OBJECTIVES: We aimed to identify a phenotype of ascending thoracic aortic aneurysm (TAA), which, more than others, evolves into type A dissection (TAD). METHODS: Aortic specimens were obtained from patients undergoing surgical repair of TAA and TAD (108 and 26, respectively). Histopathological and immunohistochemical analyses were performed by using adequate tissue specimens, appropriate techniques and criteria. RESULTS: We identified the three following TAA phenotypes: phenotype I (cystic medial degeneration balanced by a substitutive fibrosis, in absence of medial apoptosis and with a faint collagenase concentration), phenotype II (cystic medial degeneration of higher grade, respectively, than substitutive fibrosis, with focal medial apoptosis and moderate collagenase concentration), and phenotype III (elevated cystic medial degeneration without substitutive fibrosis, with plurifocal medial apoptosis and severe collagenase concentration). The same medial degenerative lesions of TAA phenotype III were observed in TAD tissue samples. CONCLUSIONS: The morphological identity of medial lesions observed in both the TAA phenotype III and in TAD aortas might be assumed to be the precursor-and consequently the optimal biomarker- of dissection, independently of aneurysm diameter or valvular disorder. Identification of genetic risk factors, useful both in diagnostics and in developing more targeted treatment for individual patients, might also be needed

Pisano, C., Maresi, E., Merlo, D., Balistreri, C., Candore, G., Caruso, M., et al. (2012). A particular phenotype of ascending aorta aneurysms as precursor of type A aortic dissection. INTERACTIVE CARDIOVASCULAR AND THORACIC SURGERY, 15(5), 840-846 [10.1093/icvts/ivs347].

A particular phenotype of ascending aorta aneurysms as precursor of type A aortic dissection.

Pisano, C;RUVOLO, GIOVANNI
2012-01-01

Abstract

OBJECTIVES: We aimed to identify a phenotype of ascending thoracic aortic aneurysm (TAA), which, more than others, evolves into type A dissection (TAD). METHODS: Aortic specimens were obtained from patients undergoing surgical repair of TAA and TAD (108 and 26, respectively). Histopathological and immunohistochemical analyses were performed by using adequate tissue specimens, appropriate techniques and criteria. RESULTS: We identified the three following TAA phenotypes: phenotype I (cystic medial degeneration balanced by a substitutive fibrosis, in absence of medial apoptosis and with a faint collagenase concentration), phenotype II (cystic medial degeneration of higher grade, respectively, than substitutive fibrosis, with focal medial apoptosis and moderate collagenase concentration), and phenotype III (elevated cystic medial degeneration without substitutive fibrosis, with plurifocal medial apoptosis and severe collagenase concentration). The same medial degenerative lesions of TAA phenotype III were observed in TAD tissue samples. CONCLUSIONS: The morphological identity of medial lesions observed in both the TAA phenotype III and in TAD aortas might be assumed to be the precursor-and consequently the optimal biomarker- of dissection, independently of aneurysm diameter or valvular disorder. Identification of genetic risk factors, useful both in diagnostics and in developing more targeted treatment for individual patients, might also be needed
2012
Pubblicato
Rilevanza internazionale
Articolo
Comitato scientifico
Settore MED/23 - CHIRURGIA CARDIACA
English
Pisano, C., Maresi, E., Merlo, D., Balistreri, C., Candore, G., Caruso, M., et al. (2012). A particular phenotype of ascending aorta aneurysms as precursor of type A aortic dissection. INTERACTIVE CARDIOVASCULAR AND THORACIC SURGERY, 15(5), 840-846 [10.1093/icvts/ivs347].
Pisano, C; Maresi, E; Merlo, D; Balistreri, C; Candore, G; Caruso, M; Codispoti, M; Ruvolo, G
Articolo su rivista
File in questo prodotto:
File Dimensione Formato  
Article 3.pdf

solo utenti autorizzati

Licenza: Copyright dell'editore
Dimensione 239.74 kB
Formato Adobe PDF
239.74 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/138571
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 11
  • ???jsp.display-item.citation.isi??? 7
social impact