scholarly journals Proliferation of Coronary Adventitial Vasa Vasorum in Patients With Spontaneous Coronary Artery Dissection

2016 ◽  
Vol 9 (7) ◽  
pp. 891-892 ◽  
Author(s):  
Taek-Geun Kwon ◽  
Rajiv Gulati ◽  
Yasushi Matsuzawa ◽  
Tatsuo Aoki ◽  
Raviteja R. Guddeti ◽  
...  
2017 ◽  
Vol 11 (3) ◽  
pp. 144-147 ◽  
Author(s):  
Farshad Tahmasebi ◽  
Alice Hurrell ◽  
Amie Ford ◽  
Manish Gupta ◽  
Damien Geindreau ◽  
...  

Spontaneous coronary artery dissection is a rare but important cause of acute coronary syndrome. Its relevance for women during the puerperium mandates awareness and understanding amongst obstetric healthcare professionals. The aetiology of the increased risk in pregnancy has not been fully elucidated, but include medial eosinophilic angitis, pregnancy-induced degeneration of collagen in conjunction with the stresses of parturition, and rupture of the vasa vasorum. The risk of mortality necessitates prompt diagnosis, usually by angiography. There is no one-size-fits-all treatment; management must be individualised according to haemodynamic status and affected vessel(s) and includes conservative management, percutaneous coronary intervention, or bypass grafting. Recovery complications include extension of the haematoma or false lumen, valvular pathology secondary to ischaemia, and sudden cardiac death. Close post-operative surveillance is mandatory. We present a 41-year-old lady with post-partum spontaneous coronary artery dissection, complicated by ischaemic papillary rupture and mitral regurgitation requiring valve replacement. Additionally, we present a literature review, including guidance on management and critical analysis of potential complications.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Margaritis ◽  
F Saini ◽  
A Baranowska ◽  
S Parsons ◽  
A Vink ◽  
...  

Abstract Introduction Spontaneous coronary artery dissection (SCAD) is a cause of acute coronary syndromes and rarely sudden cardiac death (SCD). SCAD is characterised by medial false lumen haematoma formation and periadventitial inflammatory cell infiltrate. Although SCAD has been linked to connective tissue disorders, its pathophysiology remains poorly understood and the role of inflammation unknown. Purpose We sought to establish the definitive histopathological features of SCAD and explore pathophysiological mechanisms through assessment of dermal connective tissue ultrastructure. Methods N=36 SCD cases diagnosed as SCAD on autopsy were identified in pathology archives at four international centres. Their demographic and clinical characteristics were compared with n=359 survivors recruited in a SCAD survivors cohort. Haematoxylin & eosin sections were examined under light microscope. Immunohistochemistry (IHC) was employed for quantification of inflammatory cell infiltrate (CD68, CD3) and vasa vasorum density (CD31) of SCAD cases (n=20) compared to age- and sex-matched controls (n=10). Dermal extracellular matrix components (EMC) of n=32 SCAD survivors and n=16 healthy volunteers (HV) were compared using electron microscopy (EM). Results The autopsy series cases were more likely to be male (p=0.0256) and had higher incidence of left main stem (p=0.0475) and proximal left anterior descending (p<0.001) disease compared to SCAD survivors. N=24 (66%) of SCAD autopsy case showed no evidence of myocardial necrosis. N=17 (47%) showed mild-moderate atherosclerotic changes but no features of fibromuscular dysplasia. There were no differences in vasa vasorum density between SCAD and control cases (A). The degree of inflammatory cell infiltrate varied greatly but significantly higher than controls (B), comprising CD68+ macrophages, eosinophils and CD3+ positive T-cells. There was a statistically significant association (p=0.006) between the degree of inflammatory cell infiltrate and the length of time from onset of symptoms to death (Panel C), as well as significantly (p<0.001) denser inflammatory cell infiltrate adjacent to the dissection plane (D, exemplary sections E&F). EM revealed no differences between SCAD and HV in dermal fibroblast size & activity or elastin size & damage indicators, but possible changes in subgroups with more extreme clinical phenotype or pregnancy-related SCAD (G). Conclusions To our knowledge this is the largest SCAD pathology case series so far. We show for the first time that periadvential inflammation in SCAD appears to be time-dependent and localising to the dissected coronary segment, suggesting healing response to injury rather than causal contribution. We found no evidence to suggest increased vasa vasorum density is pathophysiologically important. Connective tissue changes were only linked to a small proportion of cases. These novel findings may have important implications for the management of SCAD patients. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation, Leicester NIHR Biomedical Research Centre


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Kotecha ◽  
A.D.P.E Premawardhana ◽  
M Garcia-Guimaraes ◽  
D Pellegrini ◽  
A.D Wood ◽  
...  

Abstract Background Spontaneous Coronary Artery Dissection (SCAD) is an important cause of acute coronary syndrome particularly in young-middle aged women. Revascularisation is challenging due to an underlying disrupted and friable coronary vessel wall leading to widely reported worse outcomes than for atherosclerotic coronary disease. Therefore, a conservative approach where possible is favoured however in some cases haemodynamic instability, ongoing ischaemia and reduced distal flow mandates consideration of revascularisation. Purpose To compare SCAD survivors managed with PCI or conservatively in terms of presentation characteristics, complications and long-term outcomes. Methodology and results 226 angiographically confirmed SCAD survivors (95% female,47±9.7yrs) who underwent PCI were compared in a case control study with two hundred and twenty-five angiographically confirmed SCAD survivors (92% female, 49±9.9yrs) who were conservatively managed. Patients were recruited from UK, Spanish and Dutch SCAD registries and both groups were well matched in terms of baseline demographics. Those treated with PCI were more likely to present with proximal SCAD (30.8% vs 7.6% P<0.01) and ST elevation myocardial infarction (STEMI) or cardiac arrest with reduced flow (32.3% vs 6.3% P<0.01). Intervention was performed with stents in 72.4%, plain old balloon angioplasty in 21.1% and wiring in 6.4% of cases and more often for multi-segment disease (40.8% vs 26.3% P<0.01). In cases with initial reduced flow undergoing PCI an improvement in flow was seen in 83%. Analysis of UK PCI cases (n=144) reveal complications in 56 (38.8%). However, when assessed for significance defined by a reduction in flow in a proximal/mid vessel, stent extension into left main stem, iatrogenic dissection requiring PCI and CABG as a consequence of PCI only 13 cases (9%) met criteria. Iatrogenic dissection accounts for the majority (76.9%). SCAD lesion length was associated with presence of complications (P=0.025). There was a non-significant trend towards major adverse cardiovascular events (MACE) occurring more frequently in those undergoing PCI (18% vs 11% P=0.067) driven by revascularisation (5% vs 1% P=0.036). Median follow up was 2.7 years. Conclusions PCI in SCAD is often performed in higher risk patients; in those presenting with reduced flow, the majority demonstrate improvement. Importantly whilst overall complication rates were similar to those widely reported, clinically significant complications were low. Multivariate modelling will reveal factors associated with complications to aid future decision making in this challenging patient group. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): British Heart Foundation


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