Characterization of the inflammatory and apoptotic cells in the aortas of patients with ascending thoracic aortic aneurysms and dissections

Abstract

The coexistence of inflammatory cells with markers of apoptotic vascular cell death in the media of ascending aortas with aneurysms and type A dissections raises the possibility that activated T cells and macrophages may contribute to the elimination of smooth muscle cells and degradation of the matrix associated with thoracic aortic aneurysms and dissections.

Genetic contribution in sporadic thoracic aortic aneurysm? Emerging evidence of genetic variants related to TLR-4-mediated signaling pathway as risk determinants

“…An active participation of both innate/inflammatory and clonotypic responses has been evidenced. Infiltration of inflammatory/immune cells has been actually identified through immune-histochemical assays both in the media and adventitia from aorta samples of patients with sporadic TAA [46,47]. Accordingly, we observed significant increased amounts of CD3 + CD4 + CD8 + CD68 + CD20 + cells in tissue aorta samples from patients with Stanford type A aortic dissection [32].…”

Copy number variation in patients with cervical artery dissection

“…Because of the small size of our study sample we did not perform an open GO Term Finder search, but restricted the GO search to predefined biological processes. These GO terms were chosen as candidates that may be involved in the development of medial degeneration, 20,21 that were assumed to be associated with the risk for CeAD, or were involved in the development of the arterial system. Strength of our study was the precise phenotype of the patients.…”

“…We selected these GO process terms as medial degeneration, the putative cause of arterial dissections, is characterized by smooth muscle proliferation, apoptosis, connective tissue remodeling and proteoglycan accumulation. 20,21 Disruption of TGF-beta receptor signaling, inflammation and connective tissue disorders are known risk factors for arterial dissections. 3,22,23 RESULTS Data sets from 70 (out of 77) CeAD-patients and 403 (out of 1262) control subjects were included in the final analysis.…”

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease: Executive Summary

“…Recent literature supports the presence of inflammatory cell infiltration in this disease. 11,12 Aortic pathology associated with myosin heavy chain 11, smooth muscle (MYH11) and actin, alpha 2, smooth muscle aorta (ACTA2) mutations leading to ascending aortic aneurysms demonstrates a hyperplastic response by smooth muscle cells in the aortic media. The aortic media in aneurysm tissue taken from patients harboring mutations in these genes demonstrated focal hyperplasia associated with smooth muscle cells that were remarkable for a lack of structured orientation parallel to the lumen of the aorta, but instead, the smooth muscle cells were oriented randomly with respect to one another.…”