Spontaneous coronary artery dissection causes: Difference between revisions

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===Fibromuscular Dysplasia===
===Fibromuscular Dysplasia===


FMD is a non-[[atherosclerotic]] [[vasculopathy]] characterized by thickening, [[fibrosis]], and disarray of the arterial wall that primarily affects small and medium-sized vessels.  The association between FMD and SCAD has been well described,<ref name="SawPoulter2012">{{cite journal|last1=Saw|first1=J.|last2=Poulter|first2=R.|last3=Fung|first3=A.|last4=Wood|first4=D.|last5=Hamburger|first5=J.|last6=Buller|first6=C. E.|title=Spontaneous Coronary Artery Dissection in Patients With Fibromuscular Dysplasia: A Case Series|journal=Circulation: Cardiovascular Interventions|volume=5|issue=1|year=2012|pages=134–137|issn=1941-7640|doi=10.1161/CIRCINTERVENTIONS.111.966630}}</ref><ref name="SawRicci2013">{{cite journal|last1=Saw|first1=Jacqueline|last2=Ricci|first2=Donald|last3=Starovoytov|first3=Andrew|last4=Fox|first4=Rebecca|last5=Buller|first5=Christopher E.|title=Spontaneous Coronary Artery Dissection|journal=JACC: Cardiovascular Interventions|volume=6|issue=1|year=2013|pages=44–52|issn=19368798|doi=10.1016/j.jcin.2012.08.017}}</ref><ref name="ToggweilerPuck2012">{{cite journal|last1=Toggweiler|first1=S|last2=Puck|first2=M|last3=Thalhammer|first3=C|last4=Manka|first4=R|last5=Wyss|first5=M|last6=Bilecen|first6=D|last7=Corti|first7=R|last8=Amann-Vesti|first8=B|last9=Lüscher|first9=T|last10=Wyss|first10=C|title=Associated vascular lesions in patients with spontaneous coronary artery dissection|journal=Swiss Medical Weekly|year=2012|issn=1424-7860|doi=10.4414/smw.2012.13538}}</ref><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> and the biological proof of causation has been supported by histopathologic reports.<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><ref>{{cite journal |vauthors=Mather PJ, Hansen CL, Goldman B, Inniss S, Piña I, Norris R, Jeevanandam V, Bove AA |title=Postpartum multivessel coronary dissection |journal=J. Heart Lung Transplant. |volume=13 |issue=3 |pages=533–7 |year=1994 |pmid=8061031 |doi= |url=}}</ref><ref name="BrodskyRamaswamy2007">{{cite journal|last1=Brodsky|first1=Sergey V.|last2=Ramaswamy|first2=Gita|last3=Chander|first3=Praveen|last4=Braun|first4=Alex|title=Ruptured Cerebral Aneurysm and Acute Coronary Artery Dissection in the Setting of Multivascular Fibromuscular Dysplasia|journal=Angiology|volume=58|issue=6|year=2007|pages=764–767|issn=0003-3197|doi=10.1177/0003319707303645}}</ref>  It has been suggested that the presence of FMD may weaken the artery architecture and lead to [[aneurysm]] formation or [[coronary dissection]].<ref name="OlinGornik2014">{{cite journal|last1=Olin|first1=J. W.|last2=Gornik|first2=H. L.|last3=Bacharach|first3=J. M.|last4=Biller|first4=J.|last5=Fine|first5=L. J.|last6=Gray|first6=B. H.|last7=Gray|first7=W. A.|last8=Gupta|first8=R.|last9=Hamburg|first9=N. M.|last10=Katzen|first10=B. T.|last11=Lookstein|first11=R. A.|last12=Lumsden|first12=A. B.|last13=Newburger|first13=J. W.|last14=Rundek|first14=T.|last15=Sperati|first15=C. J.|last16=Stanley|first16=J. C.|title=Fibromuscular Dysplasia: State of the Science and Critical Unanswered Questions: A Scientific Statement From the American Heart Association|journal=Circulation|volume=129|issue=9|year=2014|pages=1048–1078|issn=0009-7322|doi=10.1161/01.cir.0000442577.96802.8c}}</ref>
FMD is a non-[[atherosclerotic]] [[vasculopathy]] characterized by thickening, [[fibrosis]], and disarray of the arterial wall that primarily affects small and medium-sized vessels.  The association between FMD and SCAD has been well described,<ref name="SawPoulter2012">{{cite journal|last1=Saw|first1=J.|last2=Poulter|first2=R.|last3=Fung|first3=A.|last4=Wood|first4=D.|last5=Hamburger|first5=J.|last6=Buller|first6=C. E.|title=Spontaneous Coronary Artery Dissection in Patients With Fibromuscular Dysplasia: A Case Series|journal=Circulation: Cardiovascular Interventions|volume=5|issue=1|year=2012|pages=134–137|issn=1941-7640|doi=10.1161/CIRCINTERVENTIONS.111.966630}}</ref><ref name="SawRicci2013">{{cite journal|last1=Saw|first1=Jacqueline|last2=Ricci|first2=Donald|last3=Starovoytov|first3=Andrew|last4=Fox|first4=Rebecca|last5=Buller|first5=Christopher E.|title=Spontaneous Coronary Artery Dissection|journal=JACC: Cardiovascular Interventions|volume=6|issue=1|year=2013|pages=44–52|issn=19368798|doi=10.1016/j.jcin.2012.08.017}}</ref><ref name="ToggweilerPuck2012">{{cite journal|last1=Toggweiler|first1=S|last2=Puck|first2=M|last3=Thalhammer|first3=C|last4=Manka|first4=R|last5=Wyss|first5=M|last6=Bilecen|first6=D|last7=Corti|first7=R|last8=Amann-Vesti|first8=B|last9=Lüscher|first9=T|last10=Wyss|first10=C|title=Associated vascular lesions in patients with spontaneous coronary artery dissection|journal=Swiss Medical Weekly|year=2012|issn=1424-7860|doi=10.4414/smw.2012.13538}}</ref><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> and the biological proof of causation has been supported by histopathologic reports.<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><ref>{{cite journal |vauthors=Mather PJ, Hansen CL, Goldman B, Inniss S, Piña I, Norris R, Jeevanandam V, Bove AA |title=Postpartum multivessel coronary dissection |journal=J. Heart Lung Transplant. |volume=13 |issue=3 |pages=533–7 |year=1994 |pmid=8061031 |doi= |url=}}</ref><ref name="BrodskyRamaswamy2007">{{cite journal|last1=Brodsky|first1=Sergey V.|last2=Ramaswamy|first2=Gita|last3=Chander|first3=Praveen|last4=Braun|first4=Alex|title=Ruptured Cerebral Aneurysm and Acute Coronary Artery Dissection in the Setting of Multivascular Fibromuscular Dysplasia|journal=Angiology|volume=58|issue=6|year=2007|pages=764–767|issn=0003-3197|doi=10.1177/0003319707303645}}</ref>  It has been suggested that the presence of FMD may weaken the artery architecture and lead to [[aneurysm|aneurysm formation]] or [[coronary dissection]].<ref name="OlinGornik2014">{{cite journal|last1=Olin|first1=J. W.|last2=Gornik|first2=H. L.|last3=Bacharach|first3=J. M.|last4=Biller|first4=J.|last5=Fine|first5=L. J.|last6=Gray|first6=B. H.|last7=Gray|first7=W. A.|last8=Gupta|first8=R.|last9=Hamburg|first9=N. M.|last10=Katzen|first10=B. T.|last11=Lookstein|first11=R. A.|last12=Lumsden|first12=A. B.|last13=Newburger|first13=J. W.|last14=Rundek|first14=T.|last15=Sperati|first15=C. J.|last16=Stanley|first16=J. C.|title=Fibromuscular Dysplasia: State of the Science and Critical Unanswered Questions: A Scientific Statement From the American Heart Association|journal=Circulation|volume=129|issue=9|year=2014|pages=1048–1078|issn=0009-7322|doi=10.1161/01.cir.0000442577.96802.8c}}</ref>


===Takotsubo Cardiomyopathy===
===Takotsubo Cardiomyopathy===

Revision as of 20:07, 29 November 2017

Spontaneous Coronary Artery Dissection Microchapters

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Spontaneous coronary artery dissection from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Approach

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

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CT

MRI

Echocardiography

Other Imaging Findings

Other Diagnostic Studies

Treatment

Treatment Approach

Medical Therapy

Percutaneous Coronary Intervention

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Type 1

Type 2A

Type 2B

Type 3

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

Synonyms and keywords: SCAD

Overview

Causes

The exact etiology of spontaneous coronary artery dissection (SCAD) remains elusive and appears to be multifactorial. It has been postulated that the phenotypic expression of SCAD may occur as a result of predisposing factors compounded by precipitating stressors.[1] Among the conditions associated with the occurrence of SCAD, fibromuscular dysplasia (FMD) and takotsubo cardiomyopathy (TCM) have been suggested to have a causal relationship with SCAD.

Fibromuscular Dysplasia

FMD is a non-atherosclerotic vasculopathy characterized by thickening, fibrosis, and disarray of the arterial wall that primarily affects small and medium-sized vessels. The association between FMD and SCAD has been well described,[2][3][4][5] and the biological proof of causation has been supported by histopathologic reports.[6][7][8] It has been suggested that the presence of FMD may weaken the artery architecture and lead to aneurysm formation or coronary dissection.[9]

Takotsubo Cardiomyopathy

References

  1. ↑ 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.
  2. ↑ Saw, J.; Poulter, R.; Fung, A.; Wood, D.; Hamburger, J.; Buller, C. E. (2012). "Spontaneous Coronary Artery Dissection in Patients With Fibromuscular Dysplasia: A Case Series". Circulation: Cardiovascular Interventions. 5 (1): 134–137. doi:10.1161/CIRCINTERVENTIONS.111.966630. ISSN 1941-7640.
  3. ↑ Saw, Jacqueline; Ricci, Donald; Starovoytov, Andrew; Fox, Rebecca; Buller, Christopher E. (2013). "Spontaneous Coronary Artery Dissection". JACC: Cardiovascular Interventions. 6 (1): 44–52. doi:10.1016/j.jcin.2012.08.017. ISSN 1936-8798.
  4. ↑ Toggweiler, S; Puck, M; Thalhammer, C; Manka, R; Wyss, M; Bilecen, D; Corti, R; Amann-Vesti, B; Lüscher, T; Wyss, C (2012). "Associated vascular lesions in patients with spontaneous coronary artery dissection". Swiss Medical Weekly. doi:10.4414/smw.2012.13538. ISSN 1424-7860.
  5. ↑ 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.
  6. ↑ Lie, J.T.; Berg, K.K. (1987). "Isolated fibromuscular dysplasia of the coronary arteries with spontaneous dissection and myocardial infarction". Human Pathology. 18 (6): 654–656. doi:10.1016/S0046-8177(87)80368-4. ISSN 0046-8177.
  7. ↑ Mather PJ, Hansen CL, Goldman B, Inniss S, Piña I, Norris R, Jeevanandam V, Bove AA (1994). "Postpartum multivessel coronary dissection". J. Heart Lung Transplant. 13 (3): 533–7. PMID 8061031.
  8. ↑ Brodsky, Sergey V.; Ramaswamy, Gita; Chander, Praveen; Braun, Alex (2007). "Ruptured Cerebral Aneurysm and Acute Coronary Artery Dissection in the Setting of Multivascular Fibromuscular Dysplasia". Angiology. 58 (6): 764–767. doi:10.1177/0003319707303645. ISSN 0003-3197.
  9. ↑ Olin, J. W.; Gornik, H. L.; Bacharach, J. M.; Biller, J.; Fine, L. J.; Gray, B. H.; Gray, W. A.; Gupta, R.; Hamburg, N. M.; Katzen, B. T.; Lookstein, R. A.; Lumsden, A. B.; Newburger, J. W.; Rundek, T.; Sperati, C. J.; Stanley, J. C. (2014). "Fibromuscular Dysplasia: State of the Science and Critical Unanswered Questions: A Scientific Statement From the American Heart Association". Circulation. 129 (9): 1048–1078. doi:10.1161/01.cir.0000442577.96802.8c. ISSN 0009-7322.
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