Clinical Features, Management, and Prognosis of Spontaneous Coronary Artery DissectionClinical Perspective
Background—Spontaneous coronary artery dissection (SCAD) is an acute coronary event of uncertain origin. Clinical features and prognosis remain insufficiently characterized.
Methods and Results—A retrospective single-center cohort study identified 87 patients with angiographically confirmed SCAD. Incidence, clinical characteristics, treatment modalities, in-hospital outcomes, and long-term risk of SCAD recurrence or major adverse cardiac events were evaluated. Mean age was 42.6 years; 82% were female. Extreme exertion at SCAD onset was more frequent in men (7 of 16 versus 2 of 71; P<0.001), and postpartum status was observed in 13 of 71 women (18%). Presentation was ST-elevation myocardial infarction in 49%. Multivessel SCAD was found in 23%. Initial conservative management (31 of 87) and coronary artery bypass grafting (7 of 87) were associated with an uncomplicated in-hospital course, whereas percutaneous coronary intervention was complicated by technical failure in 15 of 43 patients (35%) and 1 death. During a median follow-up of 47 months (interquartile range, 18–106 months), SCAD recurred in 15 patients, all female. Estimated 10-year rate of major adverse cardiac events (death, heart failure, myocardial infarction, and SCAD recurrence) was 47%. Fibromuscular dysplasia of the iliac artery was identified incidentally in 8 of 16 femoral angiograms (50%) undertaken before closure device placement and in the carotid arteries of 2 others with carotid dissection.
Conclusions—SCAD affects a young, predominantly female population, frequently presenting as ST-elevation myocardial infarction. Although in-hospital mortality is low regardless of initial treatment, percutaneous coronary intervention is associated with high rates of complication. Risks of SCAD recurrence and major adverse cardiac events in the long term emphasize the need for close follow-up. Fibromuscular dysplasia is a novel association and potentially causative factor.
- fibromuscular dysplasia
- myocardial infarction
- percutaneous coronary intervention
- spontaneous coronary artery dissection
Spontaneous coronary artery dissection (SCAD) is an infrequent cause of acute coronary syndrome (ACS), typically affecting a younger, otherwise healthy population.1–6 The spectrum of clinical presentation can range from chest pain symptoms alone to ST-segment–elevation myocardial infarction (STEMI), ventricular fibrillation, and sudden death,3,7,8 as well as from single to multiple coronary artery involvement.9,10 Although dissection of the coronary intima or media is a hallmark finding, hematoma formation deeper within the vessel wall is often present.1,11 It remains unclear whether dissection or hematoma is the primary event, but both may cause luminal stenosis and occlusion.1,11 The diagnosis of SCAD is made principally with invasive coronary angiography, although adjunctive imaging modalities such as computed tomography angiography, intravascular ultrasound, and optical coherence tomography may increase the diagnostic yield.1,12–16
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The population-based incidence of SCAD is unknown. Retrospective registry studies have reported SCAD detection in 0.07% to 1.1% of all coronary angiograms performed.3,4,17–20 This wide range relates primarily to the variable inclusion of atherosclerotic plaque dissection within study populations. This heterogeneity is a limitation of a number of prior studies4,19,21,22 in that it seems most likely that plaque dissection represents a variant of a typical ACS caused by underlying atherosclerosis, whereas true SCAD occurring outside the setting of atherosclerosis represents a distinct clinical entity.1,18 In this regard, data from SCAD case series that by and large excluded atherosclerotic dissection demonstrate a younger, female preponderance and an association with peripartum or postpartum status.1,4,5,23–25 Other SCAD associations identified from case reports include connective tissue disorders, vasculitides, and exercise,1,23,26–29 suggesting an underlying vascular predisposition in some, although a unifying structural vessel wall abnormality has not yet been identified.
The optimal treatment strategy for acute SCAD presentation remains undetermined and may vary according to the type and severity of presentation. Reports have demonstrated favorable outcomes with conservative management (with documented angiographic resolution),9,19,30 fibrinolysis,31 percutaneous coronary intervention (PCI),32 and coronary artery bypass grafting (CABG),7,32 but there have been no comparative studies of treatment modalities. Regardless of initial treatment strategy, in-hospital and early outcomes have in general been reported to be favorable,3,4,17,23,33 with the 2 largest, non–atherosclerosis-predominant SCAD series to date demonstrating in-hospital death in 1 of 22 patients3 and 0 of 23 patients.4 Longer-term follow-up in these studies revealed death of 1 of 21 and 1 of 23 survivors at 1 and 3.5 years and recurrence of SCAD in 0 of 21 and 1 of 23, respectively, over the same period.3,4
The objective of the present retrospective study was to evaluate the incidence, clinical characteristics, associations, and treatment modalities of SCAD, as well as early and late outcomes, in a large consecutive series of patients with SCAD.
This retrospective study was approved by the Mayo Foundation Institutional Review Board. Only patients who had provided authorization for use of their records for research were included per Minnesota state statute. Record screening (1979–2011) with relevant key words yielded 508 potential patients. Individual medical record analysis and coronary angiographic review excluded patients with other diagnoses, iatrogenic coronary artery trauma, and atherosclerotic plaque dissection. Eighty-seven subjects with a compatible history and angiographic evidence of SCAD were identified. Sixty-three received initial care at a referring institution. The criteria for angiographic definition of SCAD were the presence of a dissection plane together with the absence of coronary atherosclerosis, confirmed by at least 2 nonblinded reviewing cardiologists. In 2 of the 87, angiography was equivocal and SCAD was confirmed by intravascular ultrasound (dissection flap, intramural hematoma, absence of atherosclerosis in both cases).
Variables and Definitions
Demographics, potential etiologic associations, clinical presentation, coronary distribution, treatment modality, and in-hospital and long-term outcomes were determined through medical record and angiographic review and when necessary through a mailed questionnaire and telephone follow-up. A separate analysis to determine SCAD incidence in Olmsted County, Minnesota, was conducted. The Rochester Epidemiology Project, a medical records–linkage system documenting medical care received in Olmsted County, Minnesota, was used to identify all Olmsted County residents who were diagnosed with SCAD from 1979 to 2009 (n=9). Estimated county populations from 2001 to 2010 used for the calculation of incidence were obtained from the US Census Web site (www.census.gov/popest/counties). A PCI procedure was deemed technically successful if any dilation was performed and there was any improvement in baseline Thrombolysis in Myocardial Infarction (TIMI) grade 0 to 1 flow or maintenance/improvement of TIMI grade 2 to 3 flow. Coronary flow was used as a marker for success rather than improvement in lesion stenosis, given the greater clinical relevance of flow in the acute situation and the frequent finding of residual vessel dissection distinct from the dilated segment. A subset of successful procedures was defined as complicated if ≥2 additional stents had to be placed for unanticipated propagation of dissection or hematoma during intervention.
Statistical analysis was performed with JMP version 8.0 and SAS 9.2 (both from SAS Institute, Inc, Cary, NC). Continuous data were summarized as mean (standard deviation), and comparisons were performed with a Student t test. Discrete variables were expressed as frequencies or percentages, and comparisons were performed by use of a χ2 test. Kaplan-Meier methods were used to estimate survival curves for follow-up events. End points included death, recurrent SCAD, and major adverse cardiac events (death, recurrent SCAD, myocardial infarction, and congestive heart failure subsequent to the initial SCAD event). Survival curves were compared by use of a log-rank test. A value of P<0.05 was considered statistically significant.
To place the SCAD atherosclerotic risk factor profile and long-term outcomes into a broader context, matched controls of ACS and STEMI patients were generated from the Mayo Clinic PCI database. A database including ACS patients treated medically or with CABG was not available. A greedy matching algorithm was used. PCI control patients were matched to SCAD patients if they were within 5 years of age, were the same sex, had index dates within 3 years, and had the same presentation (STEMI versus other ACS). PCI patients were excluded if they had prior MI, PCI, or CABG or refused the use of their records for research. As many matched controls as possible (up to 20) were allowed for each SCAD patient. Summary statistics for matched controls were weight based. Weights for controls were calculated as follows. For each SCAD patient, its set of controls had a total weight of the ratio of the number of overall controls to the number of overall SCAD patients. If a SCAD patient had >1 matched control, the patient's total weight was divided evenly to each control. Matches could not be identified for 6 of 87 SCAD patients.
Eighty-seven patients with SCAD were identified, of whom 71 (82%) were female. Mean age was 42.6±10 years. Demographic characteristics (overall and by sex) are detailed in Table 1. They indicate a low proportion of hypertension and diabetes mellitus without significant sex differences but statistically higher rates of hyperlipidemia and tobacco use in men. Using population data available from the Rochester Epidemiology Project, we calculated the annual incidence of SCAD among residents of Olmsted County from 1979 to 2009 at 0.26 per 100 000 persons (0.33 in women and 0.18 in men).
Clinical Presentation and Angiographic Distribution
STEMI was the presenting diagnosis in 49%, non-STEMI in 44%, and unstable angina in 7% (Table 1). Seventy-nine patients (91%) reported chest pain during presentation, and 12 (14%) experienced ventricular fibrillation or ventricular tachycardia requiring emergent defibrillation. Of the ventricular arrhythmic episodes, 9 were in the setting of STEMI and 3 with non-STEMI (Figure 1). The left anterior descending (LAD) artery was the most commonly affected vessel. Multivessel coronary dissection at presentation was evident in 20 patients (23%). Fourteen (16%) demonstrated 2-vessel and 5 (6%) demonstrated 3-vessel dissection. One postpartum woman presented with simultaneous dissection of the left main, mid LAD, obtuse marginal, and right coronary arteries.
Potential associations, including hormonal, vascular, or shear-stress–related factors, were identified in 48 patients (55%; Table 2). The most common association in women was postpartum status (18%), with a mean maternal age of 33 years and mean postpartum period of 38 days. In contrast, extreme physical activity was the principal precipitant in men (44% versus 2.8%; P<0.001). Thirty-four patients underwent formal genetic consultation. Of these, testing was not performed in 12 either because of low clinical suspicion for usefulness (n=7) or because it was not pursued by the patient (n=5). Testing was performed in 22 patients; the relevant positive findings are shown in Table 2. Details of specific genetic test type and findings (both positive and negative) for all those tested are shown in Table I in the online-only Data Supplement. Of the 39 patients without identified disease associations, 9 underwent genetic screening that was negative, and the remaining 30 patients were not investigated.
A notable finding was the detection of fibromuscular dysplasia (FMD) in noncoronary vascular territories of 10 patients. All patients with FMD were female. Contrast injection through the femoral sheath performed routinely before placement of arteriotomy closure devices revealed the irregular beaded appearance of FMD in the external iliac arteries of 8 of 16 (50%). A case example is shown in Figure 2. Because these femoral angiograms were unilateral and visualization was restricted to just the distal external iliac and common femoral region, the possibility of iliac FMD being present in angiogram-negative patients cannot be excluded. One of these patients underwent distal aortic angiography indicating bilateral iliac and superficial femoral artery involvement, and another experienced catheter dissection requiring iliac stent placement. Two additional patients were diagnosed with concomitant carotid FMD and carotid dissection by computed tomography angiography. Both underwent additional vascular computed tomography angiographic imaging and were found to have FMD in the renal, iliac, and vertebral arteries, with 1 incidental vertebral dissection. None of the remaining 69 patients (79%) in the cohort underwent vascular angiography; thus, it seems likely that the true prevalence of FMD in patients with SCAD is higher than identified in this study.
Initial Management Strategy and Early Outcomes
Those treated with an initial conservative strategy (n=31) appeared to demonstrate an uncomplicated in-hospital course (Figure 3), although there were 2 deaths during the long-term follow-up. Angiography was repeated in 13 of 31 patients for chest pain during follow-up (4 of 13 for recurrent SCAD) and provided the opportunity to observe the evolution of conservatively managed dissection. Of 17 initially dissected vessels, 9 demonstrated resolution or near resolution of dissection (mean time to repeat angiography, 40 months). Partial resolution was seen in 3 of 17 (mean, 27 months), one of which was treated with PCI on day 52 because of ongoing pain. Persistent dissection was evident in 4 of 17 vessels (mean, 12 months), two of which were treated with PCI, both on day 24, for ongoing symptoms. In 1 patient, a dissected but patent LAD progressed to symptomatic acute occlusion 88 days after the initial event and was successfully treated with PCI.
A total of 43 patients underwent PCI during their first SCAD hospitalization; in 4 of these 43 patients, PCI followed initial fibrinolytic therapy. Notably, technical success was achieved in only 28 (65%). Moreover, 7 of these 28 PCI procedures, while ultimately successful, were complicated by unanticipated propagation of the dissection flap or intramural hematoma requiring placement of ≥2 further stents. Reasons for failure in the remaining 15 PCI procedures (35%) were failure to cross into the distal true lumen with a wire (n=9), failure to cross the lesion with a balloon (n=1), or propagation of dissection/hematoma during intervention with a reduction in final TIMI grade flow (n=5).
A total of 12 patients underwent CABG as an index treatment strategy (n=4), after fibrinolysis (n=3), or after unsuccessful PCI (n=5). The left main coronary artery was involved in 6 of the 12. The single in-hospital death occurred in a 51-year-old woman who presented with STEMI caused by left main SCAD and TIMI grade 2 flow into the circumflex and LAD. PCI was attempted although wire passage was unsuccessful, and there was hemodynamic instability progressing to cardiac arrest. Emergency CABG was performed, but the patient developed multiorgan failure and died on postoperative day 2. Eight patients underwent repeat angiography during follow-up. Of the 15 bypass grafts that had been placed, 11 were found to be occluded (5 left internal mammary artery grafts to the LAD artery, 1 right internal mammary artery graft to the right coronary artery, and 5 vein grafts). The patent grafts comprised 1 left internal mammary artery graft to the LAD and 3 vein grafts.
During a median follow-up of 47 months (interquartile range, 18–106), 15 patients (17%) experienced a recurrent SCAD episode. Figure 4A illustrates the Kaplan-Meier–estimated rate of SCAD recurrence. After a primary SCAD event, the 10-year SCAD recurrence rate was 29.4%. Of those with recurrent SCAD, median time to a second episode was 2.8 years (range, 3 days to 12 years). In 12 of 15, recurrence was seen in previously unaffected coronary arteries. Two patients experienced a third episode of SCAD at 1 and 11 months after the prior episode.
All 15 patients with SCAD recurrence were female (P=0.026 versus male patients). Although this relatively small sample size precluded meaningful statistical analysis for predictors of recurrence, 3 aspects are notable. First, 4 of 10 women with noncoronary FMD experienced recurrence, of whom 2 also had prior carotid dissection. Second, none of the remaining 11 patients had identifiable precipitating factors at recurrence, although 2 had possible hormonal associations at the time of their index event (fertility treatment and postmenopausal hormone replacement). Whether any of these 11 had FMD is unknown because vascular imaging was not undertaken. Third, there was no clear association between cardiac medications begun during the index admission on subsequent risk of SCAD recurrence (Table II in the online-only Data Supplement), although sample size remains a limitation for analysis. An exception appeared to be statin use, which was higher in the SCAD recurrence group. However, because the median index event year was 2007 for those prescribed statins versus 2002 for those not prescribed statins, the date of event is a potential confounding factor. More so, it is certainly possible that those not prescribed statins initially were prescribed them at a later date. Lack of information on statin use is a limitation of the analysis.
Mortality and Major Adverse Cardiac Events
During the median follow-up of 47 months (interquartile range, 18–106), 5 persons developed heart failure, 16 had a myocardial infarction, and 3 had died at 10 years. The observed 1- and 10-year mortality rates were 1.1% and 7.7%, respectively, and the 10-year rate of major adverse cardiac events (death, recurrent SCAD, myocardial infarction, and congestive heart failure) was 47.4% (Kaplan-Meier estimates; Figure 4B and 4C).
Two patients died during follow-up. The first was an 85-year-old woman (the oldest SCAD subject) who died of end-stage heart failure and pneumonia 7 years after her SCAD episode. The second was a 49-year-old woman who died 4 years after SCAD as a result of multiple pulmonary emboli in the setting of essential thrombocythemia.
To place the long-term outcomes of SCAD patients into a broader context of patients with acute coronary events, comparisons were performed with matched controls of STEMI and other ACS patients generated from the Mayo Clinic PCI database, with matches available for 81 of 87 SCAD patients. There were significantly lower proportions of atherosclerotic risk factors in the SCAD group (Table 3). Long-term follow-up indicated significantly better survival in the SCAD group compared with matched ACS controls (P=0.02, Figure 5A). However, survival free of MI and survival free of MI and congestive heart failure were similar in both groups (P=NS; Figure 5B and 5C).
The major findings of this long-term study of a large series of patients with SCAD are the following. First, SCAD affects a young, predominantly female population and presents as a life-threatening condition in more than half of cases. Second, hormonal, shear stress, or vascular structural factors are identifiable in the majority, with the presence of noncoronary FMD being a striking and likely underestimated association. Third, although early mortality is low regardless of initial treatment modality, PCI is associated with high rates of complication and procedural failure. Fourth, 1 in 5 women but none of the men experienced recurrence of SCAD during long-term follow-up. Fifth, although long-term survival after an index SCAD episode appears better compared with that for typical ACS, rates of major adverse cardiac events are similar.
The population incidence calculated in this study translates to ≈800 new cases of SCAD in the United States per year. Although there are limitations in generalizing epidemiological findings from a single population, the true incidence may be underestimated for 3 reasons. First, the presentation of SCAD as STEMI or unstable ventricular arrhythmia in more than half the patients in this series implies that it may be an underappreciated cause of sudden cardiac death in the community. Second, the well-defined age and sex bias in the evaluation of chest pain suggests that younger patients (particularly female) may be underreferred for coronary disease evaluation or misdiagnosed as having noncardiac symptoms.34 This is due in part to the perception that coronary disease should not affect the young and otherwise healthy. Third, there may be underrecognition at angiography. The diagnostic criterion for SCAD in the present series was the presence of a dissection plane, visualized primarily by contrast angiography. However, the disease process may include the formation of hematoma deeper in the vessel wall between the media and adventitial layers, which can be seen in the absence of dissection.1,11,16 In these cases, coronary angiography would simply indicate luminal narrowing, without dissection, which could easily be misinterpreted as atherosclerotic plaque or coronary spasm rather than luminal compression from intramural hematoma. This underscores the need to maintain a high index of suspicion in relevant clinical situations and to consider adjunctive intravascular imaging studies for diagnostic clarification when appropriate.
The prevalence of FMD in the general population is unknown, but one study identified renal artery FMD in 3.8% of renal donors.35 Thus, the incidental and unexpected detection of FMD in the iliac artery of 50% of those who underwent limited angiography in the present study is a notable association. It seems likely that FMD would have been detected in an even greater proportion had more extensive vascular imaging been undertaken, particularly because the disease more commonly affects the renal and carotid arteries. In support of this, a recent study reported individual examples of peripheral arterial FMD in patients with SCAD.36 However, because this was not a consecutive series, the true prevalence of FMD in patients with SCAD remains uncertain.
It seems reasonable to speculate that FMD may be both present in the coronary arteries and mechanistically linked to the occurrence of SCAD in a significant proportion. FMD in the peripheral circulation can progress to dissection37–41; indeed, 2 patients in the present series exhibited concomitant dissection and FMD of the carotid arteries. Although none of the coronary angiograms in the present series exhibited the “string of beads” pattern that is associated with advanced FMD in peripheral arteries, it is well recognized that angiographic findings can be subtle or even absent.40,42 More so, autopsy studies have identified FMD in the coronary arteries of young patients with sudden death.43 The propensity for SCAD to occur at times of sex hormone level alteration (peripartum status, fertility treatment) might suggest a direct hormonal effect on the coronary vasculature, although certain proteoglycan changes that occur after pregnancy may not occur with other hormonal manipulations. That said, only a minority of such women experience SCAD. Whether the presence of FMD is the “missing link” between sex hormone changes and the occurrence of SCAD is an intriguing possibility and warrants further study. The association described above suggests that vascular screening for FMD in all patients with SCAD should be strongly considered and that SCAD should be considered in the differential diagnosis of chest pain occurring in patients with known FMD.
The optimal treatment for SCAD remains undetermined. However, it is notable that all patients who were treated with an initial conservative strategy experienced a benign in-hospital course, and a number exhibited angiographic resolution on follow-up studies. Clearly, there will have been some bias in the selection of management according to severity of presentation, but these data support a conservative strategy in otherwise stable patients with normal flow in the affected coronary artery. A challenge may be that some continue to experience chest pain in the absence of ischemia, perhaps relating to perturbation in the vessel wall or alteration in vascular tone. Due consideration should be given to this possibility before revascularization is pursued on symptomatic grounds alone.
In this regard, PCI was associated with elevated rates of technical failure relating to passage of coronary wire into the false lumen of the dissected vessel or loss of coronary flow through propagation of dissection and displacement of intramural hematoma by stent placement. This underscores the different mechanism of coronary obstruction in SCAD compared with atherothrombotic occlusion. It also highlights a major challenge in management, particularly in situations of ongoing ischemia and infarction when time to restoration of coronary flow is critical in limiting myocardial injury.44 Although it is important to recognize a potential critical role for PCI in the management of acute SCAD, the findings of this study suggest 3 particular considerations in this patient population. First, PCI could perhaps be restricted to situations of ongoing ischemia or infarction, given the relatively good early outcomes seen with initial conservative management. Second, it could be argued that the minimum intervention necessary to restore coronary flow is undertaken. Because complications from SCAD intervention were frequently related to the placement of stents (with resulting propagation of hematoma), the risk of stent placement should be weighed against the expectation of a favorable clinical outcome and of resolution of dissection with conservative management in suitable patients. Third, due consideration should be given to the periprocedural use of adjunctive imaging technologies such as intravascular ultrasound and optical coherence tomography both to determine extent of vessel wall disruption (which may be underappreciated at angiography) and to provide real-time guidance of interventional strategy.
Acknowledging sample size limitation, it is noteworthy that patients who underwent CABG as an initial strategy fared well in the short term despite left main involvement in 50%. However, it should be emphasized that the high rate of late bypass graft occlusion demonstrated in this study suggests that bypass surgery may not provide long-term protection against the effects of recurrent native coronary artery dissection.
The occurrence of repeat SCAD in 17% of the study population during long-term follow-up was unexpectedly high. The 2 prior community studies with long-term follow-up revealed recurrence in 0 of 21 at 1 year3 and 1 of 21 at 3.5 years.4 Possible reasons for higher rates in the present study include a larger sample size and a longer duration of follow-up. It is notable that recurrent SCAD occurred exclusively in women and in 4 of the 10 patients in whom FMD was identified. This, together with sex differences in SCAD origin, raises the possibility of sex-specific disease processes and differences in prognosis that warrants further research. Although long-term survival after SCAD appears favorable, the high rate of major adverse events is notable. This finding, together with the unpredictability in timing of SCAD recurrence (ranging from 3 days to 12 years in this series), highlights the need for both close and long-term follow-up. Future multicenter registry data collection and prospective study will be helpful in further defining the natural history of SCAD, its associations, and its optimal treatment.
Although this is the largest SCAD series to date, sample size remains a limitation for statistical analysis. It is possible that complication and recurrence rates may have been overestimated owing to a referral bias toward more complex patients. Although this is speculative, caution should be used in extrapolating these data to the general population. In this regard, treatment strategy was of course not randomized, and selection bias thus limits the ability to compare outcomes according to treatment modality. Many of these are universal limitations among retrospective analyses, including prior SCAD studies, and there remains a paucity of cohesive, conclusive evidence on the natural history of SCAD and optimal treatment.
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The editorial for this article was published in the August 7, 2012 (Circulation. 2012;126:667–670.) issue of Circulation.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.112.105718/-/DC1.
- Received March 15, 2012.
- Accepted May 29, 2012.
- © 2012 American Heart Association, Inc.
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Spontaneous coronary artery dissection is an infrequent but increasingly recognized cause of acute coronary syndrome. Although it is a nonatherosclerotic condition, its origin is unknown. This retrospective single-center study evaluated clinical features, associations, management strategies, and early and late outcomes in 87 patients with angiographically confirmed spontaneous coronary artery dissection. Consistent with prior studies, we found a young female preponderance with a low burden of atherosclerotic risk factors. Half of all patients presented with an ST-elevation myocardial infarction. Postpartum status was the most frequent association in women, whereas extreme exertion was the principal correlation in men. We unexpectedly identified fibromuscular dysplasia of the iliac artery in half the femoral angiograms that had been undertaken before closure device placement. This strong association raises the possibility of shared pathophysiological processes between fibromuscular dysplasia and spontaneous coronary artery dissection. The management of acute spontaneous coronary artery dissection can be challenging. We found that conservative treatment was associated with favorable early outcomes, frequently with subsequent angiographic resolution of dissection. While early clinical outcomes after percutaneous coronary interventions were not unfavorable, percutaneous coronary intervention was associated with an elevated risk of technical complications, including propagation of intramural hematoma and dissection with stent placement. Coronary artery bypass grafting, while being safe and effective in the short term, was associated with high rates of graft occlusion during follow-up, primarily as a result of resolution of the initial dissection. Spontaneous coronary artery dissection recurred in 17% of patients during long-term follow-up, all of whom were female. This underscores the need for close and continued surveillance of this challenging patient population.