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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Arzu Kalayci, M.D. [2] Associate Editor(s)-in-Chief: Nate Michalak, B.A.

Synonyms and keywords: SCAD

Overview

Spontaneous coronary artery dissection (SCAD) is a rare, but under recognized cause of acute coronary syndrome and sudden cardiac death,[1] which predominantly affects young, healthy women with few to no traditional cardiovascular risk factors. Heightened awareness along with advances in intracoronary imaging techniques have led to an increase in the number of SCAD cases reported antemortem. Multiple risk factors and precipitating stressors have been identified for SCAD, including fibromuscular dysplasia (FMD), connective tissue disorders, systemic inflammatory disorders, pregnancy and the peripartum state, hormonal therapy, and extreme physical exertion and/or emotional stress. In the majority of cases, conservative medical management is the optimal treatment strategy; however, based on the patient's clinical status and anatomy of the coronary dissection, revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) may be warranted. Based on the limited outcomes data, SCAD survivors typically have a good long-term prognosis; however, there is an increased risk for recurrent SCAD events as well as other major cardiovascular events. Future studies are needed to further elucidate the underlying pathophysiology of this complex disorder as well as to gain a better understanding of the optimal treatment strategies and long-term outcomes of this unique patient population.

Pathophysiology

At present the pathophysiology of SCAD continues to be poorly understood due to the rarity of this condition and its heterogeneous pathology. In SCAD the affected coronary artery develops a tear, causing blood to flow between the coronary arterial layers eventually forcing them apart. The pattern of dissection in SCAD is different from the pattern observed in patients with pre-existing atherosclerosis. In SCAD the plane of dissection lies within the outer third of the tunica media or between the media and adventitia. Dissections can be present in either one artery or several arteries concomitantly.[2] The dissecting plane between intima and media creates a false lumen and the resulting hematoma compresses the vessel lumen causing myocardial ischemia or myocardial infarction (MI).

Classification

SCAD may be classified according to its angiographic features:[3][4]

Type Characteristic Features
Type 1
  • Pathognomonic multiple radiolucent lumen
  • Contrast dye staining of arterial wall
  • Presence or absence of dye hang-up or slow contrast clearing from the lumen
Type 2
  • Diffuse (typically >20–30 mm)
  • Smooth narrowing varying in severity (ranging from 40 to 100% stenosis)
  • No response to intracoronary nitroglycerin
  • No atherosclerotic lesions in other coronary arteries
  • Repeat coronary angiogram showing spontaneous resolution of the dissected segment or previous angiogram showing normal artery
  • Intracoronary imaging with OCT or IVUS proving the presence of intramural hematoma and double-lumen
2A Variant Normal arterial caliber proximal and distal to dissection
2B Variant Dissection extends to the distal tip of the artery without discernible normal segment distally
Type 3
  • Mimics atherosclerosis with focal or tubular stenosis
  • Lack of atherosclerotic changes in other coronary arteries
  • Long lesions (11–20 mm)
  • Hazy stenosis
  • Linear stenosis
  • Note: requires OCT or IVUS to prove the presence of intramural hematoma or double-lumen


Shown below are animated and static angiography images exemplifying each type of SCAD. For additional angiographic images of SCAD, click here.

Type 1

Projection angle: 14 RAO, 35 CRA. Type 1 SCAD is seen in OM2.

Type 2A

Projection angle: 5 LAO, 34 CRA. Type 2A SCAD is seen in L3.

Type 2B

Projection angle: 30 RAO, 1 CRA. Type 2B SCAD is seen in OM2.

Type 3

Projection angle: 1 LAO, 35 CRA. Type 3 SCAD is seen in D1.

Differential Diagnosis

While Type 1 SCAD has a pathognomonic appearance on angiography, Type 2 may be and Type 3 typically is indistinguishable from atherosclerosis. Risk factors and patient history may help determine diagnosis. Intracoronary imaging provides the most objective tool in differentiating between SCAD and atheroma.[5]

Epidemiology and Demographics

Based on the relatively limited data that is currently available, the estimated incidence of SCAD is approximately 800 new cases per year in the US.[6] SCAD has a strong predilection for young women with no or minimal traditional atherosclerotic risk factors. Studies indicate that SCAD accounts for approximately 25% of women aged < 50 who present with MI.[7] SCAD should be highly suspected in any young subject presenting with acute myocardial ischemia, but without traditional risk factors for coronary artery disease (CAD).The left anterior descending artery (LAD) is the most commonly affected artery.[8][9] Although multivessel SCAD has been reported, single vessel SCAD is much more common. In women LAD is frequently involved[8] while in men right coronary artery is involved more often. Men tend to present at a slightly later age and also with evidence of CAD risk factors.

Observational studies have reported that SCAD is common among young women during their peripartum period[10] or in association with use of oral contraceptives. About 80% of SCAD cases reported so far have occurred in young women, especially those taking oral contraceptives (OCPs) or those in the peripartum period.[11][12][13] Possible mechanisms underlying increased prevalence of SCAD in this population include: changes in the arterial wall media due to increasing hormone levels, shear stress during labor, fragmentation of reticulin fibers, loosening of ground substance, and hypertrophy of smooth muscle.[14]

A strong association between SCAD and FMD has been reported in the literature.[6][15][16] The presence of underlying FMD is postulated to predispose affected individuals to arterial dissections. Extreme emotional stress and/or strenuous physical activity have also been identified as associated risk factors for SCAD.[2][15][16]

The prevalence of each type of SCAD is as follows:[3]

  • Type 1: <30%
  • Type 2: approximately 66%
  • Type 3: <5%

Risk Factors

Natural History, Complications and Prognosis

Natural History

The fact that the diagnosis was made so often in the past on autopsy speaks to the poor clinical outcomes that have been associated with the condition. Outcomes in the modern era of stent placement and improved antithrombins may be improved, but solid data are lacking. Based on the limited outcomes data, SCAD survivors typically have a good long-term prognosis. Majority of cases result in spontaneous healing, with improvement starting after several weeks and resolution at approximately 1-2 years.[3] However, there is an increased risk for recurrent SCAD events as well as other major cardiovascular events.[6]

Complications

Complications include:

Prognosis

Good prognosis is associated with:

  • Small, limited dissections
  • Incomplete or lesser degree of lumen obstruction

Bad prognosis is associated with:

Long term survival after an index SCAD episode appears to be better compared with that of acute coronary syndrome. However, rates of major adverse cardiac events (MACE) resulting from index episode and complications are similar.

Diagnosis

Symptoms

The symptoms of SCAD mimic other acute coronary syndromes. Patients may present with chronic stable angina, myocardial infarction[12], cardiogenic shock, sudden death and/or pericardial tamponade. 50% of sudden death cases were reported to have dissections in the left main coronary artery.

Imaging

Angiography

In the past, this disorder was often diagnosed only at the time of autopsy.[25] At present, however, angiography is most often used to diagnose SCAD.[9] Angiographic findings include:

  • Type 1: appearance on an angiography involves the presence of two intraluminal streams/lumens separated by a radioluscent flap of intima.
  • Type 2: when the dissection plane is deeper in the vessel wall between the media and adventitial layers, formation of a hematoma can result in luminal narrowing which is seen as a stenosis on an angiography.
  • Type 3: appearance mimics atherosclerosis. The dissection is typically shorter than that of type 2 (< 20 mm) and may have a hazy appearance.

Intravascular Ultrasound and Optical Coherence Tomogrpahy

In the event that diagnosis of SCAD based on angiography is ambiguous, intravascular ultrasound (IVUS)[26][27][28] or optical coherence tomography (OCT)[29] can be used for diagnostic clarification. In fact, a definitive diagnosis of type 3 SCAD requires OCT or IVUS.[4] IVUS/OCT should be considered the gold standard in diagnosing SCAD. OCT may be preferred to IVUS due to superiority in spatial resolution and clarity in identifying intramural hematomas and intimal tears, though IVUS is still quite adequate.[3]

Treatment

Medical Therapy

There are no specific guidelines regarding the optimal management of spontaneous coronary artery dissection. Based on the clinical and angiographic scenario, treatment options include conservative medical regimens similar to that for acute coronary syndrome, percutaneous coronary intervention, and/or coronary artery bypass surgery. In the majority of cases, SCAD may be managed successfully with medical treatment alone in the absence of ongoing myocardial ischemia or hemodynamic instability.[15][30] Initial conservative management typically includes antithrombotic therapy with heparin, aspirin, clopidogrel and glycoprotein IIb/IIIa inhibitors, and antiischemic therapy with beta blockers and nitrates. However, the use of antithrombotic therapy may increase the risk of bleeding in the false lumen causing an expansion of the intramural hematoma, resulting in a decreased flow through the true lumen.[31] Fibrinolytics should be avoided. Calcium channel blockers may offer relief in coronary artery spasm.

Percutaneous Coronary Intervention

PCI is indicated in the presence of ongoing myocardial ischemia or myocardial infarction.[32] Drug eluting stents (DES) are routinely used in the management of SCAD. However, their impact on long-term outcomes has not been assessed yet in clinical studies.

Surgery

Indications for surgical revascularization (CABG)[33] include:

  • Multivessel involvement
  • Left main coronary artery involvement
  • Progression/worsening of dissection so long as there is a distal target
  • Significant narrowing of the arterial lumen
  • Refractory or recurrent myocardial ischemia

In the event of severe refractory heart failure, heart transplantation may be considered.

References

  1. ↑ 1.0 1.1 Basso C, Morgagni GL, Thiene G (1996). "Spontaneous coronary artery dissection: a neglected cause of acute myocardial ischaemia and sudden death". Heart. 75 (5): 451–4. PMC 484340. PMID 8665336.
  2. ↑ 2.0 2.1 2.2 Choi JW, Davidson CJ (2002). "Spontaneous multivessel coronary artery dissection in a long-distance runner successfully treated with oral antiplatelet therapy". The Journal of Invasive Cardiology. 14 (11): 675–8. PMID 12403896. Unknown parameter |month= ignored (help)
  3. ↑ 3.0 3.1 3.2 3.3 Saw J (2014). "Coronary angiogram classification of spontaneous coronary artery dissection". Catheter Cardiovasc Interv. 84 (7): 1115–22. doi:10.1002/ccd.25293. PMID 24227590.
  4. ↑ 4.0 4.1 Saw J, Mancini GB, Humphries K, Fung A, Boone R, Starovoytov A; et al. (2016). "Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging". Catheter Cardiovasc Interv. 87 (2): E54–61. doi:10.1002/ccd.26022. PMID 26198289.
  5. ↑ Yip A, Saw J (2015). "Spontaneous coronary artery dissection-A review". Cardiovasc Diagn Ther. 5 (1): 37–48. doi:10.3978/j.issn.2223-3652.2015.01.08. PMC 4329168. PMID 25774346.
  6. ↑ 6.0 6.1 6.2 6.3 Tweet, MS.; Hayes, SN.; Pitta, SR.; Simari, RD.; Lerman, A.; Lennon, RJ.; Gersh, BJ.; Khambatta, S.; Best, PJ. (2012). "Clinical features, management, and prognosis of spontaneous coronary artery dissection". Circulation. 126 (5): 579–88. doi:10.1161/CIRCULATIONAHA.112.105718. PMID 22800851. Unknown parameter |month= ignored (help)
  7. ↑ Saw J, Aymong E, Mancini GB, Sedlak T, Starovoytov A, Ricci D (2014). "Nonatherosclerotic coronary artery disease in young women". Can J Cardiol. 30 (7): 814–9. doi:10.1016/j.cjca.2014.01.011. PMID 24726091.
  8. ↑ 8.0 8.1 Vanzetto G, Berger-Coz E, Barone-Rochette G; et al. (2009). "Prevalence, therapeutic management and medium-term prognosis of spontaneous coronary artery dissection: results from a database of 11,605 patients". European Journal of Cardio-thoracic Surgery : Official Journal of the European Association for Cardio-thoracic Surgery. 35 (2): 250–4. doi:10.1016/j.ejcts.2008.10.023. PMID 19046896. Unknown parameter |month= ignored (help)
  9. ↑ 9.0 9.1 Kamran M, Guptan A, Bogal M (2008). "Spontaneous coronary artery dissection: case series and review". J Invasive Cardiol. 20 (10): 553–9. PMID 18830003. Unknown parameter |month= ignored (help)
  10. ↑ 10.0 10.1 Fontanelli A, Olivari Z, La Vecchia L; et al. (2009). "Spontaneous dissections of coronary arteries and acute coronary syndromes: rationale and design of the DISCOVERY, a multicenter prospective registry with a case-control group". Journal of Cardiovascular Medicine (Hagerstown, Md.). 10 (1): 94–9. PMID 19708230. Unknown parameter |month= ignored (help)
  11. ↑ Narasimhan, S (2004). "Spontaneous coronary artery dissection (SCAD)" (PDF). IJTCVS. 20 (4): 189–91. doi:10.1007/s12055-004-0084-x.
  12. ↑ 12.0 12.1 Zampieri P, Aggio S, Roncon L; et al. (1996). "Follow up after spontaneous coronary artery dissection: a report of five cases". Heart (British Cardiac Society). 75 (2): 206–9. PMC 484263. PMID 8673763. Unknown parameter |month= ignored (help)
  13. ↑ Cohen DE, Strimike CL (2000). "A case of multiple spontaneous coronary artery dissections". Catheterization and Cardiovascular Interventions : Official Journal of the Society for Cardiac Angiography & Interventions. 49 (3): 318–20. PMID 10700066. Unknown parameter |month= ignored (help)
  14. ↑ Van den Branden BJ, Bruggeling WA, Corbeij HM, Dunselman PH (2008). "Spontaneous coronary artery dissection in the postpartum period". Neth Heart J. 16 (12): 412–4. PMC 2612109. PMID 19127318. Unknown parameter |month= ignored (help)
  15. ↑ 15.0 15.1 15.2 15.3 15.4 Saw J, Aymong E, Sedlak T, Buller CE, Starovoytov A, Ricci D; et al. (2014). "Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes". Circ Cardiovasc Interv. 7 (5): 645–55. doi:10.1161/CIRCINTERVENTIONS.114.001760. PMID 25294399.
  16. ↑ 16.0 16.1 16.2 16.3 16.4 Saw J, Ricci D, Starovoytov A, Fox R, Buller CE (2013). "Spontaneous coronary artery dissection: prevalence of predisposing conditions including fibromuscular dysplasia in a tertiary center cohort". JACC Cardiovasc Interv. 6 (1): 44–52. doi:10.1016/j.jcin.2012.08.017. PMID 23266235.
  17. ↑ Archives of cardiovascular diseases. Volume 102, n° 12 pages 857-858 (décembre 2009).
  18. ↑ Ijsselmuiden A, Verheye S (2009). "Cocaine-induced coronary artery dissection". JACC. Cardiovascular Interventions. 2 (10): 1031. doi:10.1016/j.jcin.2009.07.011. PMID 19850267. Unknown parameter |month= ignored (help)
  19. ↑ Jaffe BD, Broderick TM, Leier CV (1994). "Cocaine-induced coronary-artery dissection". The New England Journal of Medicine. 330 (7): 510–1. doi:10.1056/NEJM199402173300719. PMID 8289869. Unknown parameter |month= ignored (help)
  20. ↑ 20.0 20.1 Tanis W, Stella PR, Kirkels JH, Pijlman AH, Peters RH, de Man FH (2008). "Spontaneous coronary artery dissection: current insights and therapy". Neth Heart J. 16 (10): 344–9. PMC 2570766. PMID 18958258. Unknown parameter |month= ignored (help)
  21. ↑ Vijayaraghavan R, Verma S, Gupta N, Saw J (2014). "Pregnancy-related spontaneous coronary artery dissection". Circulation. 130 (21): 1915–20. doi:10.1161/CIRCULATIONAHA.114.011422. PMID 25403597.
  22. ↑ Cade JR, Szarf G, de Siqueira ME, Chaves Á, Andréa JC, Figueira HR; et al. (2016). "Pregnancy-associated spontaneous coronary artery dissection: insights from a case series of 13 patients". Eur Heart J Cardiovasc Imaging. doi:10.1093/ehjci/jew021. PMID 26928981.
  23. ↑ Sherrid MV, Mieres J, Mogtader A, Menezes N, Steinberg G (1995). "Onset during exercise of spontaneous coronary artery dissection and sudden death. Occurrence in a trained athlete: case report and review of prior cases". Chest. 108 (1): 284–7. PMID 7606975. Unknown parameter |month= ignored (help)
  24. ↑ Aldoboni AH, Hamza EA, Majdi K, Ngibzadhe M, Palasaidi S, Moayed DA (2002). "Spontaneous dissection of coronary artery treated by primary stenting as the first presentation of systemic lupus erythematosus". The Journal of Invasive Cardiology. 14 (11): 694–6. PMID 12403902. Unknown parameter |month= ignored (help)
  25. ↑ Narasimhan, S (2004). "Spontaneous coronary artery dissection (SCAD)" (PDF). IJTCVS. 20 (4): 189–91. doi:10.1007/s12055-004-0084-x.
  26. ↑ Maehara A, Mintz GS, Castagna MT; et al. (2002). "Intravascular ultrasound assessment of spontaneous coronary artery dissection". The American Journal of Cardiology. 89 (4): 466–8. PMID 11835932. Unknown parameter |month= ignored (help)
  27. ↑ Porto I, Banning AP (2004). "Intravascular ultrasound imaging in the diagnosis and treatment of spontaneous coronary dissection with drug-eluting stents". The Journal of Invasive Cardiology. 16 (2): 78–80. PMID 14760197. Unknown parameter |month= ignored (help)
  28. ↑ Arnold JR, West NE, van Gaal WJ, Karamitsos TD, Banning AP (2008). "The role of intravascular ultrasound in the management of spontaneous coronary artery dissection". Cardiovascular Ultrasound. 6: 24. doi:10.1186/1476-7120-6-24. PMC 2429898. PMID 18513437.
  29. ↑ Ishibashi K, Kitabata H, Akasaka T (2009). "Intracoronary optical coherence tomography assessment of spontaneous coronary artery dissection". Heart (British Cardiac Society). 95 (10): 818. doi:10.1136/hrt.2008.158485. PMID 19401282. Unknown parameter |month= ignored (help)
  30. ↑ Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ; et al. (2012). "Clinical features, management, and prognosis of spontaneous coronary artery dissection". Circulation. 126 (5): 579–88. doi:10.1161/CIRCULATIONAHA.112.105718. PMID 22800851.
  31. ↑ Vrints, CJ. (2010). "Spontaneous coronary artery dissection". Heart. 96 (10): 801–8. doi:10.1136/hrt.2008.162073. PMID 20448134. Unknown parameter |month= ignored (help)
  32. ↑ Adlam D, Cuculi F, Lim C, Banning A (2010). "Management of spontaneous coronary artery dissection in the primary percutaneous coronary intervention era". The Journal of Invasive Cardiology. 22 (11): 549–53. PMID 21041853. Unknown parameter |month= ignored (help)
  33. ↑ Shamloo BK, Chintala RS, Nasur A; et al. (2010). "Spontaneous coronary artery dissection: aggressive vs. conservative therapy". The Journal of Invasive Cardiology. 22 (5): 222–8. PMID 20440039. Unknown parameter |month= ignored (help)

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