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Spontaneous Coronary Artery Dissection and Hemodynamic Instability: Can Emergent PCI Be Life Saving? Report of Two Cases and Literature Review.

ABSTRACT: Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome. It occurs predominantly among younger females and typically in the absence of atherosclerotic coronary artery disease. It is associated with peripartum period, connective tissue disorders, vasculitides, and extreme exertion. Presentations vary greatly, and this condition can be fatal. Given its rarity, there are no guidelines for management of SCAD. We present the cases of two female patients, with no coronary artery disease risk factors or recent pregnancy, who were presented with non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI), respectively, secondary to SCAD. Both had excellent outcome after emergent percutaneous intervention. Our first patient was presented with NSTEMI with ongoing chest pain and dynamic electrocardiogram (ECG). Emergent left heart catheterization was significant for first obtuse marginal (OM1) dissection, confirmed by optical coherence tomography. Percutaneous coronary intervention (PCI) with two bare metal stents was performed with resolution of symptoms and ECG changes. The second patient is known to have syndrome, presented with STEMI and emergent coronary angiography showed left anterior descending dissection with intramural hematoma confirmed by intravascular ultrasound and treated with a drug-eluting stent with resolution of symptoms and ST changes. Her hospital course was complicated by post-myocardial infarction pericarditis that was improved with colchicine. Both the patients were observed in the coronary care unit for 24 hours. Both remained asymptomatic at 6-month follow-up. SCAD is a rare cause of acute coronary syndrome. In patients with early presentation, limited disease, and ongoing symptoms, emergent cardiac catheterization with percutaneous intervention has excellent outcome. More studies are needed to establish evidence-based management guidelines.

SUBMITTER: Al Emam AR

PROVIDER: S-EPMC4244243 | biostudies-other | 2014 Dec

REPOSITORIES: biostudies-other

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Project description:ImportanceSpontaneous coronary artery dissection (SCAD) is an increasingly recognized nonatherosclerotic cause of acute myocardial infarction enriched among individuals with early-onset myocardial infarction but is of unclear etiology.ObjectiveTo assess which genes contribute to the development of SCAD.Design, setting, and participantsTo prioritize genes influencing risk for SCAD, whole-exome sequencing was performed among individuals with SCAD in the discovery and replication cohorts from a tertiary care hospital outpatient specialty clinic, and gene set enrichment analyses were also performed for disruptive coding variants. All patients were sequentially enrolled beginning July 2013. Aggregate prevalence of rare disruptive variants for prioritized gene sets was compared between individuals with SCAD with population-based controls comprising 46 468 UK Biobank participants with whole-exome sequencing. Complementary mice models were used for in vivo validation. Analysis took place between June 2020 and January 2021.Main outcomes and measuresThe frequency and identity of rare genetic variants in individuals with SCAD.ResultsOf 130 patients, 109 (83.8%) were female (26 of 32 [81.2%] in the discovery cohort and 83 of 98 [84.7%] in the replication cohort) with mean (SD) age at first SCAD event of 48.41 (8.76) years in the discovery cohort and 47.74 (10.09) years in the replication cohort. Across all patients with SCAD, rare disruptive variants were found within 10 collagen genes (COL3A1, COL5A1, COL4A1, COL6A1, COL5A2, COL12A1, COL4A5, COL1A1, COL1A2, and COL27A1) were 17-fold (P = 1.5 × 10-9) enriched among individuals with SCAD compared with a background of 2506 constrained genes expressed in coronary artery. Furthermore, compared with individuals from the UK Biobank, individuals with SCAD were 1.75-fold (P = .04) more likely to carry disruptive rare variants within fibrillar collagen genes. Complementary mice models haploinsufficient for Col3a1 or Col5a1, the 2 most common collagen gene variants identified in SCAD cases, demonstrated increased risk of arterial dissection and increased size of arterial diameters especially in female mice, with resulting changes in collagen fibril organization and diameter.Conclusions and relevanceUnbiased gene discovery in patients with SCAD with independent human and murine validation highlights the role of the extracellular matrix dysfunction in SCAD.

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Spontaneous Coronary Artery Dissection and Hemodynamic Instability: Can Emergent PCI Be Life Saving? Report of Two Cases and Literature Review.

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