Lymphangiogenesis is increased in heart valve endocarditis.

BACKGROUND: Inflammation-associated lymphangiogenesis (IAL) has been identified as part of several acute and chronic inflammation. Sparse data exist on lymphatics during endocarditis. MATERIALS AND METHODS: Fifty-two patients with surgically resected valves were included. Endocarditis was present in 18 aortic and 10 mitral valves. Controls consisted of 15 degenerative aortic and 9 degenerative mitral valves. There were 22 males with endocarditis and 17 males in controls. The mean age was 58 (SD 15) years with endocarditis vs. 62 (SD 13) years for controls. Lymphatics were detected by podoplanin antibody immunohistochemistry and morphometrical analysis was performed. RESULTS: The lymphatic density in endocarditis was 833 (SD 529) vessels/mm(2) (range 0-1707) as compared with 39 (SD 60) vessels/mm(2) (range 0-250) in controls (p=0.000). In endocarditis, the mean lymphatic size was 153 (SD 372) µm(2) ranging from 1 to 2034µm(2), whereas it was 30 (SD 29) µm(2), with maximum 90µm(2) and minimum 2µm(2) in controls (p=0.000). CONCLUSIONS: IAL is increased in valves with endocarditis as compared with controls. Lymphatics in heart valves may provide a novel means for treatment strategies against endocarditis.

Carbonic anhydrase IX deposits are associated with increased ascending aortic dilatation.

OBJECTIVES: Carbonic anhydrase IX (CA IX) expression is induced by local hypoxia. We studied whether CA IX deposits associate with ascending aortic dilatation. DESIGN: Aortic wall histology, CA IX expression, presence of leukocytes, plasma cells, macrophages, endothelial cells, smooth muscle cells, cell proliferation, elastin and collagen were studied in histological specimens collected from 30 patients who underwent surgery for ascending aorta. The samples were grouped according to presence of CA IX deposits. RESULTS: Twenty out of 30 patients had CA IX-positive deposits within the adventitia, whereas 10 specimens remained negative. Adventitial inflammation was increased in CA IX-positive samples as compared with CA IX-negative ones (p < 0.01). The mean diameter of the ascending aorta at the sinotubular junction increased significantly in patients with CA IX-positive staining as compared with CA IX-negative cases (63 ± 3 vs 53 ± 2 mm, p < 0.02). Receiver operating characteristic curve analysis confirmed the association of CA IX positivity with increased ascending aortic dilatation (AUC 0.766; S.E. 0.090; p = 0.020; 95% C.I. 0.590-0.941). CONCLUSIONS: Positive CA IX staining in certain aortic specimens suggests that increased CA activity may contribute to ascending aortic dilatation.

Aiming at one-stage corrective surgery for extended thoracic aortic dilatation.

Definitive treatment of extended thoracic aortic dilatation is a major surgical challenge. Histopathology of resected thoracic aortic wall may reveal undiagnosed aortitis affecting outcome. We sought to investigate the benefit of thorough histopathology after one-stage corrective surgery for the treatment of extended thoracic aortic dilatation. Five patients underwent one-stage corrective surgery using the hybrid open arch repair by the frozen elephant trunk together with endovascular aortic grafting. A representative sample of the resected aortic arch was procured for histology. T- and B-lymphocytes, plasma cells, macrophages, and immunoglobulin G4 (IgG4) positivity were evaluated by immunohistochemistry. The mean preoperative maximum aortic diameter was 54 mm (range, 41-79 mm). The mean follow-up was 18 months (range, 1-24 months). As confirmed by computed tomography (CT) upon follow-up, complete thrombosis of the false lumen at the level of the frozen elephant trunk was achieved in all patients with dissection. One patient was operated due to atherosclerotic dilatation of the thoracic aorta, and postoperative CT showed successful exclusion of the atherosclerotic dilatation; this 75-year-old man was diagnosed with IgG4-positive aortitis and experienced unexpected blindness after surgery without evidence of emboli or long-term neurological impairment upon repeated brain CT. The hybrid open arch repair by the frozen elephant trunk and simultaneous endovascular repair is a feasible choice for one-stage surgery through sternotomy aiming at definitive treatment of extended thoracic aortic pathology. However, systematic evaluation of inflammation may reveal concealed aortitis affecting postoperative outcome and need for long-term surveillance.

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.