Clinical Update

Spontaneous Coronary Artery Dissection: An Update for the Interventionalist

Daniela R. Crousillat, MD, Malissa J. Wood, MD, Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts

Daniela R. Crousillat, MD, Malissa J. Wood, MD, Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts

Spontaneous coronary artery dissection (SCAD) is increasingly recognized as a cause of acute coronary syndrome (ACS) and sudden cardiac death, particularly among young women. Although previously estimated to be rare, increasing awareness of heart disease among young women and detection by coronary angiography has increased the recognition of SCAD. SCAD is defined as the spontaneous separation of the coronary vessel wall in the absence of atherosclerosis or iatrogenic trauma. The dissection can involve any of the three layers of the coronary artery wall: the intima, the media, and/or the adventitia. There are two plausible hypotheses regarding the inciting event that leads to the development of SCAD. SCAD can result from an initial intimal tear leading to creation of a false lumen or from primary spontaneous hemorrhage of the vasa vasorum within the vessel wall, leading to formation of an intramural hematoma (IMH). Both mechanisms result in creation of a false lumen and separation of the coronary artery wall, resulting in compromised coronary artery flow through the true lumen.1


Although the true incidence of SCAD is not known, multiple case series suggest SCAD may be implicated as the cause of up to 5% of acute coronary syndromes (ACS). SCAD is primarily a disease of women, who account for greater than 90% of affected in most contemporary series. Although racial differences in the prevalence of SCAD are not known, SCAD has predominantly been reported among a majority white population.2-4 On average, most women present with SCAD during the fourth and fifth decades of life.5 In women less than 50 years of age, SCAD has been implicated as the cause of ACS in up to 35% of cases.5 SCAD is most common among young women and accounts for up to 43% of pregnancy-associated SCAD (p-SCAD), most commonly occurring in the third trimester or post partum.6 However, overall, p-SCAD only accounts for a minority of all SCAD cases.3,7,8 

Risk Factors

Multiple observational studies have consistently reported several associated conditions and predisposing risk factors for SCAD. The predisposition for SCAD is likely multifactorial and caused by a complex array of factors that increase hemodynamic stress and/or increase vessel wall fragility, thereby contributing to the final common pathway of coronary dissection (Figure 1). 

Given SCAD’s predisposition among women and in the peripartum state, female sex factors likely play a role through hormonal influences on the connective tissue and microvasculature, although the exact mechanisms remain to be elucidated. In a retrospective review of the Massachusetts General Hospital SCAD registry, 15% of women had a prior history of fertility treatment and 47% of postmenopausal women had a history of prior hormone replacement therapy4, further suggesting the important role of hormonal factors in the pathophysiology of this disease. Additional predisposing risk factors have been linked to over half of clinical presentations of SCAD.3 These risk factors include intense, isometric physical exercise, labor and delivery, emotional stress, exogenous hormones, and sympathomimetic drugs, which are hypothesized to predispose to dissection by increasing arterial shear stress. Importantly, SCAD is less frequently associated with traditional cardiovascular risk factors including obesity, hypertension, and diabetes. 

Additionally, vascular and inflammatory disorders can affect the integrity of the arterial vessel walls and have been associated with the incidence of SCAD. The most common arteriopathy associated with SCAD is fibromuscular dysplasia (FMD), a non-inflammatory vascular disorder that manifests as alternating stenosis and dilatation, aneurysms, and dissections, typically in the absence of atherosclerosis. FMD has been associated with SCAD in 11 to 86% of patients9, with renal, cervico-cephalic, and iliac arteries being the most commonly affected vascular beds. However, the prevalence of FMD in SCAD is difficult to discern, as routine screening of all patients has not been uniformly performed, leading to the high variability in the reported co-prevalence across multiple observational registries.5 At the time of coronary angiography, non-selective angiography of the neck, renal, and pelvic arteries can be performed, if feasible. However, given the increased procedural time and risks of iatrogenic dissection associated with this strategy, computed tomography angiography (CTA) of the head, neck, and pelvis is recommended to decrease procedural risks and to additionally allow for the interrogation of intracerebral aneurysms, which have been reported to be as high as 14% in patients presenting with SCAD.1 In contrast to FMD, other connective tissue disorders associated with inherited arteriopathies (ie, Marfan’s, vascular Ehlers-Danlos) and systemic inflammatory diseases are less commonly associated with SCAD.

Diagnosis and Classification

SCAD requires careful evaluation of coronary angiograms, as in many cases there are only subtle features, including abrupt change in vessel diameter. Familiarity with the distinct features and types of SCAD by practicing cardiologists is essential in making the correct diagnosis in a timely manner. Caution should be taken when performing coronary angiography in presumed SCAD, due to the reported increased risk of iatrogenic dissection in SCAD patients, with a risk of 2% during coronary angiography (0.2% in non-SCAD patients) and 14.3% during percutaneous coronary intervention.10

SCAD lesions are frequently quite subtle and are not associated with significant flow reduction on angiography, with TIMI-III flow present in 63.8% of lesions at the time of coronary angiography.11 Given the frequently subtle, non-occlusive appearance of SCAD lesions, caution must be taken in order to avoid missing SCAD lesions on angiography in patients with ACS. SCAD must be considered in patients with myocardial infarction and non-obstructive coronary arteries (MINOCA) and the differential diagnosis for SCAD includes atherosclerotic coronary disease, coronary vasospasm, coronary thromboembolism, and Takotsubo cardiomyopathy, which may also occur simultaneously with SCAD.12-15

The diagnosis of SCAD has been defined and classified by Saw et al and colleagues into four different types, based on diagnostic coronary angiographic findings (Table 1, Figure 2).16,17 

  • Type 1 SCAD is defined by the classic, pathognomonic appearance of a dissection flap with two separate lumens, commonly visualized as arterial wall contrast staining with “dye hang up.” 
  • Type 2 SCAD is characterized by diffuse narrowing and tapering of the affected vessel. Type 2 SCAD can either affect a discreet segment of the coronary vessel with angiographically normal adjacent proximal and distal vessels (Type 2a) or the affected vessel can terminate distally in dissection (Type 2b). 
  • Type 3 SCAD is defined by more discrete, tubular narrowings that can mimic atherosclerotic disease and can only be differentiated by the use of intravascular imaging at the time of coronary angiography.1 
  • Type 4 SCAD has additionally been proposed as an additional presentation of coronary SCAD, characterized by complete distal vessel occlusion in the absence of thromboembolism.16,17 Therefore, a high index of suspicion is necessary to detect SCAD, given its often subtle angiographic findings and more common involvement of mid to distal vessels.

Intracoronary imaging using intravascular ultrasound (IVUS) or optical coherence tomography (OCT) is now increasingly used to aid in the diagnosis of SCAD when the etiology of myocardial infarction is uncertain (Figure 3). IVUS can be used to distinguish SCAD from atherosclerosis (ie, type 3 SCAD) and can be employed to visualize the entire depth of the vessel wall. In contrast, OCT has increased spatial resolution and allows for a more detailed characterization of the relationship between the true and false lumen. OCT also provides superior guidance for coronary revascularization. However, careful consideration must be given to the need for intracoronary imaging, given data that suggest an increased risk of iatrogenic secondary dissection in SCAD patients at the time of coronary angiography and intervention.10 Due to these risks, computed tomography coronary angiography (CTCA) is emerging as a diagnostic imaging tool to aid in the diagnosis of SCAD, as well as in the follow-up of patients with recurrent chest pain syndromes after their index event. However, the sensitivity and specificity of diagnosing SCAD by CTCA is not known and coronary angiography remains the gold standard imaging modality.18

Clinical Presentation

SCAD is unfortunately a commonly missed or delayed diagnosis, both due to its presentation among a traditionally low-risk population for obstructive coronary artery disease, as well as underutilization of coronary angiography among patients with low pre-test probability for ischemic disease. Patients who present with SCAD most commonly present with chest pain as the primary symptom in up to 96% of cases, with associated findings including arm pain (50%), neck pain (22%), nausea or vomiting (23%), and diaphoresis in up to 21%.19 Most cases of SCAD typically present with ACS, most commonly non-ST segment elevation myocardial infarction (N-STEMI), with about one-quarter of patients presenting with an ST-segment elevation myocardial infarction (STEMI).1 The prevalence of ventricular arrythmias and presentation with sudden cardiac death varies from 3-11% in observational studies.2,7,20

There are several typical coronary manifestations of SCAD (Table 2). Type 2 SCAD is the most common angiographic presentation of SCAD.3 In most cases, SCAD involves a single coronary artery. Less than 15% of presentations are associated with multivessel SCAD. Although SCAD can affect any coronary vessel, the left anterior descending (LAD) artery and its branches are affected in up to one-half of cases. The distal coronary arteries and branches are most often affected, with proximal disease occurring in <10% of cases.2 In contrast, patients with p-SCAD are more likely to present with STEMI, cardiogenic shock, and left ventricular dysfunction compared to non-pregnancy associated SCAD.21 A contemporary review of 120 reported cases of p-SCAD from 2000 to 2015 found that p-SCAD was associated with higher rates of left main involvement (35%), multivessel SCAD (40%), and a reduced ejection fraction (LVEF<40%) in 44% of cases.22

Treatment Options

Conservative Therapy vs Revascularization

A conservative strategy without the use of PCI has been advocated as the optimal treatment for uncomplicated SCAD, given the mounting data to suggest spontaneous resolution and healing of coronary artery dissections over time.1,3,8 The natural history of SCAD has been evaluated in an observational series, among patients undergoing repeat coronary angiography after their index SCAD event. Among the cohort of SCAD patients from the Mayo Clinic who were managed conservatively and underwent repeat angiography, 73% demonstrated evidence of complete healing of the previously dissected vessel.8 Importantly, a very small number of conservatively treated cases demonstrated a need for late revascularization.1 In a retrospective analysis of 168 patients with SCAD at Vancouver General Hospital, 80% of patients were successfully managed conservatively, with 2% needing subsequent revascularization among this group.3 Given these findings, current expert opinion recommends conservative management for most patients presenting with SCAD who are clinically stable without high-risk coronary anatomy (left main disease or proximal two-vessel disease), reserving the use of coronary intervention only for patients who are hemodynamically unstable with poor coronary flow or with evidence of ongoing ischemia (Figure 4).5

In addition to the spontaneous healing observed in most cases of SCAD, observational studies have demonstrated an increased risk of poor outcomes associated with PCI among patients with SCAD. Importantly, in addition to low procedural success rates, coronary intervention has not been associated with improvement in outcomes. The Mayo Clinic contemporary series of 189 SCAD patients demonstrated a procedural failure rate of 53% with coronary intervention, but a lower rate of need for later revascularization among 10% of the patients who were managed conservatively. In the long term, revascularization of the target vessel and recurrent SCAD were equal in both treatment groups, highlighting that revascularization is not associated with improved outcomes.8 As a result of these findings, expert guidelines recommend against the routine use of percutaneous or surgical revascularization for stable patients presenting with SCAD. However, revascularization outcomes appear to be different among patients presenting with SCAD in the setting of a STEMI. A retrospective analysis of two large centers in 2019 shed additional light on the management of this unique cohort of patients. SCAD patients who presented with STEMI had higher rates of cardiogenic shock, and involvement of the left main or left anterior descending coronary artery territories. Compared to patients presenting with STEMI secondary to atherosclerotic disease, revascularization among SCAD patients (62% percutaneous revascularization vs 8% coronary artery bypass surgery) was associated with successful outcomes in >90% of patients and a higher 3-year survival.23 

Increasing awareness of SCAD among interventional cardiologists is of paramount importance, along with the disease-specific risks associated with attempted coronary intervention. These risks include iatrogenic secondary dissection, distal propagation of the dissection, and guidewire passage into the false lumen. Several strategies to optimize PCI in this patient population have been described, including plain old balloon angioplasty (POBA) to restore coronary flow without additional coronary intervention, and the placement of stents both proximal and distal to the dissected segment to help seal the intramural hematoma, thereby preventing propagation of the dissection. The best interventional approach to revascularization remains to be ascertained. For patients with failed PCI and ongoing ischemia, or in whom multivessel disease precludes the ability for conservative management, coronary artery bypass surgery has been used, although the known outcomes for this approach are limited.5,15

Adjunctive Therapy

There is no randomized control trial data to guide the medical management of SCAD, and recommendations are based on expert opinion and observational data. The medical management of confirmed SCAD presenting with ACS differs in several important ways from the management of ACS in the setting of atherosclerotic disease. Based on the pathophysiology of SCAD and the theoretical risk of increased bleeding into the false lumen with extension of the dissection, anticoagulation should not be routinely used and should be discontinued once the diagnosis of SCAD has been confirmed. Likewise, the use of antiplatelet agents has not been well studied in the treatment of SCAD, but carries increased theoretical risks of bleeding without known benefit to long-term outcomes. Expert consensus guidelines recommend the use of aspirin for at least 1 year to indefinitely with a weaker recommendation for short term (1-3 months and up to a year) dual antiplatelet therapy with a P2Y12 inhibitor in patients managed conservatively.5 However, SCAD patients treated with PCI should be treated similarly post-PCI to non-SCAD patients, with the use of dual antiplatelet agents per treatment guidelines.24 The only medical therapy routinely used by clinical experts in the treatment of SCAD is beta-blockers, due to their association with a reduction in the risk of recurrent SCAD.1 The use of other adjunctive therapies, including angiotensin-converting enzyme inhibitors (ACEi) and statins, should be guided by traditional indications for their use in left ventricular dysfunction and primary or secondary prevention of atherosclerosis, respectively, as there is no data to support or refute their use specifically in the setting of SCAD.5 Due to the high rate of recurrent SCAD and recurrent chest pain syndromes, anti-anginal therapies can be used for symptomatic relief. Importantly, all patients with SCAD should be referred for cardiac rehabilitation with a recommendation for avoidance of prolonged high-intensity exercise, highly competitive contact sports, and Valsalva maneuvers during exercise. These recommendations are based largely on clinical practice and extrapolation from the management of other arteriopathies.5  

Prognosis and Outcomes

Overall, long-term prognosis among patients with SCAD is excellent, with very low mortality rates.2 Despite the excellent clinical outcomes, however, SCAD survivors remain at long-term risk for recurrent SCAD and its diagnosis is associated with an exorbitantly high morbidity.1,2 In the Mayo Clinic series, SCAD recurred in 17% of patients with a median time to second event of 2.8 years. Notably, the rate of recurrence at 10 years was 29%, highlighting the high burden of morbidity associated with this disease, both in the short and long term.2 Similarly, the Vancouver series reported recurrent SCAD in a different coronary artery segment in up to 11% of patients within 30 days of the index event.25 There has been much interest regarding the potential contributors to recurrent SCAD. In a retrospective analysis of the Vancouver General Hospital SCAD registry, the use of beta-blockers was associated with a decreased risk of recurrent SCAD secondary to its decrease in myocardial demand and intracoronary shear stress. Conversely, the presence of hypertension was associated with an increased risk of SCAD.1 Other risk factors for SCAD recurrence include coronary tortuosity, which is four times more common among patients with SCAD and can be a sign of an underlying arteriopathy.26


Despite all we have accomplished in the recognition of SCAD as an important cause of acute MI among young women and less commonly, in men, much work remains to be done in our understanding of this disease. Although there are limited data and no randomized, controlled trials in SCAD, emerging data from multiple prospective registries have helped to better characterize this clinical entity. Additional research is essential to improve knowledge regarding the pathophysiology, diagnosis, and the best treatment strategies to improve outcomes among this vulnerable, young patient population. 

Disclosures: The authors report no conflicts of interest regarding the content herein.

The authors can be contacted via Malissa J. Wood, MD, at

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