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

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.

Is the mean blood leukocyte telomere length a predictor for sporadic thoracic aortic aneurysm? Data from a preliminary study.

Telomeres have been postulated as a universal clock that shortens in parallel with cellular aging. They are specialized DNA-protein structures at the ends of chromosome with remarkable functions--preventing their recognition as double-stranded DNA breaks, protecting their recombination and degradation, and avoiding a DNA damage cellular response. Telomere shortening is currently considered the best aging marker, but is also a predictor for age-related diseases, including cardiovascular diseases. Biological age clearly seems to be a better predictor of vascular risk rather than chronological age. This concept is supported by key assumptions that peripheral blood leukocyte telomere content accurately reflects that of the vascular wall and its decrease is associated with premature vascular disease. Thus, we are analyzing whether the mean of blood leukocyte telomere length might also be a predictor for sporadic thoracic aortic aneurysm (S-TAA). The preliminary results seem to be promising. Shorter telomeres were detected in patients than in controls. Thus, mean of blood leukocyte telomere length could contribute to identify individuals at S-TAA risk.

Histological and genetic studies in patients with bicuspid aortic valve and ascending aorta complications.

OBJECTIVES: Aneurysm diameter and growing rate does not represent a definite parameter for operation in bicuspid aortic valve (BAV), ascending aortic aneurysm and normal root patients. Thus, we investigated histological and immunohistochemical aspects of different segments of ascending aorta (precisely, aortic root without dilatation, aneurysmatic tubular portion, dissected ascending aorta) and genetic features of patients with BAV and ascending aorta complication (aneurysm or dissection). METHODS: Aorta tissue samples of 24 BAV patients were examined. The patients comprised of 18 men and 6 women; the mean age was 54.2 ± 14.3 years. All patients underwent composite aortic root replacement (button Bentall operation). Multiple histological sections were prepared from each aortic specimen. The evaluated features included elastic fibre fragmentation, cystic medial change, smooth muscle cell necrosis, medial fibrosis, and the markers of medial apoptosis and the metalloproteinases. Furthermore, genetic risk factors were also investigated. RESULTS: The same medial degenerative lesions in tissue samples of different aorta segments (precisely of aortic root without dilatation, and aneurysmatic ascending aorta portion) were observed. More significant associations between single nucleotide polymorphisms (-786T/C endothelial nitric oxide synthase enzyme, D/I angiotensin-converting enzyme, -1562C/T metalloproteinase-9 and -735C/T metalloproteinase-2) and aneurysm risk were detected in BAV patients than in controls. CONCLUSIONS: Based on our histological and genetic data, we underline that a surgical approach in patients with BAV, ascending aortic aneurysm and normal root, should consider not only the diameter of the aneurysmatic aortic portion but also the histological features of the whole ascending aorta and the genetic risk profile.