Clot or Not? A Meta-Analysis of Autopsy Findings in Spontaneous Coronary Artery Dissection

CIRCULATION(2021)

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摘要
Introduction: Spontaneous coronary artery dissection (SCAD) is an uncommon but likely underdiagnosed cause of acute coronary syndrome. Current treatment of SCAD commonly includes antiplatelet agents, though pathogenesis relates to intramural hematoma, rather than atherothrombosis as in typical myocardial infarction. Our goal was to determine whether thrombus in the true lumen is part of the pathophysiology of fatal cases of SCAD, which could help guide treatment decisions. Methods: A review of electronic databases including PubMed and EMBASE was conducted from inception through June 2021. Citations were included that provided pathology images of dissected coronary arteries acquired from autopsies of patients who died of SCAD. Images were independently reviewed by a pathologist who described the presence or absence of thrombus and inflammatory cells. Results: A total of 35 citations containing autopsy images were identified. These included 42 cases of which 88% were female, with an average age of 44 years. The most common vessel involved was the left anterior descending (74%), with 40% involving multiple vessels. Most decedents had no medical history, though 5% had systemic vasculitis and 17% were pregnant or peri-partum. On independent review of the pathology images, all had intramural hematoma, none had evidence of thrombus in the true lumen, and 16% had evidence of thrombus in the false lumen. There was eosinophilic inflammation of the affected artery in 64% of cases. Conclusions: There was no evidence of thrombus in the true lumen in any of 42 cases of fatal SCAD for whom autopsy images were available. This suggests that the use of antiplatelet agents in the treatment of SCAD should be re-evaluated. Clinical trials are necessary to determine whether antiplatelet agents are beneficial for patients with SCAD. Additionally, further research is necessary to better understand the role of eosinophils in the pathophysiology of SCAD.
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