Spontaneous coronary artery dissection risk factors: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Spontaneous coronary artery dissection}} | {{Spontaneous coronary artery dissection}} | ||
{{CMG}}; {{AE}}{{NRM}} {{AKK}} | {{CMG}}; {{AE}} {{Sara.Zand}} {{NRM}} {{AKK}} | ||
{{SK}} SCAD | {{SK}} SCAD | ||
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==Overview== | ==Overview== | ||
The risk factors for [[spontaneous coronary artery dissection]] include predisposing factors ( [[vasculopathy]], [[pregnancy]], [[connective tissue disorder]], [[systemic inflammation]]) and precipitating stressors (e.g., [[exercise|strenuous exercise]], [[emotional stress]], [[recreational drugs]]).Features that raise the index of suspicion for [[SCAD]] include [[myocardial infarction]] in young women (age ≤50), absence of traditional [[Cardiovascular disease#Risk factors|cardiovascular risk factors]], little or no evidence of [[coronary atherosclerosis]], [[peripartum|peripartum state]], history of [[fibromuscular dysplasia]], history of [[connective tissue disorder]] or [[systemic inflammation]]. | The [[risk factors]] for [[spontaneous coronary artery dissection]] include predisposing factors ( [[vasculopathy]], [[pregnancy]], [[connective tissue disorder]], [[systemic inflammation]]) and precipitating stressors (e.g., [[exercise|strenuous exercise]], [[emotional stress]], [[recreational drugs]]).Features that raise the index of suspicion for [[SCAD]] include [[myocardial infarction]] in young women (age ≤50), absence of traditional [[Cardiovascular disease#Risk factors|cardiovascular risk factors]], little or no evidence of [[coronary atherosclerosis]], [[peripartum|peripartum state]], history of [[fibromuscular dysplasia]], history of [[connective tissue disorder]] or [[systemic inflammation]]. | ||
==Risk Factors== | ==Risk Factors== | ||
*The phenotypic manifestation of [[spontaneous coronary artery dissection]] ([[SCAD]]) may occur as a result of predisposing factors compounded by precipitating [[stressors]].<ref name="SawMancini2016">{{cite journal|last1=Saw|first1=Jacqueline|last2=Mancini|first2=G.B. John|last3=Humphries|first3=Karin H.|title=Contemporary Review on Spontaneous Coronary Artery Dissection|journal=Journal of the American College of Cardiology|volume=68|issue=3|year=2016|pages=297–312|issn=07351097|doi=10.1016/j.jacc.2016.05.034}}</ref> | *The phenotypic manifestation of [[spontaneous coronary artery dissection]] ([[SCAD]]) may occur as a result of predisposing factors compounded by precipitating [[stressors]].<ref name="SawMancini2016">{{cite journal|last1=Saw|first1=Jacqueline|last2=Mancini|first2=G.B. John|last3=Humphries|first3=Karin H.|title=Contemporary Review on Spontaneous Coronary Artery Dissection|journal=Journal of the American College of Cardiology|volume=68|issue=3|year=2016|pages=297–312|issn=07351097|doi=10.1016/j.jacc.2016.05.034}}</ref> | ||
* The potential risk factors for [[SCAD]] include:<ref name="SawAymong2014">{{cite journal|last1=Saw|first1=J.|last2=Aymong|first2=E.|last3=Sedlak|first3=T.|last4=Buller|first4=C. E.|last5=Starovoytov|first5=A.|last6=Ricci|first6=D.|last7=Robinson|first7=S.|last8=Vuurmans|first8=T.|last9=Gao|first9=M.|last10=Humphries|first10=K.|last11=Mancini|first11=G. B. J.|title=Spontaneous Coronary Artery Dissection: Association With Predisposing Arteriopathies and Precipitating Stressors and Cardiovascular Outcomes|journal=Circulation: Cardiovascular Interventions|volume=7|issue=5|year=2014|pages=645–655|issn=1941-7640|doi=10.1161/CIRCINTERVENTIONS.114.001760}}</ref><ref name="AdlamAlfonso2018">{{cite journal|last1=Adlam|first1=David|last2=Alfonso|first2=Fernando|last3=Maas|first3=Angela|last4=Vrints|first4=Christiaan|last5=al-Hussaini|first5=Abtehale|last6=Bueno|first6=Hector|last7=Capranzano|first7=Piera|last8=Gevaert|first8=Sofie|last9=Hoole|first9=Stephen P|last10=Johnson|first10=Tom|last11=Lettieri|first11=Corrado|last12=Maeder|first12=Micha T|last13=Motreff|first13=Pascal|last14=Ong|first14=Peter|last15=Persu|first15=Alexandre|last16=Rickli|first16=Hans|last17=Schiele|first17=Francois|last18=Sheppard|first18=Mary N|last19=Swahn|first19=Eva|title=European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection|journal=European Heart Journal|year=2018|issn=0195-668X|doi=10.1093/eurheartj/ehy080}}</ref> | *The presence of either predisposing or precipitating factors increases the risk of developing a [[dissection]]. | ||
* The potential risk factors for [[SCAD]] include:<ref name="SawAymong2014">{{cite journal|last1=Saw|first1=J.|last2=Aymong|first2=E.|last3=Sedlak|first3=T.|last4=Buller|first4=C. E.|last5=Starovoytov|first5=A.|last6=Ricci|first6=D.|last7=Robinson|first7=S.|last8=Vuurmans|first8=T.|last9=Gao|first9=M.|last10=Humphries|first10=K.|last11=Mancini|first11=G. B. J.|title=Spontaneous Coronary Artery Dissection: Association With Predisposing Arteriopathies and Precipitating Stressors and Cardiovascular Outcomes|journal=Circulation: Cardiovascular Interventions|volume=7|issue=5|year=2014|pages=645–655|issn=1941-7640|doi=10.1161/CIRCINTERVENTIONS.114.001760}}</ref><ref name="AdlamAlfonso2018">{{cite journal|last1=Adlam|first1=David|last2=Alfonso|first2=Fernando|last3=Maas|first3=Angela|last4=Vrints|first4=Christiaan|last5=al-Hussaini|first5=Abtehale|last6=Bueno|first6=Hector|last7=Capranzano|first7=Piera|last8=Gevaert|first8=Sofie|last9=Hoole|first9=Stephen P|last10=Johnson|first10=Tom|last11=Lettieri|first11=Corrado|last12=Maeder|first12=Micha T|last13=Motreff|first13=Pascal|last14=Ong|first14=Peter|last15=Persu|first15=Alexandre|last16=Rickli|first16=Hans|last17=Schiele|first17=Francois|last18=Sheppard|first18=Mary N|last19=Swahn|first19=Eva|title=European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection|journal=European Heart Journal|year=2018|issn=0195-668X|doi=10.1093/eurheartj/ehy080}}</ref><ref name="HayesKim2018">{{cite journal|last1=Hayes|first1=Sharonne N.|last2=Kim|first2=Esther S.H.|last3=Saw|first3=Jacqueline|last4=Adlam|first4=David|last5=Arslanian-Engoren|first5=Cynthia|last6=Economy|first6=Katherine E.|last7=Ganesh|first7=Santhi K.|last8=Gulati|first8=Rajiv|last9=Lindsay|first9=Mark E.|last10=Mieres|first10=Jennifer H.|last11=Naderi|first11=Sahar|last12=Shah|first12=Svati|last13=Thaler|first13=David E.|last14=Tweet|first14=Marysia S.|last15=Wood|first15=Malissa J.|title=Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association|journal=Circulation|volume=137|issue=19|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000564}}</ref> | |||
{| class="wikitable" style="font-size: 85%;" | {| class="wikitable" style="font-size: 85%;" | ||
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* '''[[Fibromuscular dysplasia]]''' | * '''[[Fibromuscular dysplasia]]''' | ||
* '''[[Pregnancy|Pregnancy-related]]:''' [[antepartum]], [[postpartum|early post-partum]], [[postpartum|late post-partum]], [[postpartum|very late post-partum]] | * '''[[Pregnancy|Pregnancy-related]]:''' [[antepartum]], [[postpartum|early post-partum]], [[postpartum|late post-partum]], [[postpartum|very late post-partum]] | ||
* '''[[Pregnancy|Recurrent pregnancies]]:''' [[Parity (medicine)|multiparity ≥ 4 births]] | * '''[[Pregnancy|Recurrent pregnancies]]:''' [[Parity (medicine)|multiparity ≥ 4 births]], [[multigravida]] | ||
* '''[[Connective tissue disorder]]:''' [[Marfan syndrome]], [[Loeys-Dietz syndrome]], [[Ehlers-Danlos syndrome|Ehlers-Danlos syndrome type 4]], [[neurofibromatosis type I]], [[cystic medial necrosis]], [[alpha-1 antitrypsin deficiency]], [[polycystic kidney disease]], [[lysyl oxidase|lysyl oxidase deficiency]], [[Alport syndrome]], [[pseudoxanthoma elasticum]] | * '''[[Connective tissue disorder]]:''' [[Marfan syndrome]], [[Loeys-Dietz syndrome]], [[Ehlers-Danlos syndrome|Ehlers-Danlos syndrome type 4]], [[neurofibromatosis type I]], [[cystic medial necrosis]], [[alpha-1 antitrypsin deficiency]], [[polycystic kidney disease]], [[lysyl oxidase|lysyl oxidase deficiency]], [[Alport syndrome]], [[pseudoxanthoma elasticum]] | ||
* '''[[Systemic inflammation|Systemic inflammatory disease]]:''' [[systemic lupus erythematosus]], [[Crohn's disease]], [[ulcerative colitis]], [[polyarteritis nodosa]], [[sarcoidosis]], [[Churg-Strauss syndrome]], [[Wegener's granulomatosis]], [[rheumatoid arthritis]], [[Kawasaki disease]], [[giant cell arteritis]], [[celiac disease]], [[Takayasu arteritis]], [[cryoglobulinemia]], [[Behçet's disease]] | * '''[[Systemic inflammation|Systemic inflammatory disease]]:''' [[systemic lupus erythematosus]], [[Crohn's disease]], [[ulcerative colitis]], [[polyarteritis nodosa]], [[sarcoidosis]], [[Churg-Strauss syndrome]], [[Wegener's granulomatosis]], [[rheumatoid arthritis]], [[Kawasaki disease]], [[giant cell arteritis]], [[celiac disease]], [[Takayasu arteritis]], [[cryoglobulinemia]], [[Behçet's disease]] | ||
| Line 41: | Line 43: | ||
* '''[[Drugs]]:''' [[Calcineurin|calcineurin inhibitors]], [[5-FU]], [[fenfluramine]], [[corticosteroids]], [[methylphenidate]], [[ergotamine]], [[sumatriptan]] | * '''[[Drugs]]:''' [[Calcineurin|calcineurin inhibitors]], [[5-FU]], [[fenfluramine]], [[corticosteroids]], [[methylphenidate]], [[ergotamine]], [[sumatriptan]] | ||
|} | |} | ||
*After adjusting for cardiovascular risk factors, predisposing [[arteriopathies]], [[precipitating stressors]], [[medications]], and [[revascularization]], [[hypertension]] increased the risk of [[SCAD]] recurrence by 2.5 times, whereas [[beta-blocker]] usage reduced the recurrence risk by 64%.<ref name="SawHumphries2017">{{cite journal|last1=Saw|first1=Jacqueline|last2=Humphries|first2=Karin|last3=Aymong|first3=Eve|last4=Sedlak|first4=Tara|last5=Prakash|first5=Roshan|last6=Starovoytov|first6=Andrew|last7=Mancini|first7=G.B. John|title=Spontaneous Coronary Artery Dissection|journal=Journal of the American College of Cardiology|volume=70|issue=9|year=2017|pages=1148–1158|issn=07351097|doi=10.1016/j.jacc.2017.06.053}}</ref> | |||
==References== | ==References== | ||
Latest revision as of 23:19, 5 May 2021
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Spontaneous Coronary Artery Dissection Microchapters |
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Differentiating Spontaneous coronary artery dissection from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Type 1 Type 2A Type 2B Type 3 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Nate Michalak, B.A. Arzu Kalayci, M.D. [3]
Synonyms and keywords: SCAD
Overview
The risk factors for spontaneous coronary artery dissection include predisposing factors ( vasculopathy, pregnancy, connective tissue disorder, systemic inflammation) and precipitating stressors (e.g., strenuous exercise, emotional stress, recreational drugs).Features that raise the index of suspicion for SCAD include myocardial infarction in young women (age ≤50), absence of traditional cardiovascular risk factors, little or no evidence of coronary atherosclerosis, peripartum state, history of fibromuscular dysplasia, history of connective tissue disorder or systemic inflammation.
Risk Factors
- The phenotypic manifestation of spontaneous coronary artery dissection (SCAD) may occur as a result of predisposing factors compounded by precipitating stressors.[1]
- The presence of either predisposing or precipitating factors increases the risk of developing a dissection.
- The potential risk factors for SCAD include:[2][3][4]
- After adjusting for cardiovascular risk factors, predisposing arteriopathies, precipitating stressors, medications, and revascularization, hypertension increased the risk of SCAD recurrence by 2.5 times, whereas beta-blocker usage reduced the recurrence risk by 64%.[5]
References
- ↑ Saw, Jacqueline; Mancini, G.B. John; Humphries, Karin H. (2016). "Contemporary Review on Spontaneous Coronary Artery Dissection". Journal of the American College of Cardiology. 68 (3): 297–312. doi:10.1016/j.jacc.2016.05.034. ISSN 0735-1097.
- ↑ Saw, J.; Aymong, E.; Sedlak, T.; Buller, C. E.; Starovoytov, A.; Ricci, D.; Robinson, S.; Vuurmans, T.; Gao, M.; Humphries, K.; Mancini, G. B. J. (2014). "Spontaneous Coronary Artery Dissection: Association With Predisposing Arteriopathies and Precipitating Stressors and Cardiovascular Outcomes". Circulation: Cardiovascular Interventions. 7 (5): 645–655. doi:10.1161/CIRCINTERVENTIONS.114.001760. ISSN 1941-7640.
- ↑ Adlam, David; Alfonso, Fernando; Maas, Angela; Vrints, Christiaan; al-Hussaini, Abtehale; Bueno, Hector; Capranzano, Piera; Gevaert, Sofie; Hoole, Stephen P; Johnson, Tom; Lettieri, Corrado; Maeder, Micha T; Motreff, Pascal; Ong, Peter; Persu, Alexandre; Rickli, Hans; Schiele, Francois; Sheppard, Mary N; Swahn, Eva (2018). "European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection". European Heart Journal. doi:10.1093/eurheartj/ehy080. ISSN 0195-668X.
- ↑ Hayes, Sharonne N.; Kim, Esther S.H.; Saw, Jacqueline; Adlam, David; Arslanian-Engoren, Cynthia; Economy, Katherine E.; Ganesh, Santhi K.; Gulati, Rajiv; Lindsay, Mark E.; Mieres, Jennifer H.; Naderi, Sahar; Shah, Svati; Thaler, David E.; Tweet, Marysia S.; Wood, Malissa J. (2018). "Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association". Circulation. 137 (19). doi:10.1161/CIR.0000000000000564. ISSN 0009-7322.
- ↑ Saw, Jacqueline; Humphries, Karin; Aymong, Eve; Sedlak, Tara; Prakash, Roshan; Starovoytov, Andrew; Mancini, G.B. John (2017). "Spontaneous Coronary Artery Dissection". Journal of the American College of Cardiology. 70 (9): 1148–1158. doi:10.1016/j.jacc.2017.06.053. ISSN 0735-1097.