Genetic diversity and pathogenic variants as possible predictors of severity in a French sample of nonsyndromic heritable thoracic aortic aneurysms and dissections (nshTAAD)

Genet Med. 2019 Sep;21(9):2015-2024. doi: 10.1038/s41436-019-0444-y. Epub 2019 Feb 11.

Abstract

Purpose: Heritable thoracic aortic aneurysms and dissections (hTAAD) are life-threatening complications of well-known syndromic diseases or underdiagnosed nonsyndromic heritable forms (nshTAAD). Both have an autosomal dominant transmission and are genetically heterogeneous. Our objective was to describe the relevance of molecular diagnosis in these patients and the contribution of each gene in nshTAAD.

Methods: Two hundred twenty-six consecutive nshTAAD probands, either young (<45 years) sporadic or familial cases were included. A next-generation sequencing capture panel comprising 23 known disease-causing genes was performed.

Results: Class 4 or 5 variants were identified in 18% of the nshTAAD probands, while class 3 variants were found in 10% of them. The yield in familial cases was greater than in sporadic cases. SMAD3 and FBN1 genes were the major disease-causing genes. Unexpectedly, no premature termination codon variant was identified in the FBN1 gene. Furthermore, we report for the first time that aortic dissection or surgery occurred significantly more often and earlier in probands with a class 4 or 5 pathogenic variant.

Conclusion: This study indicates that genetic screening using NGS is efficient in young and familial nshTAAD. The presence of a pathogenic variant has a possible predictive value, which needs to be further investigated because it may influence care.

Keywords: FBN1 gene; NGS; SMAD3 gene; class 4 and 5 variants; thoracic aortic aneurysms and dissections.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aortic Aneurysm, Thoracic / diagnosis
  • Aortic Aneurysm, Thoracic / genetics*
  • Aortic Dissection / diagnosis
  • Aortic Dissection / genetics*
  • Aortic Dissection / physiopathology
  • Child
  • Codon, Nonsense / genetics
  • Female
  • Fibrillin-1 / genetics*
  • Genetic Predisposition to Disease
  • Genetic Testing / methods
  • High-Throughput Nucleotide Sequencing
  • Humans
  • Male
  • Middle Aged
  • Mutation
  • Pathology, Molecular / methods
  • Pedigree
  • Smad3 Protein / genetics*
  • Young Adult

Substances

  • Codon, Nonsense
  • FBN1 protein, human
  • Fibrillin-1
  • SMAD3 protein, human
  • Smad3 Protein

Supplementary concepts

  • Aortic Aneurysm, Familial Thoracic 1