Search

Progress in protein chemistry in the 1950s revealed that the biologic activities of proteins, such as hemoglobin and enzymes, are based on partial structures in the protein molecules. This principle suggested to us the possibility that the human antibodies responsible for induction of reaginic hypersensitivity reactions might have unique structures that are lacking in the antibody molecules involved in immunity and that the differences in the structures of human antibody molecules can be recognized by the immune systems of experimental animals. Our studies were based on the hypothesis that reaginic antibody activity is associated with a unique immunoglobulin isotype, which is now called IgE. As expected, identification of IgE facilitated the analysis of immunologic mechanisms of reaginic hypersensitivity. Subsequent studies revealed that IgE specifically bound to basophilic granulocytes and mast cells through the Fc portion of the molecules and that cross-linking of the cell-bound IgE antibody molecules by allergen induced the release of bioactive mediators, such as histamine and leukotrienes, which initiate allergic reactions., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: Functional tricuspid regurgitation (TR) often develops secondary to left heart disease. Tricuspid annuloplasty (TAP) is usually the treatment of choice for significant TRs, but recurrence of TR after surgery can occur. Previous studies have not clearly demonstrated the cause of the recurrent TR after TAP. By using an electrocardiogram-gated 320-detector-row multislice computed tomography (CT), we sought to delineate the morphologic cause of the incompetent tricuspid valve and identify the risk factors for recurrent TR., Methods: From August 2010 to September 2011, 35 patients underwent preoperative CT of the tricuspid valve. The distance between each commissure, the tethering angle of each leaflet, and the tethering height were measured. TAP using a rigid annuloplasty ring was performed in 22 patients. Risk factors for recurrent TR were determined by multivariate analyses., Results: End-diastolic and end-systolic tricuspid valve annular diameters (TVAD) correlated significantly with preoperative TR severity (R(2), 0.2734-0.4287; P < .05). However, compared with TVAD, tethering angles and height showed stronger correlation with preoperative TR severity (R(2): tethering angles, 0.5769-0.6810; tethering height, 0.6854). Multivariate analysis revealed that tethering height was an independent risk factor of postoperative recurrent TR (P = .0069)., Conclusions: TVAD, tethering angles, and tethering height correlated significantly with preoperative TR severity. The tethering height of the tricuspid valve showed significant correlation with recurrent TR., (Copyright © 2014 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.)

Objectives: Atrial tachyarrhythmia is a common complication late after the atriopulmonary connection Fontan procedure. The P-wave duration and dispersion have been regarded as useful markers for its prediction. The purpose of this study was to analyze change in the P-wave characteristics over time after the atriopulmonary connection Fontan procedure, with a special emphasis on the timing of the Fontan conversion., Methods: We reviewed clinical and electrocardiographic data in 18 patients with classic tricuspid atresia who underwent the atriopulmonary connection Fontan procedure. Their median age at operation was 4.1 years (range, 1.1-22 years), and the median follow-up period was 18.1 years (range, 10-25 years). We measured the P-wave duration, dispersion, and axis from consecutive 12-lead electrocardiograms in each patient., Results: There was a significant increase in the maximum P-wave duration as well as the P-wave dispersion over time. Transient ectopic atrial rhythm was observed in 16 patients during follow-up. Atrial tachyarrhythmia developed subsequent to transient ectopic atrial rhythm in 8 patients. Ten patients underwent the conversion. Atrial tachyarrhythmia recurred in 2 patients who had sustained arrhythmia (6.0 and 8.0 years) before the conversion. In contrast, the other 8 patients with transient ectopic atrial rhythm alone or nonsustained atrial tachyarrhythmia have been free from arrhythmia after the conversion., Conclusions: Patients commonly and increasingly had prolonged P-wave duration, larger P-wave dispersion, and ectopic atrial rhythm, along with an atrial tachyarrhythmia propensity, late after the atriopulmonary connection Fontan procedure. These P-wave characteristics were informative when considering the Fontan conversion before a sustained atrial tachyarrhythmia ensued.

Objective: Left ventricular outflow tract obstruction remains an early and late complication after repair of interrupted aortic arch and ventricular septal defect. We reviewed our experience with the selective management of the infundibular septum during primary repair to address left ventricular outflow tract obstruction., Methods: From 1991 through 2001, all 27 patients presenting with interrupted aortic arch/ventricular septal defect and posterior deviation of the infundibular septum were analyzed. Fifteen patients with the smallest subaortic areas underwent myectomy or myotomy of the infundibular septum concomitant with interrupted aortic arch/ventricular septal defect repair., Results: Patients undergoing myectomy-myotomy (Group I) had significantly smaller subaortic diameter indexes (0.83 +/- 0.16 cm/m2) when compared with those who had only interrupted aortic arch/ventricular septal defect repair (group 2: 0.99 +/- 0.13 cm/m2, P = .012). Two hospital deaths occurred in group 1, and 1 occurred in group 2. No late deaths occurred. No patient in group 2 required reoperation. Six group 1 patients required 9 reoperations for left ventricular outflow tract obstruction. Five patients underwent resection of a new subaortic membrane. Only 1 patient had recurrent muscular left ventricular outflow tract obstruction. Three patients required a second reoperation, primarily related to aortic valve stenosis., Conclusions: Interrupted aortic arch/ventricular septal defect with posterior malalignment of the infundibular septum can be repaired with low mortality in the neonatal period. Tailored to the degree of subaortic narrowing, resection or incision of the infundibular septum at the time of primary repair was very effective in preventing or prolonging the interval to recurrent left ventricular outflow tract obstruction compared with the published data. However, reoperation for left ventricular outflow tract obstruction, often related to the development of a new and discrete subaortic membrane or valvar stenosis, is still required in a subset of patients.

Objective: We sought to examine midterm results of the Fontan operation with an extracardiac conduit using pedicled autologous pericardial roll, with special attention to angiographic evaluation of serial changes in conduit geometry., Methods: Of 202 patients subjected to the Fontan operation since 1996, the conduit was used in 28 patients who had intact pericardium. We retrospectively reviewed a consecutive series of these patients, and serial changes in conduit geometry were accessed in 16 patients who underwent catheter examinations twice at 1.1 +/- 0.4 and 4.5 +/- 1.4 years postoperatively., Results: There was one early and one late death. Except for a patient with apicocaval juxtaposition in whom a conduit occlusion developed caused by compression between the vertebral bodies and the ventricle, there were no important complications. Angiographically, conduit volume, estimated by using the MULTI-SLICE method, increased significantly (3490 +/- 2166 to 5426 +/- 3081 mm3, P < .001), whereas the volume per body weight remained unchanged. Conduit diameter increased significantly at both the inferior vena caval end (16.8 +/- 4.8 to 19.8 +/- 4.8 mm, P < .001) and the pulmonary artery end (11.9 +/- 3.8 to 14.2 +/- 4.2 mm, P < .001), whereas the diameter indexed to the normal right pulmonary artery remained unchanged. The cross-sectional area of the conduit increased in parallel with that of the normal right pulmonary artery. The ratio of the widest to the narrowest diameter of the conduit exhibited no significant change., Conclusions: Midterm results of the Fontan operation with pedicled autologous pericardial roll were favorable. Proportional increase of conduit size was demonstrated, with its shape preserved. This suggested a potential of the conduit to grow and that growth correlated with somatic development.

Background: Severe degree of pulmonary vascular hypoplasia remains a major limitation in congenital heart surgery. Considering the potential effect of gene transfer with hepatocyte growth factor to induce the angiogenesis in the lung, we assessed the effects of hepatocyte growth factor gene transfer in neonatal porcine lung with pulmonary vascular hypoplasia to achieve treatment for severe pulmonary vascular hypoplasia., Methods: The model of pulmonary vascular hypoplasia was introduced with left pulmonary artery banding in piglet lung. After 7 days of pulmonary artery banding, piglets were transfected selectively to the left lung via the left pulmonary artery with a hemagglutinating virus of Japan E vector bearing the cDNA encoding human hepatocyte growth factor (H group) or control vector (C group)., Results: Seven days after the transfection, selective angiography of the left pulmonary artery showed the progression of left pulmonary vascular hypoplasia of the left lung in the C group but a significant attenuation of left pulmonary vascular hypoplasia in the H group. A right pulmonary artery occlusion test showed a marked increase in right ventricular systolic pressure in the C group, but this was significantly attenuated in the H group (C: 22.0 +/- 2.9, H: 13.0 +/- 2.7 mm Hg; P < .05). Histologic examination revealed that hepatocyte growth factor gene transfection increased the pulmonary vasculature in the left lung., Conclusions: Our results demonstrated that gene transfer of hepatocyte growth factor via the pulmonary artery showed the angiogenic effects in porcine model of pulmonary vascular hypoplasia after pulmonary artery banding.

It is generally accepted that an initial step of reaginic hypersensitivity reactions is a bridging of mast cell--bound IgE antibody molecules by antigen. Since IgE molecules are firmly bound to receptors on mast cells, bridging of cell-bound IgE molecules probably brings receptor molecules into close proximity. A hypothesis was therefore presented that such a local change in membrane structure and/or possible interaction between adjacent receptor molecules may be triggering mechanisms of IgE-mediated histamine release. The hypothesis was tested by use of antibodies against "exposed portion" of receptor molecules on rat basophilic leukemia cells. It was found that antireceptor antibodies and its F(ab')2fragments induced noncytotoxic histamine release from normal rat mast cells without participation of IgE, while the monovalent Fab' fragments of the antibody failed to do so. However, sensitization of normal rat skin with the Fab' fragments followed by an intravenous injection of antirabbit IgG induced skin reactions. These findings support the concept that bridging of receptors rather than polymerization of IgE molecules is responsible for the activation of membrane-associated enzymes which in turn leads to histamine release.

The infection of rats with Nippostrongylus brasiliensis (Nb) larvae enhanced IgE synthesis prior to the formation of IgE antibody specific for parasite antigens. As early as the eighth to tenth day of infection, IgE-bearing lymphocytes appeared in lymph nodes and spleen. At this time, even bone marrow contained IgE-bearing blast cells. The IgE-forming plasma cells were detected in the lymph nodes and spleen at the tenth day and their number reached maximum at the fourteenth day. The proliferation of IgE-bearing lymphocytes in the lymphoid tissues was observed in neonatally thymectomized animals, indicating that T cells are not essential for the development of IgE-B cells in the infected animals. It appears, however, that T cells are involved in the differentiation of IgE-B cells to IgE-forming plasma cells. Nonspecific proliferation of IgE-B cells and their differentiation to IgE-forming plasma cells may explain potentiation of IgE antibody formation against unrelated antigens after infection with N. brasiliensis (Nb). It was also found that T cells specific for parasite antigens were primed by infection with Nb. Evidence was obtained tht Nb-specific T cells raised by the infection collaborated with hapten-specific IgE-B cells and IgG-B cells for the secondary antihapten antibody responses. By contrast, T cells primed by immunization with parasite antigen included in alum exerted the helper function for IgG antibody response but failed to collaborate with IgE-B cells. Dissociation between the helper function for IgE and IgG antibody response indicated that parasite infection generated a favorable condition for priming T cells for the IgE antibody response.