Inflammatory Cell Infiltrates in Acute and Chronic Thoracic Aortic Dissection.

Darrell Wu,Aryan Sameri,Charles G Minard,Ying H Shen,Joseph S Coselli,Scott A Lemaire,Justin C Choi

doi:10.12945/j.aorta.2013.13-044

Abstract

Thoracic aortic dissection (TAD) is a highly lethal cardiovascular disease. Injury to the intima and media allows pulsatile blood to enter the media, leading to dissection formation. Inflammatory cells then infiltrate the site of aortic injury to clear dead cells and damaged tissue. This excessive inflammation may play a role in aneurysm formation after dissection. Using immunohistochemistry, we compared aortic tissues from patients with acute TAD (n = 11), patients with chronic TAD (n = 35), and donor controls (n = 20) for the presence of CD68+ macrophages, neutrophils, mast cells, and CD3+ T lymphocytes. Tissue samples from patients with acute or chronic TAD generally had significantly more inflammatory cells in both the medial and adventitial layers than did the control samples. In tissues from patients with acute TAD, the adventitia had more of the inflammatory cells studied than did the media. The pattern of increase in inflammatory cells was similar in chronic and acute TAD tissues, except for macrophages, which were seen more frequently in the adventitial layer of acute TAD tissue than in the adventitia of chronic TAD tissue. The inflammatory cell content of both acute and chronic TAD tissue was significantly different from that of control tissue. However, the inflammatory cell profile of aneurysmal chronic TAD was similar to that of acute TAD. This may reflect a sustained injury response that contributes to medial degeneration and aneurysm formation.

Highlights

Aneurysm formation after thoracic aortic dissection (TAD) is a deadly cardiovascular disease and a major cause of morbidity and mortality [1]
We characterized the inflammatory infiltrate observed in aortic tissues from acute and chronic Thoracic aortic dissection (TAD) patients by means of immunohistochemistry; all TAD tissues showed significantly more CD68ϩ macrophages, neutrophils, mast cells, and CD3ϩ T lymphocytes in both the medial and adventitial layers as compared to the same vessel layer in aortic tissues from controls (Figs. 1A and 1B, 2A and 2B, 3A and 3B, and 4A and 4B, respectively)
We found a greater abundance of all inflammatory cell types in the adventitia than in the media (Figs. 1C, 2C, 3C, and 4C, respectively); this finding suggests that inflammatory cells infiltrate the aortic wall from the vasa vasorum into the media [10]

Summary

Introduction

Aneurysm formation after thoracic aortic dissection (TAD) is a deadly cardiovascular disease and a major cause of morbidity and mortality [1]. Inflammatory cells infiltrate the site of aortic injury to clear dead cells and damaged tissue. This excessive inflammation may play a role in aneurysm formation after dissection. Results: Tissue samples from patients with acute or chronic TAD generally had significantly more inflammatory cells in both the medial and adventitial layers than did the control samples. The inflammatory cell profile of aneurysmal chronic TAD was similar to that of acute TAD This may reflect a sustained injury response that contributes to medial degeneration and aneurysm formation

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