Clinical Professor
- University of British Columbia
- Vancouver General Hospital
- Section Editors
- Juan Carlos Kaski, DSc, MD, DM (Hons), FRCP, FESC, FACC, FAHA
Juan Carlos Kaski, DSc, MD, DM (Hons), FRCP, FESC, FACC, FAHA
- Section Editor — Coronary Heart Disease
- Professor of Cardiovascular Science
- Director, Cardiovascular and Cell Sciences Research Institute
- St. George's, University of London
- Patricia A Pellikka, MD, FACC, FAHA, FASE
Patricia A Pellikka, MD, FACC, FAHA, FASE
- Section Editor — Noninvasive Cardiac Imaging and Stress Testing
- Professor of Medicine
- Mayo Clinic College of Medicine
Spontaneous coronary artery dissection (SCAD) is a non-traumatic and non-iatrogenic separation of the coronary arterial wall and is a rare cause of acute myocardial infarction. It is more common in younger patients and in women. This topic will focus on non-atherosclerotic SCAD. Other aspects of coronary heart disease in women are discussed separately. (See "Clinical features and diagnosis of coronary heart disease in women".)
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 . Both result in creation of a false lumen filled with intramural hematoma . 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 . 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 . (See "Acquired heart disease and pregnancy", section on 'Myocardial infarction'.)
Intramural hematoma involving the outer two-thirds of the media is common. Histologically, an inflammatory reaction (eg, eosinophilic infiltrates) in the adventitia has been described, suggestive of periarteritis that may breakdown the medial-adventitial layer predisposing the artery to dissection. However, this inflammatory response may be reactive rather than causative .
One retrospective study has proposed that coronary artery tortuosity may be a marker for or a potential mechanism for SCAD . In this study, the coronary angiograms of 246 patients with SCAD were compared with 313 controls. Tortuosity, as defined by the presence of ≥3 consecutive curvatures of 90 to 180 degrees measured at end-diastole in a major epicardial coronary artery ≥2 mm in diameter, was found in 78 and 17 percent, respectively. However, the presence of coronary tortuosity was also associated with extracoronary vasculopathy (eg, fibromuscular dysplasia) [9,10]; as such, it is more likely that the tortuosity, similar to dissection, is a manifestation of the underlying predisposing vasculopathy.
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