Dataset Information

Unusual interventional treatment of spontaneous coronary artery dissection without stent implantation: a case series.

ABSTRACT:

Background

Spontaneous coronary artery dissection (SCAD) is a unique cause of myocardial infarction, and optimal treatment should be selected according to the ischaemic condition. Patients with ongoing ischaemia or haemodynamic instability may require revascularization. Cutting balloon (CB) angioplasty has been acknowledged as an option for revascularization. However, few observations of the coronary artery conditions after CB angioplasty in SCAD patients have been reported. Here, we demonstrate two cases in which we evaluated the angiographic morphology of targeted coronary arteries in the chronic phase after CB angioplasty.

Case summary

Patient 1 was a 46-year-old woman who presented at our hospital with chest pain. Electrocardiography suggested acute coronary syndrome and coronary angiography was performed. The coronary angiography and intravascular ultrasound (IVUS) examinations revealed SCAD in the left anterior descending artery (LAD). Revascularization with CB angioplasty was successful. Follow-up coronary angiography 15 months after the angioplasty showed no visible stenosis in the LAD. Accordingly, the patient no longer needed to antiplatelet therapy. Patient 2 was a 50-year-old woman who was transported to our hospital for ventricular tachycardia. Coronary angiography and IVUS revealed SCAD in the right coronary artery. Coronary flow was restored by CB angioplasty. Follow-up contrast-enhanced computed tomography angiography 36 months after angioplasty showed a healed appearance. Thus, she was able to discontinue antiplatelet therapy.

Discussion

Cutting balloon angioplasty may be a possible method to treat SCAD.

SUBMITTER: Fujita H

PROVIDER: S-EPMC8350351 | biostudies-literature |

REPOSITORIES: biostudies-literature

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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.