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Biomedical subjects

C Butter

Publications and source records attributed to C Butter.

At least 37 records · Page 2Linked to original sources
PubMed2000

Transvenous biventricular defibrillation.

The recent success of biventricular pacing with transvenously implantable left ventricular leads suggests that left ventricular leads may be useful for other modes of therapy. Animal studies showed small leads inserted into a left ventricular vein dramatically reduced defibrillation strength requirements. This article describes a human investigation of the feasibility of biventricular defibrillation. Fifty-one patients undergoing implantable cardioverter defibrillator (ICD) implantation were enrolled. After insertion of a standard ICD lead, a prototype over-the-wire left ventricular defibrillation lead was inserted through the coronary sinus and into a vein on the left ventricle. Lead insertion was guided by retrograde venography. The left ventricular lead's location was randomized to the anterior or posterior vein. Randomized, paired defibrillation threshold (DFT) testing was performed to compare a standard ICD shock configuration (Control: right ventricle- --> superior vena cava+ + CAN+) to 1 of 3 biventricular shock configurations. In the anterior vein, the left ventricular lead was tested with either a single biphasic shock from right ventricle + left ventricle- --> superior vena cava+ + CAN+ or a dual biphasic shock. In the posterior vein, the left ventricular lead was tested with a dual biphasic shock. Dual shocks consisted of a 40% tilt biphasic shock from right ventricle- --> superior vena cava+ + CAN+ followed by another 40% tilt biphasic shock from left ventricle- --> superior vena cava+ + CAN+, delivered from a single 225 microF capacitance. Left ventricular lead positioning was successful in 41 of 46 patients (89%). Mean left ventricular lead insertion time was 17 +/- 17 minutes and 13 +/- 15 minutes for anterior and posterior locations, respectively. Mean DFTs were not statistically lower for the left ventricular shock configurations, but retrospective analysis showed a well-defined region of the posterolateral left ventricle where consistent DFT reduction was achieved with dual shocks (14.0 +/- 2.7 J vs 7.8 +/- 0.9 J; n = 5; p = 0.04). There were no adverse events requiring intervention due to the use of the left ventricular lead. Biventricular defibrillation is feasible and safe under the conditions used in this study. Additional studies are needed to verify whether dual shocks with posterolateral left ventricular lead positions consistently reduce DFTs.

Aged↗
PubMed2000

Pacing Therapies in Congestive Heart Failure II study.

Ventricular resynchronization therapy (VRT) by left or biventricular stimulation is gaining increasing acceptance as a new therapy in addition to drugs in patients with advanced heart failure and intraventricular conduction disturbances. Several studies have demonstrated acute hemodynamic benefit of VRT in these patients, although there are only limited long-term data in small patient cohorts. Many open questions remain: whether to pace both ventricles or the left ventricle alone, the optimal left ventricular pacing site, the criteria used to identify the optimal candidate for VRT (e.g., QRS width), and the importance of an integrated defibrillator function in a VRT device. The Pacing Therapy in Congestive Heart Failure (PATH-CHF) II study is a prospective, randomized, cross-over study currently investigating the potential benefit of VRT in a population with advanced heart failure, with or without an accepted indication for an implantable defibrillator. It focuses on the effects of optimized univentricular pacing in these patients, and both acute hemodynamic and chronic functional effects are assessed. Acute hemodynamic testing mainly investigates the impact of different left ventricular pacing sites, alone or combined with right ventricular sites, on hemodynamic performance. Primary endpoint of the study is an improvement in functional capacity as assessed by cardiopulmonary exercise testing and 6-minute walk distance; secondary endpoints include improvement in quality of life (assessed by Minnesota quality of life score, New York Heart Association (NYHA) functional class, and hospitalization frequency), and improvements in prognostic and hemodynamic parameters. The trial aims to enroll 64 patients with full datum sets (separately in 2 groups with a QRS of < or = 150 or > 150 msec, respectively) in 9 European centers. The enrollment began September 1998, and is expected to conclude in summer 2000 to reach the number of necessary datum sets.

Arrhythmias, Cardiac↗
PubMed2000

Should stimulation site be tailored in the individual heart failure patient?

Right ventricular pacing at various sites and shortened atrioventricular (AV) delay has failed to demonstrate a convincing short-term and long-term improvement of left ventricular function. Left-ventricular-based stimulation offers a new therapeutic option for patients with symptomatic congestive heart failure and conduction disturbances, especially of left bundle-branch block configuration. Left ventricular mechanical improvement seems mainly dependent on the pacing site, in addition to optimizing the AV delay. Predominantly retrospective data suggest that pacing the posterolateral free wall results in the greatest hemodynamic improvement. Based on the evaluation of different pacing sites in 2 patients, we noted that site is of major importance for maximal improvement of left ventricular function, and pacing at a suboptimal site can even deteriorate left ventricular contractility. Moreover, lead technology has advanced rapidly and different areas of the left ventricle can now be reached transvenously for acute and chronic placement. Therefore, ongoing trials will help to identify the optimal pacing site and might indicate whether invasive testing will be required in the future.

Arrhythmias, Cardiac↗
PubMed1999

CD44 is involved in selective leucocyte extravasation during inflammatory central nervous system disease.

Clinical signs of experimental autoimmune encephalomyelitis (EAE) are associated with the selective recruitment of CD4+ memory (CD45RBlow CD44high) T cells into the central nervous system (CNS). However, we have found that many of these recently recruited memory cells are CD44low, suggesting that the CD44 antigen may be involved in, and transiently lost during, the extravasation process. Indeed, administration of a CD44-specific antibody (IM7.8.1) induced leucocyte CD44 shedding and both prevented the development and ameliorated the severity of established EAE by inhibiting mononuclear cell infiltration into the CNS. Trafficking of cells into lymph nodes, however, a property mainly of naïve cells, was essentially unaffected. In contrast, treatment with antibody to very late activation antigen-4 (VLA-4) prevented homing to both the CNS and to lymph nodes. This study contests previous reports that dismissed a role for CD44 in inflammation of the CNS and, coupled with observations in murine dermatitis and arthritis, suggests that CD44 is involved in the homing of primed lymphocytes to sites of inflammation. CD44 should therefore be considered a target for immunotherapy of T-cell-mediated inflammatory diseases, such as multiple sclerosis.

Animals↗
PubMed1999

Clinical evaluation of a prototype passive fixation dual chamber single pass lead for dual chamber ICD systems.

UNLABELLED: Dual chamber ICD systems use two separate leads for sensing. We developed and tested a new prototype of a single pass dual chamber passive fixation lead for dual chamber ICDs. METHODS AND RESULTS: The prototype was a modification of the Guidant CPI Endotak DSP lead. The additional sensing electrode for the right atrium consisted of a side-mounted porous atrial ring electrode (AR). Atrial signals were recorded from the lead in patients during normal sinus rhythm (NSR), atrial fibrillation (AFib), and/or atrial flutter (AFl) with the AR in stable contact with the atrial wall or floating. During NSR, with the AR in contact with the atrial wall, an average P wave amplitude of 7.2 +/- 1.5 mV (mean +/- SD, n = 12) was measured. After induction of Afib/AFl, the single amplitude decreased to 3.6 +/- 1.5 mV (n = 8) during AFib and 3.4 +/- 1.7 mV (n = 9) during AFl. Amplitudes dropped between 53% and 75% when the AR lost atrial wall contact. The atrial pacing threshold was 1.0 +/- 0.4 V (n = 16) when the AR was in contact with the atrial wall. CONCLUSIONS: In future dual chamber ICDs the signals from a passive fixation single pass lead could be used for atrial sensing and pacing as long as the sensing electrode for the right atrium remains in contact with the atrial wall. This system might lead to a simpler, less invasive implantation of dual chamber ICD systems.

Atrial Fibrillation↗
PubMed1993

Control of immune-mediated disease of the central nervous system with monoclonal (CD4-specific) antibodies.

Chronic relapsing experimental allergic encephalomyelitis (CREAE) was induced in Biozzi AB/H (H-2dq1) mice by active sensitization with spinal cord antigens. A single i.p. injection of CD8-depleting (YTS169.4) monoclonal antibody (mAb) failed to affect the clinical course of CREAE when administered prior to and during the onset of both the initial clinical and subsequent relapse phase of the disease. By contrast similar treatment with both CD4-depleting (YTS191.1) or CD4-blocking/non-depleting (YTS177.9) mAb significantly inhibited disease progression. Treatment shortly before the anticipated onset of clinical EAE prevented the subsequent development of disease, although disease could be provoked following antigen-rechallenge. In contrast, treatment with these antibodies during post-acute remission phase mainly served to delay the incidence of relapse. This suggests that, unless tolerance can be re-induced, treatment of ongoing neuroimmunological disease will require 'pulse' therapy and thus potentiate the problems of long-term immunosuppresion. Despite the findings that CD4-specific antibodies can rapidly reverse overt clinical disease shortly after the onset of disease exacerbation, once neurological dysfunction becomes established anti-CD4 treatment fails to improve the animals clinically, possibly due to the inability to rapidly reverse established demyelination. Although this study does not exclude the potential central action of the injected mAb, the failure to significantly dissociate therapeutic benefit between mAb administered directly into the CNS and that given systemically suggests that a major action of these agents is probably by selectively removing T cells in the peripheral T cell pool.

Animals↗
PubMed1991

Mononuclear cell trafficking and plasma protein extravasation into the CNS during chronic relapsing experimental allergic encephalomyelitis in Biozzi AB/H mice.

Cellular traffic and plasma protein extravasation across the blood-brain and blood-spinal cord barrier (BBB) have been studied during chronic relapsing experimental allergic encephalomyelitis in Biozzi AB/H mice, using a simultaneous double radioisotope method. There was a general correlation between the clinical course of disease and BBB breakdown, including a resealing of the barrier during remission, although breakdown appeared slightly to precede clinical presentation. The brain was markedly less affected than the spinal cord and was only minimally involved in the relapse phase of disease.

Animals↗
PubMed1991

An immunoelectron microscopical study of the expression of class II major histocompatibility complex during chronic relapsing experimental allergic encephalomyelitis in Biozzi AB/H mice.

Immunoelectron microscopical techniques have been used to study class II major histocompatibility complex (MHC) expression by cells in the spinal cords of Biozzi AB/H mice with chronic relapsing experimental allergic encephalomyelitis. Throughout the course of disease both astrocytes and endothelia failed to express significant levels of class II MHC antigens. The major central nervous system resident cell types found to express class II MHC antigens were the perivascular microglia, with infiltrating macrophages and some lymphocytes being strongly positive.

Animals↗
PubMed1991

Expression of vascular addressins and ICAM-1 by endothelial cells in the spinal cord during chronic relapsing experimental allergic encephalomyelitis in the Biozzi AB/H mouse.

The expression of adhesion molecules on central nervous system (CNS) endothelia was examined during chronic relapsing experimental allergic encephalomyelitis (CREAE) in the Biozzi AB/H mouse. Active disease episodes (acute and relapse) were associated with the up-regulation of MALA-2, the murine homologue of intercellular adhesion molecule-1 (ICAM-1), on CNS endothelia and the infiltration of ICAM-1-positive mononuclear cells. In addition, the high endothelial venule (HEV)-associated MECA-325 antigen was evident in perivascular lesions, particularly in relapsing disease. The peripheral lymph node HEV-associated vascular addressin defined by MECA-79 antibody was not detectable in the CNS during CREAE. However, the mucosal HEV addressin was evident in lesions, which ultrastructurally was found to be expressed on the surface of endothelial cells by immunoelectron microscopy. The expression of adhesion molecules, such as ICAM-1, may provide a means by which both the initial neuroantigen-specific and the subsequent antigen-non specific cells extravasate into the CNS. Such infiltration may induce the expression of the vascular addressins which may then provide a means of site-selective cellular recruitment leading to disease progression.

Animals↗
PubMed1990

Induction of chronic relapsing experimental allergic encephalomyelitis in Biozzi mice.

Experimental allergic encephalomyelitis (EAE) was induced in Biozzi AB/H (antibody high) mice by sensitization with spinal cord homogenate in adjuvant. Biozzi AB/H mice were highly susceptible to EAE induction and followed a chronic relapsing pattern of disease. Disease episodes were characterized by mononuclear infiltration of the central nervous system, with demyelination being particularly evident in relapse. The cellular infiltrates, which were associated with immunoglobulin deposition, consisted of macrophages and primarily CD4-positive T lymphocytes. However, similarly treated Biozzi AB/L (antibody low) mice were markedly less susceptible to EAE induction than AB/H mice. Thus, Biozzi mice should prove valuable for the study of chronic relapsing EAE.

Animals↗
PubMed1989

Differential expression of guinea pig class II major histocompatibility complex antigens on vascular endothelial cells in vitro and in experimental allergic encephalomyelitis.

Previous studies have shown that vascular endothelial cells do not normally express major histocompatibility complex (MHC) Class II antigens either in vivo or in vitro. In this investigation it was found that endothelial in the central nervous system (CNS) of normal guinea pigs constitutively express MHC Class II antigens recognized by the monoclonal antibodies HLA-DR, 27E7, and MSgp8. This phenotype is retained when these CNS-derived endothelial cells are propagated in tissue culture. Furthermore, examination of CNS tissue taken from animals in the acute phase of chronic relapsing experimental allergic encephalomyelitis shows that additional epitopes of the MHC Class II antigen, detected by the monoclonal antibodies CI.13.1 and 22C4, are present during the diseased state. This study not only demonstrates constitutive expression of certain MHC Class II determinants by guinea pig endothelial cells, but also shows that other Class II determinants can be differentially expressed in certain disease states.

Animals↗
PubMed1989

The localisation of fibrin, fibronectin and class II major histocompatibility complex antigen in the spinal cord in chronic relapsing experimental allergic encephalomyelitis.

Light and electron immunocytochemistry using antibodies recognising a class II major histocompatibility complex antigen, fibrin, fibronectin, albumin and factor VIII related antigen has been used to stain sections of spinal cord from normal guinea pigs and those with chronic relapsing experimental allergic encephalomyelitis (CREAE). It was found that class II MHC antigens, fibrin and fibronectin were present in normal blood vessels and at high levels in lesions from animals at all stages of the disease. The possible immunological roles of these antigens suggest their participation in the initiation and maintenance of disease state.

Animals↗
PubMed1989

An immunoelectronmicroscopical study of the expression of major histocompatibility complex (MHC) class II antigens in guinea pig sciatic nerves following induction of intraneural mycobacterial granulomas.

A guinea pig model of nerve damage in leprosy has been used to investigate the expression of major histocompatibility complex (MHC) class II antigens in granulomatous lesions in nerves. Using an immunoelectronmicroscopical technique, infiltrating mononuclear cells and endoneural fibroblast-like cells are shown to be class II-positive in the experimental neural lesions. Schwann cells are not class II-positive under these conditions, although at the light microscope level Schwann cell-like cells appear to be positively stained. This illustrates the value of immunoelectronmicroscopy in the investigation of cell surface proteins in situ as compared with conventional light immunohistochemistry.

Animals↗
PubMed1989

A quantitative immunocytochemical study of the infiltrating lymphocytes in the spinal cord of guinea pigs with chronic relapsing experimental allergic encephalomyelitis.

The production and characterization of an anti-guinea pig B cell monoclonal antibody is described. Immunocytochemical techniques using this antibody and others recognizing a Pan T cell antigen and T cell subsets were employed to study frozen sections of spinal cord from guinea pigs with chronic relapsing experimental allergic encephalomyelitis. T and B cells were found in both perivascular lesions and the central nervous system parenchyma, with the major T cell infiltration occurring by the end of the acute phase of disease. The distribution of T cell subsets suggests a phenotypic selectivity in favour of the transport of CT6 (putative CD8)+ve cells across the blood-brain barrier.

Animals↗
PubMed1988

An immunoelectron microscopical study of the expression of class II MHC and a T lymphocyte surface marker during chronic relapsing experimental allergic encephalomyelitis.

Immunoelectron microscopy using antibodies recognising Class II MHC antigens and a pan T cell marker was employed to study sections of spinal cord from guinea pigs with chronic relapsing experimental allergic encephalomyelitis (CREAE). It was found that endothelial cells expressed Class II antigens on their luminal surface throughout the course of the disease and that lymphocytes were adherent to these surfaces. In the parenchyma lymphocytes, macrophages and possibly microglia expressed Class II antigens suggesting that they might also be involved in antigen presentation. The different distribution of T cells seen in the individual lesions during the relapse phase may correlate with their respective natural histories.

Animals↗
PubMed1988

Nerve damage induced by mycobacterial granulomas in guinea pig sciatic nerves.

A possible model for nerve damage in leprosy has been developed in the sciatic nerve of the guinea pig. Intraneural injection of 10(7) BCG organisms into an unsensitized animal induces an epithelioid cell granuloma in 2 weeks similar to that found in tuberculoid leprosy patients. In contrast, intraneural injection of 10(9) cobalt-irradiated Mycobacterium leprae organisms induces a macrophage granuloma in 5 weeks, similar to that found in lepromatous leprosy patients. Histological, immunohistochemical, electron microscopical and electrophysiological studies have demonstrated that the lesions induced in the experimental animals show many of the features documented in studies of nerve damage in leprosy patients.

Animals↗
PubMed1987

The modulation of class II histocompatibility antigens and 'activated' macrophage determinant in the spinal cord during the development of chronic relapsing experimental allergic encephalomyelitis (CREAE) in the guinea pig--relevance to the induction of remission?

Cryostat sections of spinal cord of guinea pigs with chronic relapsing experimental allergic encephalomyelitis (CREAE) were stained with monoclonal antibodies recognising a Strain 13-specific Ia epitope, a non-strain-specific Ia antigen and an 'activated' macrophage determinant. It was found that both Ia antigens and the 'activated' macrophage determinant, observed on infiltrating cells within both perivascular and meningeal compartments, appeared to be modulated during the course of CREAE. This correlated with the neurological symptoms of the disease. Blood vessels and 'glial' cells expressed both Ia determinants. 'Glial' cells also expressed the 'activated' macrophage antigen. These antigens were modulated with the course of the disease.

Animals↗