Dataset Information

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy.

ABSTRACT:

Introduction

Spontaneous coronary artery dissection is a rare cardiovascular disease that can cause acute myocardial infarction and sudden cardiac death. The mechanism of this pathology and the optimal treatment are not fully understood.

Presentation of case

An acute myocardial infarction developed while a fifty five years old woman with a rectal adenocarcinoma was receiving a cisplatin and capecitabine therapy. Coronary angiography demonstrated a multivessel occlusion of coronary arteries.

Discussion

The authors discuss several factors that may lead to the spontaneous coronary artery dissection including chemotherapy-induced vasospasm. Chemotherapy based on the cisplatin and capecitabine intake can cause a cardiotoxic effect.

Conclusion

Thus, spontaneous coronary artery dissection is a disease with an extremely complex etiololy, which does not have a special treatment guide. Management should be considered individually for each case.

SUBMITTER: Somov P

PROVIDER: S-EPMC6626886 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Publications

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy.

Somov Pavel P Marchak Dmitriy D Matusov Arkhip A Viller Alexander A Shevchenko Yuri Y Miminoshvili Archili A

Annals of medicine and surgery (2012) 20190711

<h4>Introduction</h4>Spontaneous coronary artery dissection is a rare cardiovascular disease that can cause acute myocardial infarction and sudden cardiac death. The mechanism of this pathology and the optimal treatment are not fully understood.<h4>Presentation of case</h4>An acute myocardial infarction developed while a fifty five years old woman with a rectal adenocarcinoma was receiving a cisplatin and capecitabine therapy. Coronary angiography demonstrated a multivessel occlusion of coronary ...[more]

PMID: 31338186

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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.

Dataset Information

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy.

Introduction

Presentation of case

Discussion

Conclusion

Publications

Spontaneous coronary artery dissection during cisplatin and capecitabine therapy.

Similar Datasets

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