Right Ventricular Remodeling Determines Tricuspid Valve Geometry and the Severity of Functional Tricuspid Regurgitation: A Real-Time 3-Dimensional Echocardiography Study

BACKGROUND AND OBJECTIVES: Right ventricle (RV) remodeling can determine tricuspid valve (TV) geometry and the severity of functional tricuspid regurgitation (TR). SUBJECTS AND METHODS: In 53 patients with various degrees of functional TR and in sinus rhythm, RV and TV geometries were analyzed using real-time 3-dimensional echocardiography, including tenting angles of 3 leaflets, septal-lateral and antero-posterior tricuspid annulus diameters and inlet RV dimensions, mid-RV septal-lateral dimension, and the distance between annulus and apex. A mid-systole frame when the TV tenting is smallest was selected for the analysis. RV end-diastolic and end-systolic volumes were measured. The severity of functional TR was determined by distal jet area. RESULTS: TR distal jet area was mainly determined by septal-lateral annulus diameter (p<0.001) RV inlet dimension (p=0.015), RV end-systolic volume (p=0.010), septal (p=0.019), and anterior leaflet tenting angles (p=0.045) by multiple stepwise linear regression analysis. Leaflet tenting angles were mainly determined by septal-lateral RV inlet dimension. Septal-lateral annulus diameter was determined by septal-lateral RV inlet dimension (p<0.001) and mid RV dimension (p=0.033), whereas antero-posterior annulus diameter was determined by antero-posterior RV inlet dimension (p<0.001). CONCLUSION: Functional TR severity is determined by septal-lateral annulus and RV dilation, and tenting of septal and anterior leaflets. TV leaflet tenting is mainly determined by septal-lateral RV inlet dilation, and tricuspid annulus dilation is closely linked with inlet RV dilation.

Chlamydophila pneumoniae enhances secretion of VEGF, TGF-beta and TIMP-1 from human bronchial epithelial cells under Th2 dominant microenvironment

PURPOSE: Chlamydophila pneumoniae infection in the airways is thought to be associated with the pathogenesis of asthma, especially in non-atopic severe asthma with irreversible airway obstruction that may be related to airway remodeling. Here, we investigated whether C. pneumoniae infection enhances the secretion of critical chemical mediators for airway remodeling, such as VEGF, TGF-beta, and TIMP-1, in human bronchial epithelial cells (BECs) in a Th2-dominant microenvironment. METHODS: Human bronchial epithelial cells (BEAS-2B cells) were infected with C. pneumoniae strain TW183 and cultured in both a Th1-dominant microenvironment with INF-gamma and a Th2-dominant microenvironment with IL-4 or IL-13 added to the culture medium. The VEGF, TGF-beta, and TIMP-1 levels in the culture supernatants were measured using enzyme-linked immunosorbent assays (ELISA). The activation of NF-kappaB in each experimental condition was determined using an electrophoretic mobility shift assay. RESULTS: Chlamydophila pneumoniae-infected BECs showed enhanced secretion of VEGF, TGF-beta, and TIMP-1 compared with non-infected BECs. The levels of cytokines secreted from BECs were increased more when IL-13 was added to the culture medium. C. pneumoniae-infected BECs also showed increased NF-kappaB activation. CONCLUSIONS: These results suggest that C. pneumoniae plays a role in the pathogenesis of airway remodeling in asthma, revealing a Th2-dominant immune response. Further studies are required to clarify the precise mechanism of C. pneumoniae infection in airway remodeling.