Spontaneous Coronary Artery Dissection

Jacqueline Saw, MD, Division Cardiology, University of British Columbia

Spontaneous coronary artery dissection (SCAD) is an infrequent but important cause of myocardial infarction (MI), particularly in younger women. It is defined as a spontaneous non-traumatic and non-iatrogenic separation of the coronary arterial wall, creating a false lumen that may or may not be in continuity with the true lumen. Although the cause of SCAD may be atherosclerotic or non-atherosclerotic, contemporary usage of the term "SCAD" has focused on and is synonymous with the non-atherosclerotic variant, which has distinct pathophysiology, management, and outcomes from atherosclerotic coronary artery disease.
SCAD can result from an intimal-medial tear or from spontaneous intramural hemorrhage into the artery wall. Angiographically, it can manifest as multiple radiolucent lumen (type 1 appearance), diffuse smooth narrowing (type 2 appearance; mean length ~58mm), or focal/tubular stenosis (type 3 appearance; mimics atherosclerosis).1,2 Only <30% of SCAD have type 1 angiographic appearance of pathognomonic contrast staining of arterial wall with multiple lumen.3 Unfortunately, the type 2 and 3 angiographic SCAD variants are often poorly recognized and missed on coronary angiography. Thus, intracoronary imaging with optical coherence tomography (OCT) or intravascular ultrasound (IVUS) can play important roles in the diagnosis of non-type 1 angiographic SCAD, which requires the presence of intramural hematoma and/or separation of the intimal-medial membrane creating a double lumen.2
The etiology of SCAD is incompletely understood, but contemporary large series suggest that the majority of patients have underlying predisposing arteriopathy, such as fibromuscular dysplasia (FMD), connective tissue disorders, systemic inflammatory conditions, or pregnancy-related.3 Only <20% are considered idiopathic after vascular screening and detailed history. The strongest association with SCAD appears to be FMD. Since our discovery and publication of the first case series of concomitant SCAD and FMD in 2011,4 we and others had reported that extracoronary FMD was present in up to 70-80% of patients with SCAD.3-6 On the contrary, peripartum SCAD has a much lower reported frequency (<5 %) as a predisposing cause in contemporary series.7  Precipitating stressors may also trigger SCAD, especially inpatients with underlying predisposing arteriopathy. These stressors include intense emotional stress, physical activities, hormonal therapy, sympathomimetic drugs and intense Valsalva-like activities (e.g. vaginal delivery, coughing, retching, vomiting, bowel movement).3
The optimal management of SCAD remains controversial. There are no randomized trials that compared conservative therapy to revascularization. Standard medical therapies administered for acute coronary syndrome (ACS) have not been studied in the SCAD population. Thus, current recommendations on management are largely based on expert opinion. For medical management, aspirin and beta-blocker are typically administered long-term for secondary thrombotic prevention and reduction of arterial shear-stress, respectively. ACE inhibitor or ARB is administered for patients with left ventricular dysfunction; and statins for patients with underlying dyslipidemia.8
Most experts recommend conservative management as the first-line therapy, pursuing revascularization only in patients with ongoing or recurrent ischemia, hemodynamic instability, or left main dissection. Percutaneous coronary intervention can often be challenging and have suboptimal results, with reported procedural success of only 50–70%.3,9 Likewise, the results with coronary bypass surgery may also be suboptimal, with small case series reporting low long-term graft patency.10 Furthermore, the majority of dissected arteries heal spontaneously, obviating the need for revascularization unless patients are unstable.
The in-hospital and long-term outcomes of SCAD patients appear relatively good in contemporary prospective series. Most patients present with ACS with either non-ST elevation or ST-elevation MI, and a small proportion have ventricular arrhythmias. Acute in-hospital mortality was <5% in modern series, and recurrent MI or the need for revascularization in conservatively managed patients was 5–10%.3,10 However, following hospital discharge, a significant proportion of patients can have recurrent chest pains. Subacute major adverse cardiovascular events (MACE) were reported in 10–20% of patients at 2-year follow-up, with recurrent SCAD event of ~15%.3 Retrospective series with longer-term follow-up reported higher MACE rate of up to 50–60%.3,10 These findings emphasize the importance of close follow-up of SCAD survivors by cardiovascular specialists.
In summary, SCAD is an important cause and should be on the differential diagnosis for women presenting with MI. The diagnosis can be elusive on coronary angiography, and recognition of non-pathognomonic angiographic SCAD variants and selective use of intracoronary imaging are important to aid diagnosis. Conservative management is recommended unless patients are unstable. Recurrent events are frequent and SCAD survivors should be closely followed long-term. Further prospective studies should be pursued to further understand the natural history and management of this challenging condition.


Dr. Saw has received unrestricted research funding (from the Canadian Institutes of Health Research, University of British Columbia Division of Cardiology, AstraZeneca, Abbott Vascular, St Jude Medical, Boston Scientific, and Servier), speaker honoraria (AstraZeneca, St Jude Medical, Boston Scientific, Bayer and Sunovion), consultancy and advisory board honoraria (AstraZeneca, St Jude Medical, Boston Scientific, and Abbott Vascular), and proctorship honoraria (St Jude Medical and Boston Scientific).


  1. Saw J. Coronary angiogram classification of spontaneous coronary artery dissection. Catheter Cardiovasc Interv. 2014;84:1115-22. doi: 10.1002/ccd.25293.
  2. Saw J, Mancini GB, Humphries K et al. Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging. Catheter Cardiovasc Interv. 2015. [Epub ahead of print]. doi: 10.1002/ccd.26022.
  3. Saw J, Aymong E, Sedlak T et al. Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv. 2014;7:645-55. doi: 10.1161/CIRCINTERVENTIONS.114.001760.
  4. Saw J, Poulter R, Fung A, Wood D, Hamburger J, Buller CE. Spontaneous coronary artery dissection in patients with fibromuscular dysplasia. A case series. Circ Cardiovasc Interv. 2012;5:134-7. doi: 10.1161/CIRCINTERVENTIONS.111.966630.
  5. Saw J, Ricci D, Starovoytov A, Fox R, Buller CE. Spontaneous coronary artery dissection: prevalence of predisposing conditions including fibromuscular dysplasia in a tertiary center cohort. JACC Cardiovasc Interv. 2013;6:44-52. doi: 10.1016/j.jcin.2012.08.017.
  6. Prasad M, Tweet MS, Hayes SN et al. Prevalence of extracoronary vascular abnormalities and fibromuscular dysplasia in patients with spontaneous coronary artery dissection. Am J Cardiol. 2015;115:1672-7. doi: 10.1016/j.amjcard.2015.03.011.
  7. Vijayaraghavan R, Verma S, Gupta N, Saw J. Pregnancy-related spontaneous coronary artery dissection. Circulation. 2014;130:1915-20.  doi:  10.1161/CIRCULATIONAHA.114.011422.
  8. Saw J. Spontaneous coronary artery dissection. Can J Cardiol. 2013;29:1027-33. doi: 10.1016/j.cjca.2012.12.018.
  9. Tweet MS, Eleid MF, Best PJ et al. Spontaneous coronary artery dissection: revascularization versus conservative therapy. Circ Cardiovasc Interv. 2014;7:777-86. doi: 10.1161/CIRCINTERVENTIONS.114.001659.
  10. Tweet MS, Hayes SN, Pitta SR et al. Clinical Features, Management and Prognosis of Spontaneous Coronary Artery Dissection. Circulation. 2012;126:579-88. doi: 10.1161/CIRCULATIONAHA.112.105718.
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