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PubMed1997

[Invasive aspergillosis. Description of a case in an infant with severe granulocytopenia and endocardial fibroelastosis].

Invasive Aspergillosis in a child with severe granulocitopenia and endocardial fibroelastosis. A case of invasive aspergillosis in a 3-month old baby is reported. At autopsy gross examination revealed the presence of whitish nodules in the liver, spleen, kidneys and suprarenal glands. A black eschar with surrounding erythema involved the left auricle. The heart showed dilated left ventricle with porcelain-like thickening of the endocardium. The histological section of the hepatic nodular lesions showed Aspergillus colonization, vascular invasion with hyphal forms and necrotic granulomatous lesions in the other sites. Histologically, the endocardium is markedly thickened and rich in connective tissue and elastic fibres. Examination of the bone-marrow showed poor cellularity with a striking reduction of cells of the neutrophil granulocyte series. Aspergillosis may complicate the course of the child in immunocompromised state. Granulocitopenia causes an insufficient delimitation of infections and allows metastatic diffusion of fungi, through blood-vessels invasion.

Agranulocytosis↗
PubMed1997

New strategy for prolonging the preservation time of hearts for transplantation.

Our study concerned the findings that rat and rabbit heart transplants do not survive after six hours. They become dark, hard and fail to contract within 2 min after reperfusion and never regain their function. We tested the supplementation of solutions for heart transplant preservation with tetrahydrobiopterin (H4B) and L-arginine (L-ARG) to maintain the oxidative and reductive domains of the endocardial NO synthase. We decided to study the excised rabbit hearts preserved in Hank's balanced salt solution (HBSS) at 0 degrees C supplemented with different concentrations of H4B (0, 1, 5, 10 or 100 microM). At desired time intervals, successive pieces stored in the above solutions were warmed to rabbit body temperature in 4 ml of HBSS and maximally agonized by direct application of 20 microl of 200 microM bradykinin (or other agonist) onto the exposed endocardium. Nitric oxide bursts were monitored with a porphyrinic NO sensor lying on the exposed endocardium. Our goal was to find the lowest H4B concentration which would maximally agonize NO. and prolong the time of heart preservation to more than 6 hours. Ten microM are a minimum H4B concentration which achieves maximum prolongation of heart preservation time up to 90 hours. This effect was based upon maximal potentiation of NO. release and minimizing of superoxide production.

Animals↗
PubMed1996

Fibulin-1, vitronectin, and fibronectin expression during avian cardiac valve and septa development.

BACKGROUND: Extracellular matrix (ECM) proteins have been implicated as mediators of events important to valvuloseptal development (reviewed by Little and Rongish, Experentia, 51:873-882, 1995). The aim of this study was to identify connective tissue ECM proteins present at sites of valvuloseptal morphogenesis, and to determine how their patterns of expression change during the developmental process. METHODS: Immunofluorescence microscopy was used to examine the distribution of fibulin-1, vitronectin, and fibronectin in the embryonic chicken heart over a broad developmental time frame (Hamburger and Hamilton stages 14 to 44), emphasizing stages that illustrate endocardial cushion formation, growth, fusion, and development into valvuloseptal components. RESULTS AND CONCLUSIONS: Fibulin-1 immunolabeling was concentrated in endocardial cushions, notably at boundaries with the myocardium, during stages when the cushions are differentiating into valvular and septal components. Fibulin-1 was detected in the endocardial cushions prior to their seeding with cushion cells, but became undetectable by early midgestation. Vitronectin expression was similar to fibulin-1, but less restricted in its distribution. Vitronectin was observed before endocardial cushion cell migration commenced and persisted until the formation of prevalvular structures (early midgestation) in the atrioventricular cushions. Vitronectin remained detectable in the semilunar valves until late midgestation. Fibronectin was present in the endocardial cushion region and in portions of the endocardium and myocardium throughout the stages presented. Our data suggests that the ECM of the endocardial cushions undergoes remodelling in a regionally and temporally specific manner which corresponds with morphogenetic changes during valvuloseptal development.

Animals↗
PubMed1997

Polysialylated NCAM expression on endocardial cells of the chick primary atrial septum.

Septation of the tubular heart to form the multi-chambered heart involves endocardial cell mesenchymal transformation at discrete sites. These sites include the crests of endocardial cushions at the atrioventricular junction, crests of the spiral ridges within the outflow tract, and the leading edge of the atrial septum. The factors involved in this multi-step inductive process appear to include the neural cell adhesion molecule (NCAM). The down-regulation of NCAM coincident with mesenchymal transformation has been documented at the atrioventricular cushion tissue. In view of the function-regulation properties of polysialylated NCAM (PSA-NCAM), we hypothesized that this form of NCAM would be playing a role during the dramatic changes in cell-cell interactions occurring in the endocardium at the leading edge of the primary atrial septum. Chicken hearts at stages during primary atrial septum development were fixed with paraformaldehyde and either immunofluorescently stained for the light microscope analysis or immunoperoxidase stained for ultrastructural analysis. A monoclonal antibody to an NCAM polypeptide epitope (5E) was used to detect all forms of NCAM, while a monoclonal to the polysialic acid (5A5) was used to detect that subset of NCAM which is highly polysialylated (PSA-NCAM). By light microscope level analysis, an increase in immunostaining for NCAM and the appearance of PSA-NCAM was detected on embryonic chicken endocardial cells at the leading edge of the growing atrial septum. The ultrastructural analysis revealed that there is also a change in the pattern of NCAM and PSA-NCAM from a polarized localization to a more ubiquitous distribution over the endocardial cell surface as these cells send out processes, form multiple layers, and sink or move into the underlying extracellular matrix. PSA-NCAM was also detected along cell appositions of cells within the matrix. Both NCAM and PSA-NCAM levels were reduced on cells deep within the matrix. These findings indicate that during primary atrial septation, PSA-NCAM may be deployed on endocardial epithelial cells in order to down-regulate cell-cell interactions and allow the detachment and migration of some of these cells into the underlying matrix.

Animals↗
PubMed1999

Catheter microwave ablation therapy for cardiac arrhythmias.

This article describes three microwave catheter antennas for percutaneous cardiac ablation. A particular design feature of these antennas is that there is no reflected microwave current from the antenna flowing up the transmission line. Thus, it minimizes heating of the coaxial cable. The power reflection coefficients are very low (4% or less) in phantom equivalent materials. These antennas can also serve as bipolar electrodes for sensing endocardiac electrograms. Our studies in dogs, during both cardiopulmonary bypass and closed-chest operations via the femoral vein, have shown microwave energy greater than 200 joules (J) delivered to the heart through a split-tip dipole catheter antenna can produce irreversible block of the heart rhythms. This energy was achieved either by increasing the delivered power from 20 to 40 watts or by increasing the treatment duration from 7 to 11 s (210 to 330 J per application). It produced an endocardium temperature of about 65 degrees C. We found that the percutaneous, transcatheter microwave system is capable of inducing AV blocks consistently in dogs using the flexible, curved tip, split-tip catheter antenna. In addition, our studies have shown that the width and height of SAR distributions for cap-choke and split-tip catheter antennas are similar for the same antenna length. The cap-slot design had a much longer SAR distribution compared to the others. Moreover, a longer (4 mm) split-tip antenna can also induce larger lesions. These results suggest that it could be possible to ablate a ventricular tachycardia focus using the 4 mm split-tip as well as the cap-slot microwave catheter antennas.

Animals↗
PubMed1978

Cardiac candidiasis in cancer patients.

Histologically proven infection of the heart by Candida organisms occurred in 17 (10%) of 168 cancer patients with candidiasis studied at necropsy. All 17 patients were among the 85 patients with disseminated Candida infection; none of the 83 patients with localized candidiasis had involvement of the heart. Abscesses in the myocardium were present by histologic examination in all 17 patients and in 8 were evident on gross inspection as well. The mural endocardium was also affected in 5 patients from direct extension of a myocardial abscess. The valves were uninvolved. Pericardial infection was detected in 2 patients. The 17 patients with cardiac Candida infection had a higher frequency of positive premortem blood and cerebrospinal fluid cultures and of presence of Candida in the heart's blood than did the 68 patients with disseminated candidiasis but without involvement of the heart. Symptoms or signs of cardiac dysfunction resulting from the cardiac Candida infection were not readily detected in any patient. The clinical and pathologic features of cardiac candidiasis in cancer patients are distinct from those observed in Candida endocarditis.

Adolescent↗
PubMed1989

Endocardial cell arrangement: role of hemodynamics.

This paper demonstrates the presence of areas where endocardial cells are aligned with the blood flow in three distinct regions of the embryonic chick heart: on the inferior border of the growing septum primum, on the upper wall of the primitive ventricle above the developing interventricular septum, and on the part of the atrial floor that funnels into the atrioventricular canal. While orientation in the first two areas is transitory, the number of cells aligned with the blood flow in the atrial floor increases from days 3 to 5 of incubation. It is suggested that shear stress induces endocardial cell orientation in these areas. To further explore the role of hemodynamics in endocardial cell arrangement, the left vitelline vein was severed at stages 13-14. This resulted in abnormal development of the vitelline venous system. Examination of experimental embryos at 5 days of age revealed the presence of a distinct area of endocardial cell orientation in the dorsal wall of the right atrium, near the opening of the sinus venous. Changes in the venous return to the atria may modify flow patterns, thus inducing endocardial cell orientation. This experimental procedure may be a useful model not only for exploring the effects of hemodynamics upon the endocardium, but also for investigating other aspects of heart development under altered hemodynamic conditions, without manipulating any portion of the embryonic heart.

Animals↗
PubMed2003

VEGF modulates early heart valve formation.

Although hypoxic and/or nutritional insults during gestation are believed to contribute to congenital heart defects, the mechanisms responsible for these anomalies are not understood. Given the role vascular endothelial growth factor (VEGF) plays in response to hypoxia, it is a likely candidate for mediating deleterious effects of embryonic hypoxia. The ectopic or overproduction of endogenous factors such as VEGF may contribute to specific heart defects. Here we compared hypoxia-induced precocious production of VEGF during early heart valve development to normal VEGF production. Mouse prevalvular cardiac endocardial cushions were explanted onto hydrated type I collagen gels under normoxic or hypoxic conditions. The extent of transformation of cardiac endothelium into mesenchyme was inversely correlated with the levels of VEGF during the various culture conditions. A soluble VEGF antagonist confirmed that endogenous production of VEGF was specific for blocking normal cushion mesenchyme formation. We further demonstrated that E10.5 endocardium retains the ability to transform into cardiac mesenchyme in the absence of endogenous VEGF.

Animals↗
PubMed2006

Chick embryos exposed to trichloroethylene in an ex ovo culture model show selective defects in early endocardial cushion tissue formation.

BACKGROUND: Formation of the primitive heart is a critical step for establishing a competent circulatory system necessary for continued morphogenesis, and as such has significant potential as a target for environmental insult. The goal of this study was to identify the initial cellular events that precede more superficially observable abnormalities resulting from exposing early chick embryos to trichloroethylene (TCE). METHODS: A whole embryo culture method was used to assess the susceptibility of endocardial epithelial-mesenchymal transformation in the early chick heart to TCE. This method has the benefits of maintaining the anatomical relationships of developing tissues and organs, instantaneously exposing precisely staged embryos to quantifiable levels of TCE in a protein-free medium, and the ability to directly monitor developmental morphology. RESULTS: A minority of embryos (Hamburger and Hamilton [HH] stage 13-14) exposed to TCE (10-80 ppm) were not viable after 24 hr in culture and exhibited a variety of gross malformations in a dose-dependent fashion. However, the majority of treated embryos remained viable and developed into HH stage 17 embryos that were superficially indistinguishable from vehicle-treated controls. Further analysis of the hearts of these superficially normal embryos by whole-mount confocal microscopy revealed selective reduction in the number of atrioventricular canal mesenchymal cells. Additionally, those mesenchymal cells that did develop migrated abnormally as long thin cords of adherent cells. CONCLUSIONS: The regional selectivity of these effects in the chick heart suggests a critical window of susceptibility to TCE in the epithelial-mesenchymal transformation of atrioventricular canal endocardium.

Animals↗
PubMed2005

Live 3D echo guidance of catheter-based endomyocardial injection.

Local delivery of therapeutic agents into the myocardium is limited by suboptimal imaging. We evaluated the feasibility and accuracy of live 3D echo to guide left ventricular endomyocardial injection. An intramyocardial injection catheter was positioned in the left ventricle in five healthy Yorkshire pigs using fluoroscopy. All other catheter manipulations were performed with live biplane and 3D echo guidance. In each animal, a total of 12 endomyocardial injections (volume, 50-100 microl) of echo contrast mixed with blue tissue dye were performed. Four injections, 10 mm apart, were directed to three myocardial target zones: the anterior septum at the mitral valve level (zone 1); the posterolateral wall between the heads of the papillary muscles (zone 2); and the apex (zone 3). The injections were aimed to form a transverse line in zones 1 and 2 and an inverted triangular pyramid in zone 3. The animals were sacrificed, the hearts were inspected and the left ventricular endocardium was examined to create a map of injection marks. Success, defined as a visible injection of tissue dye, was 95%, and accuracy, defined as an injection into the target zone, was 83%. There was no significant difference in accuracy between the zones. Live 3D echo can successfully guide endomyocardial injections by accurately targeting specific myocardial zones, verifying catheter apposition and, when combined with echo contrast, providing real-time visualization of injectate deposition.

Animals↗
PubMed1994

Electrophysiologic characteristics at initiation of ventricular tachycardia and ventricular fibrillation in a canine infarct model.

Local ventricular activation time and the conduction time during sinus rhythm at the induction of ventricular tachycardia (VT) and ventricular fibrillation (VF) were investigated using a canine model of chronic myocardial infarction. Of 26 dogs studied, 15 had inducible VT, 10 had inducible VF, and 1 had no inducible arrhythmias. Bipolar local ventricular electrograms were recorded during sinus rhythm from 136 sites in 10 dogs with VT and 164 sites in 11 dogs with VF. Mean activation time in dogs with inducible VT was significantly longer than in dogs with inducible VF. Furthermore, simultaneous local ventricular electrograms were recorded during the induction of VT (74 episodes) or VF (38 episodes) from the infarct border zone at the endocardium (B-EN), the epicardium (B-EP), and normal sites (N-EN, N-EP). During VT induction, the activation time at N-EN and N-EP was significantly longer than during VF induction (N-EN: 94 +/- 21, 70 +/- 19 ms; N-EP: 83 +/- 21, 64 +/- 10 ms; p < 0.05). Conduction time was measured at the initiation of VT or VF induced by orthodromic or antidromic pacing. The conduction times of the last paced beat between N-EN and B-EP (35 +/- 11, 62 +/- 24 ms), N-EN and N-EP (35 +/- 12, 14 +/- 13 ms), B-EN and B-EP (16 +/- 10, 38 +/- 25 ms), and B-EP and N-EP (77 +/- 27, 44 +/- 12 ms) were significantly different in dogs with inducible VT (p < 0.05), but not in dogs with VF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Epicardial-like cells on the distal arterial end of the cardiac outflow tract do not derive from the proepicardium but are derivatives of the cephalic pericardium.

A series of recent studies strongly suggests that the myocardium of the cardiac distal outflow tract (d-OFT) does not derive from the original precardiac mesoderm but, instead, differentiates from a so-called anterior heart field. Similar findings were also reported for the endocardium of the d-OFT. However, very little information is available on the origin of the epicardium of the OFT. To address this issue, we have performed a study in which we have combined experimental in vivo and in vitro techniques (construction of proepicardial chimeras, proepicardial ablation, OFT insertion of eggshell membrane pieces, and culture on collagen gels) with molecular characterization techniques to determine this origin and define the properties of d-OFT epicardium compared with proepicardially derived epicardium. Our results demonstrate that the coelomic/pericardial epithelium in the vicinity of the aortic sac (and not the proepicardium) is the origin of d-OFT epicardium. This "pericardially" derived epicardium and the proepicardially derived epicardial tissues differ in their morphologic appearance, gene-expression profile, and in their ability to undergo epithelial-to-mesenchymal transformation. We conclude that the heterogeneity in the epicardial cell population of the OFT could be a factor in the complex developmental remodeling events at the arterial pole of the heart.

Animals↗
PubMed2004

MAP kinase activation in avian cardiovascular development.

Signaling pathways mediated by receptor tyrosine kinases (RTK) and mitogen-activated protein kinase (MAPK) activation have multiple functions in the developing cardiovascular system. The localization of diphosphorylated extracellular signal regulated kinase (dp-ERK) was monitored as an indicator of MAPK activation in the forming heart and vasculature of avian embryos. Sustained dp-ERK expression was observed in vascular endothelial cells of embryonic and extraembryonic origins. Although dp-ERK was not detected during early cardiac lineage induction, MAPK activation was observed in the epicardial, endocardial, and myocardial compartments during heart chamber formation. Endocardial expression of dp-ERK in the valve primordia and heart chambers may reflect differential cell growth associated with RTK signaling in the heart. dp-ERK localization in the epicardium, subepicardial fibroblasts, myocardial fibroblasts, and coronary vessels is consistent with MAPK activation in epicardial-derived cell lineages. The complex temporal-spatial regulation of dp-ERK in the heart supports diverse regulatory functions for RTK signaling in different cell populations, including the endocardium, myocardium, and epicardial-derived cells during cardiac organogenesis.

Animals↗
PubMed1999

Inflammatory agents regulate in vivo expression of fractalkine in endothelial cells of the rat heart.

Fractalkine is distinguished structurally from other chemokines in that it contains a mucin-like stalk that tethers a CX3C chemokine module to a transmembrane-spanning region; its expression in cultured endothelial cells has been shown to be up-regulated by tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1). The purpose of this study was to determine whether fractalkine is expressed, in a proinflammatory agent-regulated manner, by cardiac endothelial cells in vivo. Steady state levels of fractalkine mRNA were increased in rat cardiac tissues after in vivo treatment with lipopolysaccharide (LPS), IL-1, or TNF-alpha. In situ hybridization and immunohistochemical analysis revealed that endothelial cells of the coronary vasculature and endocardium were the principal source of proinflammatory agent-inducible fractalkine, although some fractalkine immunoreactivity was also found on the myocytes. These data are the first demonstration of in vivo cardiac endothelial cell fractalkine expression and regulation by proinflammatory agents such as LPS, IL-1, or TNF-alpha. Cardiac endothelial cell-expressed fractalkine may contribute to the influx of leukocytes into the heart during inflammation.

Animals↗
PubMed1993

Transmural saturation transfer analysis of the creatine kinase system in the mammalian heart.

31P NMR spatial localization and saturation transfer techniques were combined to enable the transmural measurement of the forward creatine kinase (CK) rate (ATP:creatine N-phosphotransferase, EC 2.7.3.2.) in the in vivo canine myocardium. Five epicardial towards endocardial regions of the left ventricle (LV) were simultaneously examined using spatially localized voxels. Although intraleft ventricular CP/ATP ratios were constant, the pseudo first order rate constant (k') and the forward creatine kinase rate (Rf) displayed a 61% variation across the LV wall. Because CK levels and calculated [ADP], [CP] and pH are transmurally invariant in the normal left ventricle, the observed changes in the Rf could not be explained by changes in the absolute levels of these substrates and of creatine kinase. In addition, because myocardial oxygen consumption rates are known to be higher in the endocardium, these results imply that forward creatine kinase rates are not directly related to oxidative phosphorylation rates.

Adenosine Diphosphate↗
PubMed1997

Induction of endocardial cushion tissue in the avian heart is regulated, in part, by TGFbeta-3-mediated autocrine signaling.

Valvuloseptal morphogenesis of the primitive heart tube into a four-chambered organ requires the formation of endocardial cushion tissue. The latter is the outcome of an inductive interaction in which endocardial (endothelial) cells are induced to transform into mesenchyme by paracrine signals secreted by the adjacent myocardium. In this study, we propose that transforming endothelial/mesenchymal cells themselves secrete a factor-TGFbeta-3-that functions in an autocrine mode to promote/sustain mesenchyme formation and possibly in a paracrine manner to amplify the original (myocardial) inductive event. Cushion mesenchyme-conditioned medium, previously demonstrated to be an endogenous source of autocrine, migration-promoting factors, was found in the present study to contain TGFbeta-3, as detected by immunoblot analysis. Immunoneutralization of TGFbeta-3 in preparations of cushion mesenchyme-conditioned medium resulted in a failure of treated target endocardial cells to migrate as mesenchyme, whereas inclusion of a control antibody did not inhibit the migration-promoting activity of the conditioned medium. Similar to treatment with the conditioned medium, direct addition of TGFbeta-3 to target endocardial cells also elicited invasive migration but only in cultures which had been activated in vivo by inductive interaction with the myocardium prior to treatment. Selective inhibition of TGFbeta-3-mediated autocrine signaling in continuous cocultures of endocardium plus myocardium resulted in endocardial cells which did not migrate, even though they had expressed early markers associated with endocardial cell activation (e.g., alpha-smooth muscle actin, ES/130, and TGFbeta-3). Collectively, these results suggest that (i) two signaling pathways, myocardial and endocardial, are required to start and complete epithelial-mesenchymal transformation in cushion-forming regions of the heart and (ii) the endocardial pathway signals through iteration of TGFbeta-3 and is not functionally redundant to the myocardial pathway.

Animals↗
PubMed1998

Dynamic patterns of retinoic acid synthesis and response in the developing mammalian heart.

Retinoic acid (RA) has been implicated in cardiac morphogenesis by its teratogenic effects on the heart, although its role in normal cardiogenesis remains unknown. To define the parameters of RA action in cardiac morphogenesis, we analyzed the patterns of ligand synthesis, response, and inactivation in the developing mouse heart. Activation of a lacZ transgene controlled by an RA response element (RARE) was compared to the localization of the retinaldehyde-oxidizing dehydrogenase RALDH2, the earliest RA synthetic enzyme in the mouse embryo, and to the expression of a gene encoding an RA-degrading enzyme (P450RA). We observed that RALDH2 localization and RA response were virtually superimposable throughout heart development. Initially, both RALDH2 and RARE-LacZ activity were restricted to the sinus venosa in unlooped hearts, but were high in the dorsal mesocardium, while P450RA expression was restricted to the endocardium. Later stages were characterized by a sequential, noncontiguous progression of RALDH2 accumulation and RA response, from the sinus venosa to atria, dorsal-medial conotruncus, aortic arches, and the epicardium. This dynamic pattern of RA response was a direct result of localized RALDH2, since hearts of cultured embryos were uniformly competent to respond to an exogenous RA challenge. These observations support a model in which the influence of endogenous RA on heart development depends upon localized presentation of the ligand, with only limited diffusion from the source of its synthesis.

Aldehyde Oxidoreductases↗
PubMed1999

Elucidating the origins of the vascular system: a fate map of the vascular endothelial and red blood cell lineages in Xenopus laevis.

Required to supply nutrients and oxygen to the growing embryo, the vascular system is the first functional organ system to develop during vertebrate embryogenesis. Although there has been substantial progress in identifying the genetic cascade regulating vascular development, the initial stages of vasculogenesis, namely, the origin of vascular endothelial cells within the early embryo, remain unclear. To address this issue we constructed a fate map for specific vascular structures, including the aortic arches, endocardium, dorsal aorta, cardinal veins, and lateral abdominal veins, as well as for the red blood cells at the 16-cell stage and the 32-cell stage of Xenopus laevis. Using genetic markers to identify these cell types, our results suggest that vascular endothelial cells can arise from virtually every blastomere of the 16-cell-stage and the 32-cell-stage embryo, with different blastomeres preferentially, though not exclusively, giving rise to specific vascular structures. Similarly, but more surprisingly, every blastomere in the 16-cell-stage embryo and all but those in the most animal tier of the 32-cell-stage embryo serve as progenitors for red blood cells. Taken together, our results suggest that during normal development, both dorsal and ventral blastomeres contribute significantly to the vascular endothelial and red blood cell lineages.

Animals↗