title: Inflammatory Cell Infiltrates in Acute and Chronic Thoracic Aortic Dissection.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  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. 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; ; Department of Cardiovascular Surgery, The Texas Heart Institute, Houston, Texas; ; Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas; and.
authors.forename: Darrell
authors.initials: D
authors.lastname: Wu
authors.affiliation: Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; ; Department of Cardiovascular Surgery, The Texas Heart Institute, Houston, Texas;
authors.forename: Justin C
authors.initials: JC
authors.lastname: Choi
authors.affiliation: Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; ; Department of Cardiovascular Surgery, The Texas Heart Institute, Houston, Texas;
authors.forename: Aryan
authors.initials: A
authors.lastname: Sameri
authors.affiliation: Dan L. Duncan Institute for Clinical and Translational Research, Baylor College of Medicine, Houston, Texas.
authors.forename: Charles G
authors.initials: CG
authors.lastname: Minard
authors.affiliation: Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; ; Department of Cardiovascular Surgery, The Texas Heart Institute, Houston, Texas;
authors.forename: Joseph S
authors.initials: JS
authors.lastname: Coselli
authors.affiliation: Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; ; Department of Cardiovascular Surgery, The Texas Heart Institute, Houston, Texas;
authors.forename: Ying H
authors.initials: YH
authors.lastname: Shen
authors.affiliation: Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; ; Department of Cardiovascular Surgery, The Texas Heart Institute, Houston, Texas; ; Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas; and.
authors.forename: Scott A
authors.initials: SA
authors.lastname: LeMaire
keywords: Inflammation; Macrophage; Mast cell; Neutrophil; T lymphocyte; Thoracic aortic dissection