Immunoglobulin G4-positive ascending thoracic aortitis may be prone to dissection.

OBJECTIVE: Immunoglobulin (Ig) G4-positive aortitis may determine outcome after surgery for ascending aorta. We evaluated IgG4 expression of dilated ascending aortic wall. METHODS: The study consisted of 91 patients who underwent ascending aortic surgery. For histology, hematoxylin-eosin, elastase-van Gieson, and periodic acid-Schiff stainings were performed. The amount of T and B lymphocytes, plasma cells, macrophages, cell proliferation, and IgG4 positivity were determined by immunohistochemistry. RESULTS: The aortic wall in 12 patients had IgG4 positivity that was always confined to the adventitia. Adventitial plasma cells were numerous in all but 2 of these patients (P < .0001). Aortitis was revealed in 2 patients (17%) with IgG4-positive staining of the aorta and in 6 patients (8%) with IgG4 negativity. IgG4 staining was significantly associated with total aortic wall inflammation (area under the curve, 0.865; standard error, 0.043; P = .000; 95% confidence interval, 0.779-0.950). The mean diameter of the ascending aorta was 69 ± 4.7 mm and 56 ± 1.1 mm in patients with IgG4 positivity and negativity, respectively (P < .004). Approximately half of the patients with IgG4 positivity had dissection (42%), compared with only 15 of 79 (19%) of the remaining patients (P = not significant). Two patients with IgG4 positivity had to undergo reoperation because of immediate postoperative dissection. Seven patients died, including 4 patients (33%) with IgG4 positivity; the remaining 3 patients (4%) were IgG4 negative (P < .005). CONCLUSIONS: IgG4-positive ascending aortic wall was frequent in our study cohort (13%) and revealed aortic inflammation associated with dilatation.

Lack of C4d deposition may reveal susceptibility for ascending aortic dissection.

OBJECTIVES: Complement activation as evidenced by C4d deposition indicates immunological tissue reactivity. We sought to study the vascular reactivity of the aortic wall by characterizing C4d deposits. DESIGN: Aortic wall histology and immunohistochemistry for C4d, leukocytes, T- and B-lymphocytes, plasma cells, macrophages, endothelial cells, smooth muscle cells, cell proliferation, elastase, and Van-Gieson-staining were performed to 91 consecutive patients that underwent surgery for ascending aorta, and the samples were grouped according to presence of C4d deposits. RESULTS: Fifty-three out of 91 patients had C4d deposits mainly within the adventitia (C4d +), whereas 38 patients lacked C4d deposits (C4d-) including decreased staining of intra-aortic vessels (p < 0.005). Intimal thickness and cellularity, together with inflammation consisting of plasma cells were increased in C4d- as compared with C4d + (p < 0.05). Receiver operating characteristic curve (ROC) analysis showed that C4d was associated with stabile nondissecting ascending aorta (AUC 0.792; SE 0.053; p = 0.000; 95% CI 0.688-0.895), but not with presence of aortitis per se (AUC 0.523; SE 0.069; p = 0.752; 95 % CI 0.388-0.658). CONCLUSIONS: Lack of C4d may indicate active remodeling of the aortic wall leading to aortic dissection (AD). Immunologic complement factors may be amenable to diagnosis of instability after aortic surgery.

A disintegrin and metalloprotease -8 and -15 and susceptibility for ascending aortic dissection.

BACKGROUND. Dilatation of the ascending aorta (AA) is affected by extra-cellular matrix modifications and inflammation. A disintegrin and metalloproteases (ADAMs) may reveal differences between AA and ascending aortic dissection (AD). We characterized the inflammatory histology of AD and AA and examined the role of ADAM8 and -15 in these diseases. MATERIAL AND METHODS. Aortic wall histology and immunohistochemistry for leukocytes, T- and B-lymphocytes, plasma cells, macrophages, endothelial cells, smooth muscle cells, cell proliferation, elastase and Van-Gieson-staining were performed to 40 consecutive patients that underwent surgery for AA or AD. The expressions of ADAM8 and -15 mRNA and proteins were evaluated using QRT-PCR and immunohistochemistry. RESULTS. Thirty-four patients were enrolled, of which 29 had AA and five had AD of the ascending aorta. B-cells throughout the aortic wall and intimal plasma cells were more numerous during AD as compared with AA (p < 0.05). The gene expressions for ADAM8 and -15 were notably lower in AA as compared with AD. The median for down-regulation of ADAM8 and -15 in AA was -2.7 and -1.8, respectively. ADAM8 and -15 were mainly found in the media layer in patients with AD. Two of the patients with AA and increased ADAMs developed AD of the remaining aorta. CONCLUSIONS. The involvement of ADAM8 and -15 together with inflammation consisting of B-cells may indicate active remodelling of the aortic wall leading to AD.