Papers

International journal
Dec, 2014

Evaluation of Valsalva sinus wall deformation due to compression by the Amplatzer septal occluder and the potential for erosion development.

Journal of interventional cardiology
  • Masataka Kitano
  • ,
  • Satoshi Yazaki
  • ,
  • Tadaaki Abe
  • ,
  • Yamada Osamu

Volume
27
Number
6
First page
555
Last page
62
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1111/joic.12158

OBJECTIVES: We studied whether the pressure exerted by the Amplatzer septal occluder (ASO) disk on the Valsalva sinus wall (VW) is a risk factor for erosion and attempted to determine the pressure that may trigger erosion. BACKGROUND: The causes and mechanisms of erosion after ASO placement remain unclear. METHODS: We reviewed 665 consecutive patients with atrial septal defects who underwent ASO closure at our hospital from 2005 to 2012. We used transesophageal echocardiography and other tests to evaluate disk-related VW deformation as a risk factor for erosion. RESULTS: Immediately after ASO placement, intermittent VW deformation from either disk was determined in 54 of the 665 patients (8%). Of these 54 patients, only 1 exhibited late erosion (0.15%) during a follow-up of more than 4 years (0.035% a year). The maximum VW deformation depth relative to the standard curve, or dent, was 2.6 mm in this patient, whereas that in the remaining patients ranged from 0.5 to 2.0 mm. The dent values were significantly deeper in patients with contact between the left atrial disk and posterior atrial wall than in those without contact (P = 0.03). There was a significant negative correlation between dent and the aortic side-maximum device thickness (DT)/middle part-DT ratio (P = 0.04). CONCLUSION: Although VW deformation, particularly deep VW deformation caused by pressure from either disk after ASO placement must be a recognized risk for erosion, which deformation level carries a stronger risk for erosion could not be concluded.

Link information
DOI
https://doi.org/10.1111/joic.12158
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/25346158
ID information
  • DOI : 10.1111/joic.12158
  • Pubmed ID : 25346158

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