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Conduction Tissue (conduction + tissue)
Selected AbstractsElectrophysiology and Anatomic Characterization of an Epicardial Accessory PathwayJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2001JOHN SAPP M.D. Epicardial Accessory Pathway. Pericardial access permitted epicardial catheter mapping and ablation of a rapidly conducting posteroseptal accessory pathway (AP) that had failed repeated ablation attempts. Transient block was achieved at the site of an AP potential. The AP was visible at surgery and resected. Histologic examination revealed cells typical of specialized cardiac conduction tissue. The location, size, and presence of conduction tissue likely account for failure of catheter ablation and resistance to drug therapy. [source] Aortic fat pad and atrial fibrillation: cardiac lymphatics revisitedANZ JOURNAL OF SURGERY, Issue 1-2 2009Ryszard W. Lupinski Abstract The lymphatics of the heart have not generated any broad or sustained interest among clinicians. Few publications on cardiac lymphatics are available, the anatomy is not routinely known and the true role of cardiac lymphatics remains doubtful. One important anatomical concept needing clarification is that of the lymphatic drainage of conduction tissue. The sinoatrial node lymphatic collector and right principal lymphatic trunk are both incorporated into the aortic fat pad of the ascending aorta and are the most frequently damaged lymphatic vessels during cardiac surgery. Thus, preservation of the aortic fat pad and its lymphatic collectors should reduce the incidence of new atrial fibrillation observed in patients after cardiac surgery. This review assesses current knowledge of cardiac lymphatics and shows their possible role in triggering arrhythmias in the postoperative period. [source] Role of hypoxia and cAMP in the transdifferentiation of human fetal cardiac fibroblasts: Implications for progression to scarring in autoimmune-associated congenital heart blockARTHRITIS & RHEUMATISM, Issue 12 2007Robert M. Clancy Objective Identification of isolated congenital heart block (CHB) predicts, with near certainty, the presence of maternal anti-SSA/Ro antibodies; however, the 2% incidence of CHB in first offspring of anti-SSA/Ro+ mothers, 20% recurrence in subsequent pregnancies, and discordance in identical twins suggest that an environmental factor amplifies the effect of the antibody. Accordingly, this study was carried out to explore the hypothesis that hypoxia potentiates a profibrosing phenotype of the fetal cardiac fibroblast. Methods Evidence of an effect of hypoxia was sought by immunohistologic evaluation of CHB-affected fetal heart tissue and by determination of erythropoietin levels in cord blood. The in vitro effect of hypoxia on gene expression and phenotype in fibroblasts derived from fetal hearts and lungs was investigated by Affymetrix arrays, quantitative polymerase chain reaction (PCR), immunofluorescence, and immunoblotting. Results In vivo hypoxic exposure was supported by the prominent intracellular fibroblast expression of hypoxia-inducible factor 1, in conduction tissue from 2 fetuses in whom CHB led to death. The possibility that hypoxia was sustained was suggested by significantly elevated erythropoietin levels in cord blood from CHB-affected, as compared with unaffected, anti-SSA/Ro,exposed neonates. In vitro exposure of cardiac fibroblasts to hypoxia resulted in transdifferentiation to myofibroblasts (a scarring phenotype), as demonstrated on immunoblots and immunofluorescence by increased expression of smooth muscle actin (SMA), an effect not seen in lung fibroblasts. Hypoxia-exposed cardiac fibroblasts expressed adrenomedullin at 4-fold increased levels, as determined by Affymetrix array, quantitative PCR, and immunofluorescence, thus focusing attention on cAMP as a modulator of fibrosis. MDL12,330A, an adenylate cyclase inhibitor that lowers the levels of cAMP, increased expression of fibrosis-related proteins (mammalian target of rapamycin, SMA, plasminogen activator inhibitor type 1, and type I collagen), while the cAMP activator forskolin attenuated transforming growth factor ,,elicited fibrosing end points in the cardiac fibroblasts. Conclusion These findings provide evidence that hypoxia may amplify the injurious effects of anti-SSA/Ro antibodies. Modulation of cAMP may be a key component in the scarring phenotype. Further assessment of the susceptibility of cardiac fibroblasts to cAMP modulation offers a new research direction in CHB. [source] Wnt11 and Wnt7a are up-regulated in association with differentiation of cardiac conduction cells in vitro and in vivoDEVELOPMENTAL DYNAMICS, Issue 4 2003Jacqueline Bond Abstract The heart beat is coordinated by a precisely timed sequence of action potentials propagated through cells of the conduction system. Previously, we have shown that conduction cells in the chick embryo are derived from multipotent, cardiomyogenic progenitors present in the looped, tubular heart. Moreover, analyses of heterogeneity within myocyte clones and cell birth dating have indicated that elaboration of the conduction system occurs by ongoing, localized recruitment from within this multipotent pool. In this study, we have focused on a potential role for Wnt signaling in development of the cardiac conduction system. Treatment of embryonic myocytes from chick with endothelin-1 (ET-1) has been shown to promote expression of markers of Purkinje fiber cells. By using this in vitro model, we find that Wnt11 are Wnt7a are up-regulated in association with ET-1 treatment. Moreover, in situ hybridization reveals expression, although not temporal coincidence of, Wnt11 and Wnt7a in specialized tissues in the developing heart in vivo. Specifically, whereas Wnt11 shows transient and prominent expression in central elements of the developing conduction system (e.g., the His bundle), relative increases in Wnt7a expression emerge at sites consistent with the location of peripheral conduction cells (e.g., subendocardial Purkinje fibers). The patterns of Wnt11 and Wnt7a expression observed in vitro and in the embryonic chick heart appear to be consistent with roles for these two Wnts in differentiation of cardiac conduction tissues. Development Dynamics 227:536,543, 2003. © 2003 Wiley-Liss, Inc. [source] Topographic Anatomy of the Inferior Pyramidal Space: Relevance to Radiofrequency Catheter AblationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2001DAMIÁN SÁNCHEZ-QUINTANA M.D. Inferior Pyramidal Space and Ablation.Introduction: Radiofrequency catheter ablation carried out in the vicinity of the triangle of Koch risks damaging not only the AV conduction tissues but also their arterial supply. The aim of this study was to examine the relationship of the AV nodal artery to the inferior pyramidal space, the triangle of Koch, and the right atrial endocardial surface. Methods and Results: We studied 41 heart specimens, 24 by gross dissections and 17 by histologic sections. The proximity of the AV nodal artery to the surface landmarks of the triangle of Koch was variable, but it was notable that in 75% of specimens the artery passed close to the endocardial surface of the right atrium and within 0.5 to 5 mm of the mouth of the coronary sinus. In all specimens, the mean distance of the artery to the endocardial surface was 3.5 ± 1.5 mm at the base of Koch's triangle. The location of the compact AV node and its inferior extensions varied within the landmarks of the triangle. At the mid-level of Koch's triangle, the compact node was medially situated in 82% of specimens, but it was closer to the hinge of the tricuspid valve in the remaining 18% of specimens. In 12% of specimens, the inferior parts of the node extended to the level of the mouth of the coronary sinus. Conclusion: The nodal artery runs close to the orifice of the coronary sinus, the endocardial surface of the right atrium, the middle cardiac vein, and the specialized conduction tissues in most hearts. The nodal artery and/or the AV conduction tissues can be at risk of damage when ablative procedures are carried out at the base of the triangle of Koch. [source] Complete heart block associated with lupus in a dogAUSTRALIAN VETERINARY JOURNAL, Issue 7 2003R MALIK A 5-year-old Poodle-cross was initially presented for exercise intolerance and difficulty in chewing and yawning. Some months later it acutely developed lethargy referable to complete heart block. Further investigations before and after permanent pacemaker implantation demonstrated Coombs-positive immune-mediated haemolytic anaemia, presumptive masticatory myositis and hypoadrenocorticism, suggesting the possibility of multisystem auto-immune disease. A diagnosis of systemic lupus erythematosus (SLE) was made based on these findings and a positive anti-nuclear antibody titre. It was thought that immune-mediated destruction of cardiac conduction tissues was responsible for the development of atrioventricular conduction block. Glucocorticoid deficiency was corrected using cortisone replacement therapy. SLE was controlled successfully for 10 months using azathio-prine monotherapy until signs, subsequently shown to be due to subacute bacterial endocarditis, resulted in the death of the patient. Lupus should be considered as a potential underlying aetiology in dogs that develop heart block. [source] | ||||||||||