Annals of vascular surgery · 2025
The Complicated Genetics behind Uncomplicated Type B Aortic Dissection.
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Auton Ella, Kamal Mohiuddin, Jubouri Matti, Bashir Mohamad
Аннотация
BACKGROUND: Up to 50% of uncomplicated type B aortic dissection (unTBAD) cases progress to become complicated with a mortality rate of up to 42% within 5 years of onset. Morphological and clinical parameters have previously been defined for the decision of surgical intervention in unTBAD to improve clinical outcomes. The analysis of genetic variants in this risk stratification has demonstrated a lack of evidence to influence clinical decision-making.
METHODS: A comprehensive literature review was conducted using multiple electronic databases. A selection of genes recognized in thoracic aortic aneurysms and dissections were investigated in association with clinical outcomes in type B aortic dissections.
RESULTS: Case studies highlighted the impact of variants in fibrillin-1, type III collagen, alpha-actin 2, MYH11, protein kinase cGMP-dependent type I, transforming growth factor beta 1, type I transforming growth factor β receptor, and type II transforming growth factor β receptor on clinical outcomes in type B aortic dissection. Patients who carry variants in these genes experience more rapid disease progression and benefit from surgery.
CONCLUSION: The presence of a variant in genes that underlie unTBAD etiology could impact clinical decision-making and risk stratification in unTBAD. Emerging evidence supports thoracic endovascular aortic repair for unTBAD patients who have a higher risk of developing complications. The use of genetics in the management of unTBAD patients may help to improve the adverse clinical outcomes in unTBAD.
METHODS: A comprehensive literature review was conducted using multiple electronic databases. A selection of genes recognized in thoracic aortic aneurysms and dissections were investigated in association with clinical outcomes in type B aortic dissections.
RESULTS: Case studies highlighted the impact of variants in fibrillin-1, type III collagen, alpha-actin 2, MYH11, protein kinase cGMP-dependent type I, transforming growth factor beta 1, type I transforming growth factor β receptor, and type II transforming growth factor β receptor on clinical outcomes in type B aortic dissection. Patients who carry variants in these genes experience more rapid disease progression and benefit from surgery.
CONCLUSION: The presence of a variant in genes that underlie unTBAD etiology could impact clinical decision-making and risk stratification in unTBAD. Emerging evidence supports thoracic endovascular aortic repair for unTBAD patients who have a higher risk of developing complications. The use of genetics in the management of unTBAD patients may help to improve the adverse clinical outcomes in unTBAD.