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Updated: Nov 4, 2025
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Published on: October 25, 2024
Vascular histopathology and connective tissue ultrastructure in spontaneous coronary artery dissection:
Marios Margaritis1, Francesca Saini1, Ania A Baranowska-Clarke1
1Department of Cardiovascular Sciences and National Institute for Health Research Leicester Biomedical Research Centre, Glenfield Hospital, Groby Road, Leicester LE3 9QP, UK.
Insights
Spontaneous coronary artery dissection (SCAD) is a serious condition. This study found peri-coronary inflammation is a reaction to SCAD, not a cause, and dermal connective tissue changes are uncommon in survivors.
Area of Science:
- Cardiology
- Pathology
- Histology
Background:
- Spontaneous coronary artery dissection (SCAD) can lead to acute coronary syndromes and sudden cardiac death (SCD).
- Previous research suggested connective tissue abnormalities, inflammation, increased coronary vasa vasorum (VV) density, and fibromuscular dysplasia contribute to SCAD.
- These factors have not been systematically evaluated in SCAD pathophysiology.
Purpose of the Study:
- To investigate coronary histological and dermal collagen ultrastructural findings in SCAD.
- To differentiate SCAD from other causes of sudden cardiac death.
- To clarify the role of inflammation and connective tissue in SCAD.
Main Methods:
- Compared autopsy SCAD cases (n=36) with SCAD survivors (n=359).
- Performed coronary and myocardial histology and immunohistochemistry.
- Utilized transmission electron microscopy (TEM) to analyze dermal extracellular matrix (ECM) in SCAD survivors (n=31) and healthy volunteers (n=16).
Main Results:
- Autopsy cases were more likely male and had greater proximal left coronary involvement.
- 66% of autopsy cases showed no myocardial infarction, suggesting arrhythmogenic death.
- Higher inflammation was observed in delayed-onset death cases and around dissected coronary segments; no differences in VV density or general dermal ECM ultrastructure were found.
Conclusions:
- SCAD assessment, especially in SCD without myocardial necrosis, requires careful evaluation.
- Peri-coronary inflammation appears to be a reaction to SCAD, not a cause.
- Coronary fibromuscular dysplasia and increased VV density are not considered major pathophysiological factors in SCAD; dermal connective tissue changes are uncommon in survivors.
Aims:
Spontaneous coronary artery dissection (SCAD) is a cause of acute coronary syndromes and in rare cases sudden cardiac death (SCD). Connective tissue abnormalities, coronary inflammation, increased coronary vasa vasorum (VV) density, and coronary fibromuscular dysplasia have all been implicated in the pathophysiology of SCAD but have not previously been systematically assessed. We designed a study to investigate the coronary histological and dermal collagen ultrastructural findings in SCAD.
Methods And Results:
Thirty-six autopsy SCAD cases were compared with 359 SCAD survivors. Coronary and myocardial histology and immunohistochemistry were undertaken. Transmission electron microscopy (TEM) of dermal extracellular matrix (ECM) components of n = 31 SCAD survivors and n = 16 healthy volunteers were compared. Autopsy cases were more likely male (19% vs. 5%; P = 0.0004) with greater proximal left coronary involvement (56% vs. 18%; P < 0.0001) compared to SCAD survivors. N = 24 (66%) of cases showed no myocardial infarction on macro- or microscopic examination consistent with arrhythmogenic death. There was significantly (P < 0.001) higher inflammation in cases with delayed-onset death vs. sudden death and significantly more inflammation surrounding the dissected vs. non-dissected vessel segments. N = 17 (47%) cases showed limited intimal fibro-elastic thickening but no features of fibromuscular dysplasia and no endothelial or internal elastic lamina abnormalities. There were no differences in VV density between SCAD and control cases. TEM revealed no general ultrastructural differences in ECM components or markers of fibroblast metabolic activity.
Conclusions:
Assessment of SCD requires careful exclusion of SCAD, particularly in cases without myocardial necrosis. Peri-coronary inflammation in SCAD is distinct from vasculitides and likely a reaction to, rather than a cause for SCAD. Coronary fibromuscular dysplasia or increased VV density does not appear pathophysiologically important. Dermal connective tissue changes are not common in SCAD survivors.
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