Spontaneous coronary artery dissection pathophysiology

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 Case 1 Case 2 Case 3 Case 4 Case 5 Case 6 Case 7 Type 2A Case 1 Case 2 Case 3 Case 4 Case 5 Case 6 Type 2B Case 1 Case 2 Case 3 Case 4 Type 3 Case 1 Case 2 Case 3 Case 4 Case 5 Case 6

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

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. 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. 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.