|Year : 2019 | Volume
| Issue : 1 | Page : 14-20
Spontaneous coronary artery dissection in acute coronary syndromes: A single-center experience
Suresh Madhavan, Jayaprasad Narayanapillai
Department of Cardiology, Government Medical College, Kottayam, Kerala, India
|Date of Web Publication||29-Mar-2019|
Dr. Suresh Madhavan
Department of Cardiology, Government Medical College, Kottayam - 686 008, Kerala
Source of Support: None, Conflict of Interest: None
Aim: Incidence, diagnosis, and management of spontaneous coronary artery dissection (SCAD) in the Indian subcontinent are less well understood. The present study is to find the incidence and clinical features of SCAD in acute coronary syndrome (ACS) patients undergoing coronary angiography in acute coronary settings.
Subjects and Methods: This is a prospective and retrospective analysis conducted on ACS patients who underwent emergency angiogram in the Department of Cardiology, Government Medical College, Kottayam, India, from February 19, 2008, to December 31, 2017. Those without SCAD were kept as control.
Results: Out of 3708 patients studied, SCAD was seen in 5.9% patients with 78.8% females and was responsible for 31.4% and 6% of ACS in females aged <50 and >50 years, respectively. The mean age of presentation was 47.2 years. Age <50 years, female sex, emotional and physical stress, and fibromuscular dysplasia (FMD) were the risk factors identified. In-hospital and 6-month mortality rate was 3.1% and 6.3%. 31.9% of SCAD patients were diagnosed to have FMD on follow-up. Only 4.1% of patients belonged to peripartum period. Medical management is superior in hemodynamically stable SCAD patients compared to invasive strategies.
Conclusions: SCAD is far more common than expected in this part of the world, and the awareness regarding the diagnosis, treatment, and follow-up has to be improved.
Keywords: Acute coronary syndromes, fibromuscular dysplasia, spontaneous coronary artery dissection
|How to cite this article:|
Madhavan S, Narayanapillai J. Spontaneous coronary artery dissection in acute coronary syndromes: A single-center experience. Heart India 2019;7:14-20
|How to cite this URL:|
Madhavan S, Narayanapillai J. Spontaneous coronary artery dissection in acute coronary syndromes: A single-center experience. Heart India [serial online] 2019 [cited 2019 Apr 24];7:14-20. Available from: http://www.heartindia.net/text.asp?2019/7/1/14/255286
| Introduction|| |
Spontaneous coronary artery dissection (SCAD) is defined as an epicardial coronary artery dissection that is not associated with atherosclerosis or trauma and not iatrogenic.
SCAD, previously thought to be rare entity, is now being increasingly recognized in the western world due to the improvement in coronary imaging techniques such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT). Lack of awareness of the etiopathogenesis and lack of uniform standard treatment strategies even among the interventional cardiologists complicate the scenario. Better awareness of the etiopathogenesis and incidence in our population will help in accurate treatment since the clinical presentation is almost same as that of atherosclerotic occlusive coronary artery disease.
The aim of the study is to find the incidence of SCAD in our population, to find out the precipitating factors and treatment strategy opted, and to assess the mortality for a mean duration of 6 months postevent.
| Subjects and Methods|| |
In this prospective and retrospective observational study, the database of cardiac catheterization laboratory in a single tertiary care center was reviewed to identify patients with SCAD. Data collection was started on February 12, 2015, after getting institutional ethics committee approval. Retrospective data collection from February 19, 2008, to February 12, 2015, was carried out from the database available. All available hospital records including coronary angiograms were analyzed. Patients were contacted via telephone and asked for outpatient department review to get further details when needed. Prospective data collection started on February 12, 2015. All patients with acute coronary syndrome (ACS) undergoing coronary angiography within 72 h of admission were included in the study. Out of 3708 patients who underwent emergency angiography in ACS between February 19, 2008, to December 31, 2017, 222 patients were diagnosed to have SCAD-associated ACS and 3486 non-SCAD (atherosclerosis-related) ACS. All angiograms were independently reviewed by two experienced interventional cardiologists. The diagnosis of SCAD was based on fewer or no conventional coronary risk factors, and angiographic diagnosis was based on Saw classification for SCAD. In the Saw angiographic SCAD classification, Type 1 refers to the classic appearance of multiple radiolucent lumens or arterial wall contrast staining (which is considered as the “pathognomonic” appearance of SCAD is present in only a small proportion of cases). Type 2 refers to the presence of diffuse stenosis that can be of varying severity and length (usually >20 mm), in which Variant 2A is diffuse arterial narrowing bordered by normal segments proximal and distal to the intramural hemorrhage (IMH), and variant 2B is diffuse narrowing that extends to the distal tip of the artery. Type 3 is focal or tubular stenosis, usually <20 mm in length that mimics atherosclerosis. The use of IVUS was according to the discretion of the operator, especially when there was a diagnostic confusion. The operator and treating doctors were blinded from the study. Patients were grouped into ACS due to SCAD and ACS due to atherosclerotic causes (control group). All patients were analyzed for demographic data, risk/precipitating factors, clinical profile, and treatment and followed up for a mean period of 6 months. Both in-hospital and 6-month mortality was recorded. For deceased patients, or if otherwise needed, information was obtained by telephone from the family. Those with a history of previous percutaneous intervention before index admission to our hospital and chest trauma were excluded. The study conforms to the guidelines of Declaration of Helsinki 1964 revised in 1975. The study was approved by the scientific review committee and ethical review board of Government Medical College, Kottayam.
Categorical variables were compared using the Chi-square test and the Fisher's exact test wherever appropriate. Continuous variables were analyzed using two tailed t-test or Mann–Whitney U-test. Patient characteristics were expressed as means ± standard deviations or percentages. Only factors significant in univariate testing were included in the multivariate model. Multivariate logistic regression analysis was used to determine the significant factors associated with SCAD. A two-tailed P ≤ 0.05 was used to indicate statistical significance. Statistical analysis was done using SPSS software (version 16.0, SPSS Inc., Chicago, Illinois, USA).
| Results|| |
Demographics [Table 1]
Of the 3708 ACS patients (1623 females, 2085 males) taken for emergency coronary angiography and revascularization, 222 patients (5.9%) were diagnosed to have SCAD, females 175 (78.8%) outnumbering males 47 (21.2%). The mean age of SCAD patients was 47.2 years. In non-SCAD ACS group, the mean age was 56.4 years. The mean age of females with SCAD was 47.6 years which was slightly higher than the male counterpart with SCAD, where the mean age was 45.5 years. Among the females with SCAD when the age was <50 years, the mean age of presentation was 43.2 years, which also was slightly higher than male counterpart which was 40.2 years. In the age group >50 years, the mean age in females and males was 53.1 and 59.2 years, respectively. The mean age of peripartum period-related SCAD was 33.7 years. Of the total 1623 female patients, 10.8% (175) had ACS due to SCAD. SCAD was responsible for 31.4% of ACS in females <50 years of age (96 out of 306 in number). In female subset, when the age was >50 years, this proportion was 6% (79 out of 1317). Of the total 2085 male patients, 2.2% (47) had ACS due to SCAD. SCAD was responsible for 8.6% of ACS in males <50 years of age (34 out of 392 in number). In male subset, when the age was >50 years, this proportion was 0.7% (13out of 1693). The incidence of conventional coronary risk factors was less in SCAD patients compared to the non-SCAD ACS group.
Possible precipitating/associated factors [Table 2]
Patients had more than one type of possible precipitating/associated factors. In both sex, most important precipitating factors were emotional stress and unaccustomed physical exertion. Underlying arteriopathy like fibromuscular dysplasia (FMD) was seen in 31.9% of patients with SCAD. All peripartum ACS had SCAD as the diagnosis. On multivariate analysis, only these two factors showed statistically significant association with SCAD.
Coronary involvement pattern, treatment, and mortality [Table 3] and [Table 4]
|Table 4: Logistic regression analysis for predictors of spontaneous coronary artery dissection|
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Majority of the patients had involvement of left anterior descending coronary artery (LAD, 37.8%) followed by left circumflex artery (32.4%) and right coronary artery (23.4%). Saw SCAD classification Type 1, 2, and 3 were seen in 28.8%, 56.3%, and 14.9% of patients, respectively. All pregnancy-related SCAD had diffuse involvement of mid and distal part of coronary artery. All the three cocaine-addicted SCAD patients had more than one vessel involvement and that too ostioproximal involvement. Left main coronary artery (LMCA)/multivessel involvement was seen in 14 (6.3%) of all SCAD. Of 47 male patients, 31 (66%) had proximal vessel involvement. 45.1% of females (79 patients) had proximal involvement. 54.9% of females had predominantly mid and distal involvement. Thus, the pattern of involvement had a statistically significant difference between males and females (P < 0.01). 86.5% of all SCADs were ST elevation myocardial infarction (MI) and rest 13.5% non-ST elevation ACSs. The presenting complaints of SCAD patients were indistinguishable from atherosclerotic ACS. After assessing the coronary anatomy and clinical judgment by the treating physicians, 62.1% of SCAD (138) patients and 26.7% (919) patients in non-SCAD group were given medical therapy, showed statistical significance of P < 0.001. Of those, 17 patients had to cross over to invasive strategy later based on symptoms. Of the 84 SCAD patients who received invasive strategy as primary modality of treatment, 68 SCAD patients underwent angioplasty to culprit vessels and 16 SCAD patients were taken for coronary artery bypass graft surgery (CABG). Those with LMCA involvement, ostial dissections, and hemodynamic instability were taken for invasive strategy as percutaneous coronary intervention ( PCI) or CABG. 138 patients who were detected to have SCAD were given medical treatment as the initial strategy. Of those, 17 patients had to cross over to invasive strategy later based on symptoms. In the medically treated group, there was only one in-hospital mortality, reason being abrupt onset of free wall rupture of the ventricle 18 h after the onset of angina symptoms. Six patients (7.1%) in the PCI/CABG group died due to cardiac complications. Of those, four patients had LMCA involvement and two had multivessel dissection. All were hemodynamically unstable during admission. The overall in hospital mortality for the SCAD group was seven out of 222 (3.2%). Of seven patients died, five were males and two females. In-hospital mortality in non-SCAD group was 3.6%. Six months mortality in the medically treated group was 3 (2.1%) whereas in the PCI/CABG group was 11 (13.1%), amounting to overall 6.3% mortality.
On comparison with recent studies by Rashid et al., Nakashima et al., and Nishiguchi et al. [Table 5], we noted that the prevalence of SCAD in ACS is more than expected. The percentage of female SCAD was comparable.
| Discussion|| |
Since the first description of SCAD in 1931 by Pretty and first angiographic description almost five decades later, it was believed that the disease is rare. However, widespread use of angiography and newer imaging techniques such as IVUS, OCT, and cardiac coronary computerized tomography (CT) have helped to identify more and more patients and thus helped us to understand the pathophysiology much better. The risk factors identified are female sex especially peripartumperiod, younger age. SCAD continues to be misdiagnosed or managed as atherosclerotic ACS, which may harm patients with SCAD. Compared to emergency PCI in atherosclerotic ACS, PCI for SCAD has been associated with lower technical success and higher complications than PCI., The true prevalence of SCAD remains uncertain. Recent series using careful diagnostic criteria suggest that SCAD may be a cause of up to 1%–4% of all ACS cases and may be the cause of ACS in up to 35% of MIs in women ≤50 years of age,,, and is the most common cause of pregnancy-associated MI (43%).
In our study, the SCAD was responsible for the ACS in 31.4% females and 8.6% males below the age of 50 years. The high percentage of SCAD below 50 years was rather unexpected since it was against the notion that SCAD is an extremely rare disease in our population. The high percentage of SCAD below 50 years was similar to that of recent studies by Rashid et al., Nakashima et al., and Nishiguchi et al. Thus, we can assume that SCAD is prevalent in all age groups all over the world, with more predominant in young females. The mean age of presentation in SCAD, in our study, was similar to that reported in the available literature. Compared to previous trials, the present study also noted scarcity of atherosclerotic risk factors in SCAD patients. On comparison of possible precipitating factors, occurrence of the major factors such as stress and unaccustomed exertion was almost similar in both the SCAD and the atherosclerotic group. The increased occurrence of ocular symptoms in younger SCAD patients (7.2%) needs to be carefully studied. It possibly indicates the involvement of other vascular territories suggesting possible unrecognized arteriopathies. Since the present study was retrospective and prospective observational study, we tried to get all available records related to the ocular symptoms. The time of occurrence of the ocular symptoms had no relation with occurrence of SCAD. Most of the patients who had ocular symptoms had transient sectorial field defects labeled as BRAO [Branch Retinal Arterial Occlusion].
Of the various reported series, LAD is the most common artery involved. Our study also revealed similar results. More ostioproximal SCAD was noted in males compared to females who had more mid-distal involvement.
Histopathologically, SCAD is characterized by IMH within the wall of a coronary artery and compressing the true lumen, leading to coronary insufficiency. It is not sure whether the inciting event is intimal tear leading to false lumen formation with channeling of blood from the lumen or it is the spontaneous bleeding in the vasa vasorum of the blood vessel. In all suspected death due to SCAD, histopathological examination of the vessel should include distal segments of the epicardial arteries also, due to predilection of SCAD for mid to distal coronary arteries.
The SCAD may be linked to underlying arteriopathies, genetic factors, hormonal influences, inherited or acquired arteriopathies, or systemic inflammatory diseases often compounded by environmental precipitants or stressors. The association of SCAD with multifocal FMD in extracoronary arteries has been the most commonly reported. FMD is a nonatherosclerotic, noninflammatory vascular disease that can affect nearly any arterial bed and can manifest as arterial stenosis, aneurysm, tortuosity, or dissection., Multifocal FMD is the most common type of FMD and is defined angiographically as areas of alternating stenosis and dilatation resulting in a string-of-beads pattern. Focal FMD appears angiographically as a single concentric or tubular narrowing; <10% of cases of FMD are of this type. In the US Registry for FMD, overall prevalence of SCAD in FMD was 2.7%.,
SCAD is the most common cause of ACS among patients who are pregnant or postpartum. SCAD has been reported as early as in 5th week of pregnancy to several months postpartum, even though third trimester was the most common period. The hormonal changes of pregnancy may lead to alterations in the architecture of the arterial wall which weakens the vessel wall, which culminates in arterial wall rupture, IMH, and onset of clinical symptoms. Pregnancy-related SCAD is more with black race, hypertension including gestational, dyslipidemias, depression, vascular headaches,, advanced maternal age and age at first childbirth, multiparty, and infertility treatment. Our study had only nine pregnancy-related SCAD out of 222. Under diagnosis or possible referral bias could have been the reason for low percentage. SCAD has been reported in isolated cases of systemic lupus erythematosus, inflammatory bowel disease, polyarteritis nodosa, celiac disease, hepatitis C-associated cryoglobulinemia, inherited arteriopathies, connective tissue disorders, and polycystic kidney disease.
The complex interplay between a vulnerable patient with above-mentioned factors and potential triggers is believed to initiate a spontaneous arterial tear or IMH. This may not be applicable to all patients, highlighting the poorly understood pathophysiology of SCAD. The most commonly reported precipitants are extreme physical or emotional stress, leading to increased catecholamine levels which in turn cause coronary artery shear stress that, at least in part, contributes to the pathophysiology of SCAD. From available reports, only severe coronary tortuosity has been identified as a risk factor for recurrence, with recurrence most likely to occur in a segment of tortuosity. The SCAD has to be suspected with clinical presenting features such as patient demographics, especially young age, female sex, and few or nonconventional cardiovascular risk factors. Even though arterial wall is not specifically imaged, conventional coronary angiography remains the first-line diagnostic imaging.
Newer imaging methods, including IVUS and OCT, provide detailed visualization of the arterial wall that aids the diagnosis of SCAD. Classical description of multiple lumens or contrast staining of arterial walls (type 1) is seen only in <30% patients with SCAD; hence, reliance solely on this would result in missed diagnoses of >70% of SCAD cases. Therefore, familiarity with the diffuse narrowed-lumen appearance of IMH and use of intracoronary imaging in appropriate settings are warranted. Even though they help in diagnosis, these tools have potential risks, including extending the coronary dissection with wire or imaging catheter, guide-catheter iatrogenic dissection, catheter-induced occlusion of true lumen, and hydraulic extension with contrast injection for OCT. Coronary CT angiography is not recommended as the first-line investigation for suspected acute SCAD as it is time-consuming and delays primary treatment, but it can be used for follow-up studies to assess the healing.
For ACS, all available guidelines recommend an early invasive strategy with revascularization of culprit lesions over conservative therapy alone to reduce the risk of recurrent occlusion at the lesion site and associated adverse events in atherosclerotic MI, but there have been no randomized trials or treatment analysis outcomes or comparisons between acute revascularization strategies for ACS caused by SCAD. Conservative therapy may have an edge over invasive therapy as per few observational data that have indicated angiographic “healing” of SCAD lesions in 70%–97% of patients who were selectively restudied weeks to months after a conservatively managed index episode., Recurrence of ACS requiring revascularization can happen within the first 7 days after an acute episode. Hence, inpatient monitoring for at least 7 days is typically recommended as part of a conservative strategy for SCAD management. Our study also revealed that extended stay is safer as 17 patients initially managed medically had to cross over to invasive strategy due to recurrence of symptoms predominantly toward the end of 1st week. Conservative therapy may not be appropriate in high-risk patients with ongoing ischemia, left main artery dissection, or those with hemodynamic instability.
The success rate of coronary revascularization in SCAD is less compared to that of atherosclerotic disease as per the available studies. Since majority of the patients with SCAD will be having arteriopathies, the PCI procedure itself may do harm by hydraulic extension of the dissection or extension of intramural hematoma after the stent deployment. Various techniques have been proposed to reduce the same by (1) implantation of longer or multiple stents so as to accommodate extension of the IMH when compressed by the stent; (2) direct stenting without balloon predilation; (3) balloon angioplasty without stenting; (4) cutting balloon fenestration of the IMH to allow decompression of the false lumen blood pool into the true lumen with or without additional stenting, and (5) use of bioresorbable stents to provide a temporary scaffold because complete resorption of struts occurs within 2 years. CABG can be considered for left main stem or proximal dissections, unsuccessful PCI, persistent symptoms despite optimal conservative therapy. During long-term follow-up, one study reported increased rate of graft failure as a result of subsequent healing of native SCAD vessels and competitive flow promoting graft occlusion. The study also showed that CABG was not protective against recurrent SCAD events. Even though there are no clear-cut recommendations on the use of various drugs for the treatment for ACS due to SCAD, the current treatment plan adopted by majority is almost same that of ACS due to atherosclerotic causes. Even though there is theoretical probability of IMH extension on using anticoagulants, it has not been studied in detail. In our study also, we noted that the mortality was higher in patients who underwent invasive procedures. All patients who underwent these procedures had clinical indications for the same also. Hence, a broad statement against the PCI/CABG may not be appropriate.
| Conclusions|| |
SCAD is far common than previously thought in this part of the world and was responsible for 5.9% of all ACS studied. Majority of SCAD patients were females and was responsible for nearly one third of ACS in females <50 years. Emotional stress and physical exertions in the background of arteriopathies such as FMD were the important precipitating factors. Clinical presentation of SCAD was same as that of atherosclerotic ACS, except the fact that conventional coronary risk factors were very low in SCAD group. Saw classification Type 2 (diffuse narrow appearance of the coronary) was the most common SCAD noted. For unknown reasons, males had more ostioproximal and more multivessel involvement. Females had predominant mid to distal coronary involvement. Unlike various available reports, the incidence of SCAD ACS in peripartum period is less in the present study. Whether it is referral bias or under diagnosis of the clinical situation is not known. Even though 38.9% of females had FMD on follow up, none of the peripartum related SCAD had the same on evaluation. All peripartum-associated SCAD ACS had mid to distal coronary involvement and uneventful recovery on medical management alone. Majority of the patients, who were hemodynamically stable, received medical therapy and the in-hospital and 6-month mortality was less compared to the invasive group. The difference observed was most likely due to the fact that hemodynamically unstable patients were taken for early invasive strategy like PCI or CABG. Hence, the periprocedural complications were more in the invasive group. Further research is needed on lower mean age of presentation in males <50 years and lesser incidence on pregnancy associated ACS in the study population. Not only that, we need a consensus on treatment strategy worldwide based on randomized controlled trials.
Limitations of the study
One of the important limitations of the study was nonuniform pattern of recruitment of patients – both prospective and retrospective. Before the availability of Saw classification, the physicians used to diagnose SCAD based on classical appearance of dissection, which might have missed the diagnosis in few patients which were labeled as either minor coronary artery disease or recanalized vessels. The use of IVUS/OCT was not uniform as the operators were blinded from the study. Compared to other studies, the percentage of peripartum ACS were less in number, reasons could be referral bias or decision for conservative management without doing angiography during initial 6 months after the event. Only ACS patients taken for emergency angiography were studied. Hence, the prevalence cannot be extrapolated to all patients. On follow-up, only the 6-month mortality data were collected. Collection of follow-up angiogram was not included in the study.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Saw J, Mancini GBJ, Humphries KH. Contemporary review on spontaneous coronary artery dissection. J Am Coll Cardiol 2016;68:297-312.
Rashid HN, Wong DT, Wijesekera H, Gutman SJ, Shanmugam VB, Gulati R, et al.
Incidence and characterisation of spontaneous coronary artery dissection as a cause of acute coronary syndrome – A single-centre Australian experience. Int J Cardiol 2016;202:336-8.
Nakashima T, Noguchi T, Haruta S, Yamamoto Y, Oshima S, Nakao K, et al.
Prognostic impact of spontaneous coronary artery dissection in young female patients with acute myocardial infarction: A report from the angina pectoris-myocardial infarction multicenter investigators in japan. Int J Cardiol 2016;207:341-8.
Nishiguchi T, Tanaka A, Ozaki Y, Taruya A, Fukuda S, Taguchi H, et al.
Prevalence of spontaneous coronary artery dissection in patients with acute coronary syndrome. Eur Heart J Acute Cardiovasc Care 2016;5:263-70.
Pretty HC. Dissecting aneurysm of coronary artery in a woman aged rupture. Br Med J 1931;1:667.
Tweet MS, Gulati R, Aase LA, Hayes SN. Spontaneous coronary artery dissection: A disease-specific, social networking community-initiated study. Mayo Clin Proc 2011;86:845-50.
Tweet MS, Eleid MF, Best PJ, Lennon RJ, Lerman A, Rihal CS, et al.
Spontaneous coronary artery dissection: Revascularization versus conservative therapy. Circ Cardiovasc Interv 2014;7:777-86.
Saw J, Aymong E, Sedlak T, Buller CE, Starovoytov A, Ricci D, et al.
Spontaneous coronary artery dissection: Association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv 2014;7:645-55.
Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, et al.
Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation 2012;126:579-88.
Elkayam U, Jalnapurkar S, Barakkat MN, Khatri N, Kealey AJ, Mehra A, et al.
Pregnancy-associated acute myocardial infarction: A review of contemporary experience in 150 cases between 2006 and 2011. Circulation 2014;129:1695-702.
Saw J, Aymong E, Mancini GB, Sedlak T, Starovoytov A, Ricci D, et al.
Nonatherosclerotic coronary artery disease in young women. Can J Cardiol 2014;30:814-9.
Kadian-Dodov D, Gornik HL, Gu X, Froehlich J, Bacharach JM, Chi YW, et al.
Dissection and aneurysm in patients with fibromuscular dysplasia: Findings from the U.S. Registry for FMD. J Am Coll Cardiol 2016;68:176-85.
Olin JW, Gornik HL, Bacharach JM, Biller J, Fine LJ, Gray BH, et al.
Fibromuscular dysplasia: State of the science and critical unanswered questions: A scientific statement from the American Heart Association. Circulation 2014;129:1048-78.
Bayar N, Çaǧırcı G, Üreyen ÇM, Kuş G, Küçükseymen S, Arslan Ş, et al.
The relationship between spontaneous multi-vessel coronary artery dissection and celiac disease. Korean Circ J 2015;45:242-4.
Tweet MS, Hayes SN, Codsi E, Gulati R, Rose CH, Best PJM, et al.
Spontaneous coronary artery dissection associated with pregnancy. J Am Coll Cardiol 2017;70:426-35.
Faden MS, Bottega N, Benjamin A, Brown RN. A nationwide evaluation of spontaneous coronary artery dissection in pregnancy and the puerperium. Heart 2016;102:1974-9.
Reddy S, Vaid T, Ganiga Sanjeeva NC, Shetty RK. Spontaneous coronary artery dissection as the first presentation of systemic lupus erythematosus. BMJ Case Rep 2016;2016. pii: bcr2016216344.
Srinivas M, Basumani P, Muthusamy R, Wheeldon N. Active inflammatory bowel disease and coronary artery dissection. Postgrad Med J 2005;81:68-70.
Chu KH, Menapace FJ, Blankenship JC, Hausch R, Harrington T. Polyarteritis nodosa presenting as acute myocardial infarction with coronary dissection. Cathet Cardiovasc Diagn 1998;44:320-4.
Fernández-Gutiérrez B, Zamorano J, Batlle E, Alfonso F, Conde A, Sánchez-Harguindey L, et al.
Coronary dissection associated with hepatitis C virus-related cryoglobulinaemia. Rheumatology (Oxford) 1999;38:1299-301.
Henkin S, Negrotto SM, Tweet MS, Kirmani S, Deyle DR, Gulati R, et al.
Spontaneous coronary artery dissection and its association with heritable connective tissue disorders. Heart 2016;102:876-81.
Eleid MF, Guddeti RR, Tweet MS, Lerman A, Singh M, Best PJ, et al.
Coronary artery tortuosity in spontaneous coronary artery dissection: Angiographic characteristics and clinical implications. Circ Cardiovasc Interv 2014;7:656-62.
Saw J, Mancini GB, Humphries K, Fung A, Boone R, Starovoytov A, et al.
Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging. Catheter Cardiovasc Interv 2016;87:E54-61.
Prakash R, Starovoytov A, Heydari M, Mancini GB, Saw J. Catheter-induced iatrogenic coronary artery dissection in patients with spontaneous coronary artery dissection. JACC Cardiovasc Interv 2016;9:1851-3.
Emergency Department Patients With Chest Pain Writing Panel, Rybicki FJ, Udelson JE, Peacock WF, Goldhaber SZ, Isselbacher EM, et al.
2015 ACR/ACC/AHA/AATS/ACEP/ASNC/NASCI/SAEM/SCCT/SCMR/SCPC/SNMMI/STR/STS appropriate utilization of cardiovascular imaging in emergency department patients with chest pain: A Joint Document of the American College of Radiology Appropriateness Criteria Committee and the American College of Cardiology Appropriate use Criteria Task Force. J Am Coll Radiol 2016;13:e1-29.
Rogowski S, Maeder MT, Weilenmann D, Haager PK, Ammann P, Rohner F, et al.
Spontaneous coronary artery dissection: Angiographic follow-up and long-term clinical outcome in a predominantly medically treated population. Catheter Cardiovasc Interv 2017;89:59-68.
Alfonso F, Paulo M, Dutary J. Endovascular imaging of angiographically invisible spontaneous coronary artery dissection. JACC Cardiovasc Interv 2012;5:452-3.
Alfonso F, Bastante T, García-Guimaraes M, Pozo E, Cuesta J, Rivero F, et al.
Spontaneous coronary artery dissection: New insights into diagnosis and treatment. Coron Artery Dis 2016;27:696-706.
Alkhouli M, Cole M, Ling FS. Coronary artery fenestration prior to stenting in spontaneous coronary artery dissection. Catheter Cardiovasc Interv 2016;88:E23-7.
Panoulas VF, Ielasi A. Bioresorbable scaffolds and drug-eluting balloons for the management of spontaneous coronary artery dissections. J Thorac Dis 2016;8:E1328-30.
Hayes SN, Kim ESH, Saw J, Adlam D, Arslanian-Engoren C, Economy KE, et al.
Spontaneous coronary artery dissection: Current state of the science: A scientific statement from the American Heart Association. Circulation 2018;137:e523-57.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]