Spontaneous coronary artery dissection pathophysiology: Difference between revisions

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__NOTOC__
__NOTOC__
{{Spontaneous coronary artery dissection}}
{{Spontaneous coronary artery dissection}}
{{CMG}}; {{AE}}{{NRM}}
{{CMG}}; {{AE}} {{AKK}}; {{NRM}}


{{SK}} SCAD
{{SK}} SCAD
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==Overview==
==Overview==


At present, the [[pathophysiology]] of [[non-atherosclerotic]] [[spontaneous coronary artery dissection]] (NA-[[SCAD]]) continues to be poorly understood due to the rarity of this condition and its heterogeneous [[pathology]]. Although [[intimal tear]] or [[bleeding]] of [[vasa vasorum]] with intermedial [[hemorrhage]] seems to be the most probable reason, the exact underlying mechanism is still unknown. In a [[SCAD]] registry, a total of 5% to 8% of [[patients]] were carriers of [[genetic]] [[mutations]] for [[connective tissue disorders]]. [[SCAD]] may also be associated with a variety of disorders including but not limited to [[fibromuscular dysplasia]], [[Connective tissue disorders]], and [[autoimmune diseases]] such as [[systemic lupus erythematous]].


==Pathophysiology==


==Pathophysiology==
*NA-[[SCAD]] can develop in any [[layer]] ([[intima]] , [[media]], or [[adventitia]]) of the [[coronary artery]] wall.
*The initiation and the pattern of dissection in NA-[[SCAD]] is different from the pattern observed in [[patients]] with pre-existing [[atherosclerosis]].
*The plane of [[dissection]] mostly occurs within the outer third of the [[tunica media]] or between the [[media]] and [[adventitia]] in NA-[[SCAD]].
* [[Dissections]] can be present within either one [[artery]] or several [[arteries]] concomitantly in this state.<ref name="pmid22800852">{{cite journal| author=Alfonso F| title=Spontaneous coronary artery dissection: new insights from the tip of the iceberg? | journal=Circulation | year= 2012 | volume= 126 | issue= 6 | pages= 667-70 | pmid=22800852 | doi=10.1161/CIRCULATIONAHA.112.122093 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22800852  }} </ref><ref name="pmid12403896">{{cite journal |author=Choi JW, Davidson CJ |title=Spontaneous multivessel coronary artery dissection in a long-distance runner successfully treated with oral antiplatelet therapy |journal=[[The Journal of Invasive Cardiology]] |volume=14 |issue=11 |pages=675–8 |year=2002 |pmid=12403896}}</ref>
'''Two possible mechanisms have been described for the [[arterial]] wall separation:''' <ref name="pmid27417009">{{cite journal| author=Saw J, Mancini GBJ, Humphries KH| title=Contemporary Review on Spontaneous Coronary Artery Dissection. | journal=J Am Coll Cardiol | year= 2016 | volume= 68 | issue= 3 | pages= 297-312 | pmid=27417009 | doi=10.1016/j.jacc.2016.05.034 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27417009  }} </ref>
*The first one is [[intimal]] tear hypothesis, in which [[intramural]] [[blood]] accumulation may develop through a primary entry tear which occurs due to the damaged [[intimal]] surface and causes separation of the [[arterial]] wall.
*The second one is, [[medial]] [[haemorrhage]] hypothesis, in which spontaneous rupture of newly formed [[vasa vasorum]] in response to [[injury]] can cause a [[haemorrhage]] within between the [[arterial]] wall [[layers]].
*Both of them result in a creation of false [[lumen]] filled with [[intramural]] [[haematoma]]. <ref name="pmid25336602">{{cite journal| author=Alfonso F, Bastante T| title=Spontaneous coronary artery dissection: novel diagnostic insights from large series of patients. | journal=Circ Cardiovasc Interv | year= 2014 | volume= 7 | issue= 5 | pages= 638-41 | pmid=25336602 | doi=10.1161/CIRCINTERVENTIONS.114.001984 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25336602  }} </ref>
*High pressure of the [[hematoma]] within the [[arterial]] wall may lead to a [[rupture]] through the intima and create a “reverse” [[intimal]] rupture.
*Furthermore, increasing pressure of enlarging [[haematoma]] in the false [[lumen]] may also lead to [[luminal]] compression and precipitate [[myocardial ischemia]] and [[infarction]]. [[Thrombus]] can occur in both true and false [[lumen]].
*[[Thrombosis]] of the true [[lumen]] mostly originates from [[intimal]] rupture sites.
*The current literature remains controversial regarding whether there is a [[thrombosis]] in the true [[lumen]] in patients with NA-[[SCAD]].
*Two [[angiographic]] and one [[optical coherence tomography]] (OCT) studies have proposed that there was no [[thrombus]] in the arterial true [[lumen]]. <ref name="pmid25294399">{{cite journal| author=Saw J, Aymong E, Sedlak T, Buller CE, Starovoytov A, Ricci D et al.| title=Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. | journal=Circ Cardiovasc Interv | year= 2014 | volume= 7 | issue= 5 | pages= 645-55 | pmid=25294399 | doi=10.1161/CIRCINTERVENTIONS.114.001760 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25294399  }} </ref> <ref name="pmid25406203">{{cite journal| author=Tweet MS, Eleid MF, Best PJ, Lennon RJ, Lerman A, Rihal CS et al.| title=Spontaneous coronary artery dissection: revascularization versus conservative therapy. | journal=Circ Cardiovasc Interv | year= 2014 | volume= 7 | issue= 6 | pages= 777-86 | pmid=25406203 | doi=10.1161/CIRCINTERVENTIONS.114.001659 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25406203  }} </ref> <ref name="pmid26198289">{{cite journal| author=Saw J, Mancini GB, Humphries K, Fung A, Boone R, Starovoytov A et al.| title=Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging. | journal=Catheter Cardiovasc Interv | year= 2016 | volume= 87 | issue= 2 | pages= E54-61 | pmid=26198289 | doi=10.1002/ccd.26022 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26198289  }} </ref>
* Another [[OCT]] study has detected some insignificant [[thrombosis]] in the false and also true [[lumen]].<ref name="pmid22421300">{{cite journal| author=Alfonso F, Paulo M, Gonzalo N, Dutary J, Jimenez-Quevedo P, Lennie V et al.| title=Diagnosis of spontaneous coronary artery dissection by optical coherence tomography. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 12 | pages= 1073-9 | pmid=22421300 | doi=10.1016/j.jacc.2011.08.082 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22421300  }} </ref>
*[[Atherosclerotic]] variant of [[SCAD]] has basically different characteristic which only includes medial [[atrophy]] and [[scarring]]. <ref name="pmid3776849">{{cite journal| author=Isner JM, Donaldson RF, Fortin AH, Tischler A, Clarke RH| title=Attenuation of the media of coronary arteries in advanced atherosclerosis. | journal=Am J Cardiol | year= 1986 | volume= 58 | issue= 10 | pages= 937-9 | pmid=3776849 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3776849  }} </ref>
*Unlike the [[atherosclerotic]] pattern, NA-[[SCAD]] can have an expanded [[dissection]] particularly in the presence of an underlying [[arteriopathy]] which makes the [[arterial]] wall more fragile.
* [[Intracoronary imaging]] studies showed  that NA-[[SCAD]] cases have a normal [[intimal]] structure. <ref name="pmid26198289">{{cite journal| author=Saw J, Mancini GB, Humphries K, Fung A, Boone R, Starovoytov A et al.| title=Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging. | journal=Catheter Cardiovasc Interv | year= 2016 | volume= 87 | issue= 2 | pages= E54-61 | pmid=26198289 | doi=10.1002/ccd.26022 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26198289  }} </ref> <ref name="pmid22421300">{{cite journal| author=Alfonso F, Paulo M, Gonzalo N, Dutary J, Jimenez-Quevedo P, Lennie V et al.| title=Diagnosis of spontaneous coronary artery dissection by optical coherence tomography. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 12 | pages= 1073-9 | pmid=22421300 | doi=10.1016/j.jacc.2011.08.082 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22421300  }} </ref>
* [[Pregnancy]] is a significant risk factor for NA-[[SCAD]].
* Some negative effects of [[hormones]] and elevated [[hemodynamic stress]] make the [[coronary]] [[arterial]] wall weak during [[pregnancy]].<ref name="pmid8665336">{{cite journal| author=Basso C, Morgagni GL, Thiene G| title=Spontaneous coronary artery dissection: a neglected cause of acute myocardial ischaemia and sudden death. | journal=Heart | year= 1996 | volume= 75 | issue= 5 | pages= 451-4 | pmid=8665336 | doi= | pmc=484340 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8665336  }} </ref>
*Multiparty causes a longer exposure to [[pregnancy]]-associated changes which result in an increased risk of [[SCAD]].<ref name="pmid25403597">{{cite journal| author=Vijayaraghavan R, Verma S, Gupta N, Saw J| title=Pregnancy-related spontaneous coronary artery dissection. | journal=Circulation | year= 2014 | volume= 130 | issue= 21 | pages= 1915-20 | pmid=25403597 | doi=10.1161/CIRCULATIONAHA.114.011422 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25403597  }} </ref> Histological analyses revealed a periarteritis including eosinophilic infiltrates in the tunica adventitia that may lead to a separation of the arterial wall layers resulting in dissection.
* On the other hand this [[inflammatory]] state could be a response to the [[dissection]] instead of being an underlying [[mechanism]]. <ref name="pmid22421300">{{cite journal| author=Alfonso F, Paulo M, Gonzalo N, Dutary J, Jimenez-Quevedo P, Lennie V et al.| title=Diagnosis of spontaneous coronary artery dissection by optical coherence tomography. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 12 | pages= 1073-9 | pmid=22421300 | doi=10.1016/j.jacc.2011.08.082 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22421300  }} </ref>
*A retrospective study has shown the relationship between [[coronary artery tortuosity]] and SCAD. <ref name="pmid25138034">{{cite journal| author=Eleid MF, Guddeti RR, Tweet MS, Lerman A, Singh M, Best PJ et al.| title=Coronary artery tortuosity in spontaneous coronary artery dissection: angiographic characteristics and clinical implications. | journal=Circ Cardiovasc Interv | year= 2014 | volume= 7 | issue= 5 | pages= 656-62 | pmid=25138034 | doi=10.1161/CIRCINTERVENTIONS.114.001676 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25138034}} </ref>.
* An association has  been described between [[coronary]] [[tortuosity]] and [[fibromuscular dysplasia]].
* [[Tortuosity]] is a consequence of an underlying [[vasculopathy]] likewise [[dissection]]. <ref name="pmid26957531">{{cite journal| author=Saw J, Bezerra H, Gornik HL, Machan L, Mancini GB| title=Angiographic and Intracoronary Manifestations of Coronary Fibromuscular Dysplasia. | journal=Circulation | year= 2016 | volume= 133 | issue= 16 | pages= 1548-59 | pmid=26957531 | doi=10.1161/CIRCULATIONAHA.115.020282 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26957531  }} </ref> <ref name="pmid27417009">{{cite journal| author=Saw J, Mancini GBJ, Humphries KH| title=Contemporary Review on Spontaneous Coronary Artery Dissection. | journal=J Am Coll Cardiol | year= 2016 | volume= 68 | issue= 3 | pages= 297-312 | pmid=27417009 | doi=10.1016/j.jacc.2016.05.034 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27417009  }} </ref>
 
{|
|
[[File:Scad image-pathology.jpg|500px|thumb|
[[Hematoxylin]] and trichrome stain of the [[coronary artery]] demonstrating an [[intramural hematoma]] compressing the vessel [[lumen]] from outside.
<BR>
<font size="-2">'''''(Adapted from [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3603681/figure/BJSPORTS2012091415F3/ Br J Sports Med. 2012; 46(Suppl_1): i15–i21.] under [http://creativecommons.org/licenses/by-nc/3.0/ CC BY-NC] license)'''''</font>
<ref name="pmid23097474">{{cite journal| author=Sheppard MN| title=Aetiology of sudden cardiac death in sport: a histopathologist's perspective. | journal=Br J Sports Med | year= 2012 | volume= 46 Suppl 1 | issue=  | pages= i15-21 | pmid=23097474 | doi=10.1136/bjsports-2012-091415 | pmc=3603681 | url=http://bjsm.bmj.com/content/bjsports/46/Suppl_1/i15/F3.large.jpg}} </ref>
]]
|}


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.<ref name="pmid12403896">{{cite journal |author=Choi JW, Davidson CJ |title=Spontaneous multivessel coronary artery dissection in a long-distance runner successfully treated with oral antiplatelet therapy |journal=[[The Journal of Invasive Cardiology]] |volume=14 |issue=11 |pages=675–8 |year=2002 |month=November |pmid=12403896 |doi= |url=}}</ref> 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).
==Genetics==
*In a [[SCAD]] registry, a total of 5% to 8% of [[patients]] with [[SCAD]] were carriers of [[genetic]] [[mutations]] for [[connective tissue disorders]].<br>
*[[Genes]] involved in the pathogenesis of [[SCAD]] include but not limited to:<br>
*[[COL3A1]] <ref name="poster">{{cite journal|doi=10.1161/circ.138.suppl_1.15404 and 28570239}}</ref>
*[[FBN1]] <ref name="LitwokLau2019">{{cite journal|last1=Litwok|first1=Yonathan|last2=Lau|first2=Joe|last3=Soni|first3=Mihir|title=THE ASSOCIATION OF CONNECTIVE TISSUE DISEASE AND CORONARY VASCULATURE: A CASE REPORT OF SPONTANEOUS CORONARY ARTERY DISSECTION IN A YOUNG FEMALE|journal=Journal of the American College of Cardiology|volume=73|issue=9|year=2019|pages=2675|issn=07351097|doi=10.1016/S0735-1097(19)33281-4}}</ref>
*[[COL4A5]] <ref name="poster">{{cite journal|doi=10.1161/circ.138.suppl_1.15404}}</ref>
*[[PKD1]] <ref name="pmid26069747">{{cite journal |vauthors=Klingenberg-Salachova F, Limburg S, Boereboom F |title=Spontaneous coronary artery dissection in polycystic kidney disease |journal=Clin Kidney J |volume=5 |issue=1 |pages=44–6 |date=February 2012 |pmid=26069747 |pmc=4400459 |doi=10.1093/ndtplus/sfr158 |url=}}</ref><ref name="pmid19557720">{{cite journal |vauthors=Basile C, Lucarelli K, Langialonga T |title=Spontaneous coronary artery dissection: One more extrarenal manifestation of autosomal dominant polycystic kidney disease? |journal=J Nephrol |volume=22 |issue=3 |pages=414–6 |date=2009 |pmid=19557720 |doi= |url=}}</ref>
*[[PKD2]] <ref name="pmid26069747">{{cite journal |vauthors=Klingenberg-Salachova F, Limburg S, Boereboom F |title=Spontaneous coronary artery dissection in polycystic kidney disease |journal=Clin Kidney J |volume=5 |issue=1 |pages=44–6 |date=February 2012 |pmid=26069747 |pmc=4400459 |doi=10.1093/ndtplus/sfr158 |url=}}</ref>
*[[SMAD3]] <ref name="pmid27986426">{{cite journal |vauthors=Garcia-Bermúdez M, Moustafa AH, Barrós-Membrilla A, Tizón-Marcos H |title=Repeated Loss of Consciousness in a Young Woman: A Suspicious SMAD3 Mutation Underlying Spontaneous Coronary Artery Dissection |journal=Can J Cardiol |volume=33 |issue=2 |pages=292.e1–292.e3 |date=February 2017 |pmid=27986426 |doi=10.1016/j.cjca.2016.09.004 |url=}}</ref><ref name="pmid26409702">{{cite journal |vauthors=Blinc A, Maver A, Rudolf G, Tasič J, Pretnar Oblak J, Berden P, Peterlin B |title=Clinical Exome Sequencing as a Novel Tool for Diagnosing Loeys-Dietz Syndrome Type 3 |journal=Eur J Vasc Endovasc Surg |volume=50 |issue=6 |pages=816–21 |date=December 2015 |pmid=26409702 |doi=10.1016/j.ejvs.2015.08.003 |url=}}</ref>
*[[COL1A1]] <ref name="poster">{{cite journal|doi=10.1161/circ.138.suppl_1.15404}}</ref>
*[[COL1A2]] <ref name="poster">{{cite journal|doi=10.1161/circ.138.suppl_1.15404}}</ref>


Although intimal tear or bleeding of vasa vasorum with intramedial hemorrhage seems to be most probable reason, the exact underlying mechanism of non-atherosclerotic spontaneous coronary artery dissection (NA-SCAD) is still unknown [1]. Consequently intramural hematoma creates a false lumen [2]. Progressive expansion of the false lumen may cause subsequent myocardial ischemia and infarction.
==Associated Conditions==
[[Conditions]] associated with SCAD include:
*[[Connective tissue disorders]] such as: <ref name="HenkinNegrotto2016">{{cite journal|last1=Henkin|first1=Stanislav|last2=Negrotto|first2=Sara M|last3=Tweet|first3=Marysia S|last4=Kirmani|first4=Salman|last5=Deyle|first5=David R|last6=Gulati|first6=Rajiv|last7=Olson|first7=Timothy M|last8=Hayes|first8=Sharonne N|title=Spontaneous coronary artery dissection and its association with heritable connective tissue disorders|journal=Heart|volume=102|issue=11|year=2016|pages=876–881|issn=1355-6037|doi=10.1136/heartjnl-2015-308645}}</ref>
**[[Vascular]] [[Ehlers–Danlos syndrome]]
**[[Marfan’s syndrome]]
**[[Loeys–Dietz syndrome]]
*[[Pregnancy]] <ref name="FadenBottega2016">{{cite journal|last1=Faden|first1=Majed S|last2=Bottega|first2=Natalie|last3=Benjamin|first3=Alice|last4=Brown|first4=Richard N|title=A nationwide evaluation of spontaneous coronary artery dissection in pregnancy and the puerperium|journal=Heart|volume=102|issue=24|year=2016|pages=1974–1979|issn=1355-6037|doi=10.1136/heartjnl-2016-309403}}</ref>
*[[Fibromuscular dysplasia]] <ref name="LieBerg1987">{{cite journal|last1=Lie|first1=J.T.|last2=Berg|first2=K.K.|title=Isolated fibromuscular dysplasia of the coronary arteries with spontaneous dissection and myocardial infarction|journal=Human Pathology|volume=18|issue=6|year=1987|pages=654–656|issn=00468177|doi=10.1016/S0046-8177(87)80368-4}}</ref>
**In a prospective cohort of SCAD [[patients]], approximately 50% demonstrated the evidence of [[fibromuscular dysplasia]].<ref name="KimLongo2020">{{cite journal|last1=Kim|first1=Esther S.H.|last2=Longo|first2=Dan L.|title=Spontaneous Coronary-Artery Dissection|journal=New England Journal of Medicine|volume=383|issue=24|year=2020|pages=2358–2370|issn=0028-4793|doi=10.1056/NEJMra2001524}}</ref>
*[[Inflammatory]] [[disorders]] such as:
**[[Systemic lupus erythematosus]] <ref name="ReddyVaid2016">{{cite journal|last1=Reddy|first1=Sravan|last2=Vaid|first2=Tejasvini|last3=Ganiga Sanjeeva|first3=Naveen Chandra|last4=Shetty|first4=Ranjan K|title=Spontaneous coronary artery dissection as the first presentation of systemic lupus erythematosus|journal=BMJ Case Reports|year=2016|pages=bcr2016216344|issn=1757-790X|doi=10.1136/bcr-2016-216344}}</ref>
**[[Sarcoidosis]] <ref name="KanaroglouNair2015">{{cite journal|last1=Kanaroglou|first1=Savas|last2=Nair|first2=Vidhya|last3=Fernandes|first3=John R|title=Sudden cardiac death due to coronary artery dissection as a complication of cardiac sarcoidosis|journal=Cardiovascular Pathology|volume=24|issue=4|year=2015|pages=244–246|issn=10548807|doi=10.1016/j.carpath.2015.01.001}}</ref>
**[[Celiac disease]] <ref name="BayarÇağırcı2015">{{cite journal|last1=Bayar|first1=Nermin|last2=Çağırcı|first2=Göksel|last3=Üreyen|first3=Çağın Mustafa|last4=Kuş|first4=Görkem|last5=Küçükseymen|first5=Selçuk|last6=Arslan|first6=Şakir|title=The Relationship between Spontaneous Multi-Vessel Coronary Artery Dissection and Celiac Disease|journal=Korean Circulation Journal|volume=45|issue=3|year=2015|pages=242|issn=1738-5520|doi=10.4070/kcj.2015.45.3.242}}</ref>


==References==
==References==  
{{Reflist|2}}
{{Reflist|2}}


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[[Category:Angiographic Definitions]]
[[Category:Angiographic Definitions]]
[[Category:Disease]]
[[Category:Disease]]
[[Category:Up-to-date]]

Latest revision as of 23:30, 5 May 2021

Spontaneous Coronary Artery Dissection Microchapters

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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]; Nate Michalak, B.A.

Synonyms and keywords: SCAD

Overview

At present, the pathophysiology of non-atherosclerotic spontaneous coronary artery dissection (NA-SCAD) continues to be poorly understood due to the rarity of this condition and its heterogeneous pathology. Although intimal tear or bleeding of vasa vasorum with intermedial hemorrhage seems to be the most probable reason, the exact underlying mechanism is still unknown. In a SCAD registry, a total of 5% to 8% of patients were carriers of genetic mutations for connective tissue disorders. SCAD may also be associated with a variety of disorders including but not limited to fibromuscular dysplasia, Connective tissue disorders, and autoimmune diseases such as systemic lupus erythematous.

Pathophysiology

Two possible mechanisms have been described for the arterial wall separation: [3]

Hematoxylin and trichrome stain of the coronary artery demonstrating an intramural hematoma compressing the vessel lumen from outside.
(Adapted from Br J Sports Med. 2012; 46(Suppl_1): i15–i21. under CC BY-NC license) [14]

Genetics

Associated Conditions

Conditions associated with SCAD include:

References

  1. Alfonso F (2012). "Spontaneous coronary artery dissection: new insights from the tip of the iceberg?". Circulation. 126 (6): 667–70. doi:10.1161/CIRCULATIONAHA.112.122093. PMID 22800852.
  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.
  3. 3.0 3.1 Saw J, Mancini GBJ, Humphries KH (2016). "Contemporary Review on Spontaneous Coronary Artery Dissection". J Am Coll Cardiol. 68 (3): 297–312. doi:10.1016/j.jacc.2016.05.034. PMID 27417009.
  4. Alfonso F, Bastante T (2014). "Spontaneous coronary artery dissection: novel diagnostic insights from large series of patients". Circ Cardiovasc Interv. 7 (5): 638–41. doi:10.1161/CIRCINTERVENTIONS.114.001984. PMID 25336602.
  5. 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.
  6. Tweet MS, Eleid MF, Best PJ, Lennon RJ, Lerman A, Rihal CS; et al. (2014). "Spontaneous coronary artery dissection: revascularization versus conservative therapy". Circ Cardiovasc Interv. 7 (6): 777–86. doi:10.1161/CIRCINTERVENTIONS.114.001659. PMID 25406203.
  7. 7.0 7.1 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.
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