Spontaneous coronary artery dissection pathophysiology

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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

Angiography

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., Arzu Kalayci, M.D. [2]

Synonyms and keywords: SCAD

Overview

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.[1] 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).

Spontaneous arterial dissection can develop in any layer (intima , media, or adventitia) of the coronary artery wall. Two possible mechanisms may be responsible for the arterial wall separation.[2] The first one is, the 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 hemorrhage hypothesis, in which spontaneous rupture of newly formed vasa vasorum in response to injury can cause a haemorrhage in between the arterial wall layers. High pressure of the haematoma within the aortic wall may rupture through the intima and create a “reverse” intimal rupture.


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.

References

  1. 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)
  2. 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.