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PubMed1993

Inhibition of urokinase synthesis and cell surface binding alters the motile behavior of embryonic endocardial-derived mesenchymal cells in vitro.

The expression of the serine protease urokinase is elevated during the epithelial-mesenchymal transformation of the endocardium in the developing avian heart. Elevated urokinase expression is associated with the migrating mesenchymal cells of the atrioventricular canal and bulbotruncus and not the myocardium. Treatment of isolated endocardial-derived mesenchymal cells with phosphatidyinositol-specific phospholipase C released urokinase and its receptor from the cell surface and caused significant alterations in cell morphology and motility. Likewise inhibition of urokinase synthesis by treatment of cells with antisense oligonucleotides also inhibited the migration and motility of the endocardial-derived cells. These results suggest an important role for this enzyme in cell-matrix interactions and cell migration during development.

Animals↗
PubMed1994

Cardiovascular development in the zebrafish. II. Endocardial progenitors are sequestered within the heart field.

We have examined the zebrafish embryo to ascertain the location of endocardial and myocardial progenitors prior to gastrulation, in an attempt to define the earliest stages of cardiac patterning. Currently there is uncertainty as to the spatial and lineage relationship of the progenitors for these two phenotypically distinct cell types that form the two concentric layers of the primitive heart tube. By single-cell injection and tracking, we distinguish a region in the early and midblastula which has the properties of a heart field, in that it defines a zone of cardiac progenitors within which there is a spatial gradient of propensity to generate heart cells, and which regulates, in the sense of adapting to the transplantation of pluripotential cells. This zone extends from the future ventral axis dorsally along the margin, with cardiogenic propensity tapering off laterally and dorsally. Myocardial progenitors are spread throughout this region, but endocardial precursors are restricted to the ventral marginal region. The cardiovascular progeny of the ventral cells include, in addition to endocardium and myocardium, cells in the endothelium and blood.

Animals↗
PubMed2001

A novel role for VEGF in endocardial cushion formation and its potential contribution to congenital heart defects.

Normal cardiovascular development is exquisitely dependent on the correct dosage of the angiogenic growth factor and vascular morphogen vascular endothelial growth factor (VEGF). However, cardiac expression of VEGF is also robustly augmented during hypoxic insults, potentially mediating the well-established teratogenic effects of hypoxia on heart development. We report that during normal heart morphogenesis VEGF is specifically upregulated in the atrioventricular (AV) field of the heart tube soon after the onset of endocardial cushion formation (i.e. the endocardium-derived structures that build the heart septa and valves). To model hypoxia-dependent induction of VEGF in vivo, we conditionally induced VEGF expression in the myocardium using a tetracycline-regulated transgenic system. Premature induction of myocardial VEGF in E9.5 embryos to levels comparable with those induced by hypoxia prevented formation of endocardial cushions. When added to explanted embryonic AV tissue, VEGF fully inhibited endocardial-to-mesenchymal transformation. Transformation was also abrogated in AV explants subjected to experimental hypoxia but fully restored in the presence of an inhibitory soluble VEGF receptor 1 chimeric protein. Together, these results suggest a novel developmental role for VEGF as a negative regulator of endocardial-to-mesenchymal transformation that underlies the formation of endocardial cushions. Moreover, ischemia-induced VEGF may be the molecular link between hypoxia and congenital defects in heart septation.

Animals↗
PubMed2002

Cardiovascular ephrinB2 function is essential for embryonic angiogenesis.

EphrinB2, a transmembrane ligand of EphB receptor tyrosine kinases, is specifically expressed in arteries. In ephrinB2 mutant embryos, there is a complete arrest of angiogenesis. However, ephrinB2 expression is not restricted to vascular endothelial cells, and it has been proposed that its essential function may be exerted in adjacent mesenchymal cells. We have generated mice in which ephrinB2 is specifically deleted in the endothelium and endocardium of the developing vasculature and heart. We find that such a vascular-specific deletion of ephrinB2 results in angiogenic remodeling defects identical to those seen in the conventional ephrinB2 mutants. These data indicate that ephrinB2 is required specifically in endothelial and endocardial cells for angiogenesis, and that ephrinB2 expression in perivascular mesenchyme is not sufficient to compensate for the loss of ephrinB2 in these vascular cells.

Animals↗
PubMed2001

Regional effects of voluntary exercise on cell size and contraction-frequency responses in rat cardiac myocytes.

A model of voluntary exercise, in which rats are given free access to a running wheel over a 14-week period, led to left ventricular hypertrophy. To test whether the hypertrophic response to exercise was uniformly distributed across the ventricular wall, single ventricular myocytes were isolated from the sub-epicardium (EPI) and sub-endocardium (ENDO) of exercised rats and from sedentary rats for comparison. Cellular hypertrophy (approximately 20 % greater cell volume) was seen in ENDO cells from exercised animals, but no significant changes were observed in EPI cells when compared with sedentary controls. This regional effect of exercise may be a response to transmural changes in ventricular wall stress and/or strain. Cell contraction was measured as cell shortening in ENDO and EPI cells at stimulation frequencies between 1 and 9 Hz at 37 degrees C. Exercise training had no effect on cell shortening. Positive and negative contraction-frequency relationships (CFRs) were found in both EPI and ENDO cells between 1 and 5 Hz; at higher frequencies (5-9 Hz), all myocytes displayed a negative CFR. The CFR of a myocyte was, therefore, independent of regional origin and unaffected by exercise. These results suggest that, in vivo, the rat heart displays a negative CFR. We conclude that increased cell size may be a more important adaptive response to exercise than a modification of excitation-contraction coupling.

Animals↗
PubMed1975

The effect of malignant neoplasms on the heart. A study on the electrocardiographic abnormalities and the anatomical findings in cases with and without cardiac involvement.

Six hundred and twenty-two autopsies of patients with malignant neoplasm were used for this study. The incidence of cardiac involvement in relation to the sites of the primary tumor, the anatomical distribution within the heart, and the ECG findings in the patients with and without cardiac involvement were analysed. The incidence of cardiac involvement by malignant tumor was 12.7% (79 out of 622 cases). Involvement by breast and pulmonary cancer was found to be very common, while intestinal and gastric cancer uncommonly metastasised to the heart. The incidence of epicardial involvement was higher than that of the pericardium, myocardium, or endocardium. A significant difference was observed in the ECG findings recorded within 3 months before death between the groups with and without cardiac involvement. Cases of myocardial metastasis were always associated with the pattern of myocardial damage in the ECG. The findings in this study are discussed in the light of previous reports.

Arrhythmias, Cardiac↗
PubMed1984

Ultrastructural features of the endomyocardium in patients with eosinophilic heart disease. An endomyocardial biopsy study.

In a series of studies with endomyocardial biopsy, 7 adult cases with cardiac disease and eosinophilia were studied clinically and electro-microscopy. Degranulation of the eosinophils in the peripheral blood was observed ultrastructurally in 3 of the 4 cases studied. The clinical expression of the 7 patients were, restrictive cardiomyopathy in 2, dilated cardiomyopathy in 2 and sick sinus syndrome in 1 and others in 2. Endocardial thickening was observed in 5 cases, one of whom showed a marked cellular infiltration with macrophages, plasma cells, lymphocytes and mast cells. One other case showed cell debris of degranulated eosinophils. Degeneration of the myocytes was manifested by an increase in Z-bands of the myofibrils as well as streaming (1 case), disarrangement of the myofibrils, and mitochondrial change (1 case) which was characterized by giant mitochondria (1 case) as well as by a numerical increase in mitochondria. Increase of atrial granules and mitochondria in a right atrial biopsy of a case with sick sinus syndrome was noteworthy. Basal lamina layering of the capillaries of the myocardium and pyknosis of an endothelial cell cytoplasm were also noted in each case. These observations may reveal that various disease processes are taking place in the endocardium and adjacent myocardium.

Adult↗
PubMed1999

Gadolinium suppresses stretch-induced increases in the differences in epicardial and endocardial monophasic action potential durations and ventricular arrhythmias in dogs.

We tested whether acute pressure overloading of the left ventricle (LV) had spatially different effects on repolarization, thereby causing arrhythmias. The effects of gadolinium (Gd3+), a nonspecific blocker of stretch-activated channels were also examined. In anesthetized dogs, 5 s clamping of the ascending aorta (AC), separated by 5-min intervals, was repeated while monophasic action potentials (MAPs) were recorded from the LV endocardium and epicardium. Gd3+ was injected into the left atrium before the second (500 micromol) and third AC (2500 micromol) (n=10). In a separate group (n=7), the effects of Gd3+ in the presence of verapamil were examined. Epicardial MAP durations at 50% and 90% repolarization (APD50; APD90) shortened in response to LV pressure rise and elongation of the segment length induced by the first AC, whereas endocardial MAP durations remained unchanged. Thus, the difference in APD50 and APD90 increased. Consistent with these changes, premature ventricular contractions (PVCs) developed. Gd3+ had no effect on baseline MAP durations, however it prevented an AC-induced increase in the difference by suppressing epicardial MAP shortening. Gd3+ also reduced PVCs in a dose-dependent manner at plasma concentrations of 1-4 micromol/L. The effects were also evident after administration of verapamil. Thus, gadolinium suppressed an increase in the spatial dispersion of repolarization and arrhythmias via a mechanism of action different from that of verapamil.

Action Potentials↗
PubMed1991

Diffuse endocardial thrombus in left ventricle associated with a case of hypereosinophilic syndrome.

A 16-year-old girl appeared with fever and dyspnea. In her peripheral blood, leukocytes were found to have increased up to 25,200/mm3, and eosinophils occupied 49% of the leukocyte population. By echocardiography, an abnormal echo layer which appeared to be thrombus was observed over the entire left ventricular endocardium including the posterior leaflet of the mitral valve, and mild mitral valve regurgitation was noted. After treatment, the abnormal echoes were markedly reduced simultaneously with the improvement of subjective symptoms.

Adolescent↗
PubMed1996

Efficacy of direct injection of ethanol into the myocardium to control aconitine-induced ventricular tachycardia in anesthetized dogs.

The effect of injecting ethanol directly into the myocardium to control aconitine-induced ventricular tachycardia (VT) was evaluated in anesthetized dogs. In 17 dogs, VT was induced by injecting aconitine (1.0 microgram, median dose) directly into the epicardium. After inducing persistent VT for up to 3 min, 0.6 ml (median volume) of 96% ethanol was injected into the same epicardial region. Regular sinus rhythm reappeared in 15 dogs with no change in systolic blood pressure; the other 2 dogs died of ventricular fibrillation (VF). In another 13 dogs, VT was induced by injecting aconitine directly into the endocardium using a Variocath needle catheter. After persistent VT for up to 3 min, a regular sinus rhythm was restored in 7 dogs by injecting 2.0 ml (median volume) of 96% ethanol; the remaining 6 dogs died of VF. Histology showed no transmural necrosis and the subendocardial necrotic areas were essentially the same in the dogs that recovered from VT as in those that died. There was no statistically significant relationship between doses of ethanol and VT duration. These preliminary results suggest that the injection of ethanol into the myocardium may efficiently terminate VT when other techniques fail.

Aconitine↗
PubMed1977

Ultrasonic studies on endocardial fibroelastosis.

Four patients with endocardial fibroelastosis were studied by two-dimensional and M-mode echocardiography. The two-dimensional echocardiography showed the characteristic echo from the abnormally thickened endocardium of the left ventricle in every case. Of the 4 cases, 2 were still suffering from congestive heart failure at the time of the study and the other 2 had been already free from clinical symptoms. In the former group, the ultrasonic findings revealed an enlargement of the left ventricle (large left ventricular dimension index) and poor movement of the anterior mitral leaflet which was indicated by a decrease in the diastolic descent rate. The latter group presented almost normal findings concerning the above points. The ultrasonic method is thus proved to be very useful for the diagnosis and evaluation of clinical conditions in cases of endocardial fibroelastosis.

Child↗
PubMed1975

Ultrastructure research of the endocardial endothelium of monkeys.

The surface structure of the endocardial endothelium of normal monkeys (Macaca fuscata and M. irus) was studied using scanning and transmission electron microscopy. The endocardium was covered by a layer of endothelial cells, each of which was recognized by the presence of nuclear bulge and marginal folds. The free cell surface was covered by a number of microvilli. The size of the endothelial cell and its surface morphology varied considerably in the different portions of the heart. The endothelial cells were packed more densely along the free margin of the valves especially at the noduli valvularum semilunarum. The microvilli over the cell surface were denser and longer on the ventricular side of the mitral valve and on the aortic valve, where the marginal folds were not "folds" but were formed by an array of numerous microvillous projections. These cytoplasmic projections had a topographical correlation with micro- and macro-pinocytotic vesicles, thus suggesting their role in the interaction with circulating biologically active substances.

Animals↗
PubMed2001

Invasive pulmonary aspergillosis with thrombosis in the left atrium.

We report a female patient with left atrial wall invasion from pulmonary aspergillosis. She had been treated for diabetes mellitus. Pulmonary aspergillosis extended to the left atrial wall via the left pulmonary vein and formed a polypoid lesion in the left atrium. The polypoid lesion was composed of thrombus, and the thrombus increased in size to become large, and it showed invagination into the mitral valve during diastole. We considered that the thrombus was formed on the injured endocardium. Severe invasive aspergillosis thus could occur in a mild systemic immunocompromised host.

Aspergillosis↗
PubMed1983

Echocardiography of cardiac metastases.

Metastatic disease to the heart is a relatively common entity that may involve the pericardium, myocardium, or endocardium singly or in combination. Echocardiography, particularly two-dimensional imaging, is the most sensitive tool for detecting metastatic disease to the heart. Simple, safe, and noninvasive, it can provide better anatomic detail than can more invasive studies. This information is helpful not only in diagnosis and treatment planning, but in differential diagnoses of unusual cardiac configurations and guidance for pericardiocentesis of loculated effusions.

Aged↗
PubMedDate not supplied

An open environment for quantitative analysis of left ventricular function using ultrasound images.

We have developed an open environment for quantitative analysis of left ventricular function using ultrasound images. The system is primarily intended for experimental purposes, i.e. clinical research and the evaluation of quantification algorithms. The modular design allows easy expansion with new analysis methods. The core of our system is the user-interface and image presentation. Image analysis methods are included as a set of tools available to the operator. Using this approach, the expensive, expert knowledge of the cardiologist is used more efficiently than in most delineation systems. During delineation, images of a complete heart cycle can be simultaneously displayed dynamically ('cine mode') in a separate window. This feature improves visual edge perception and enables accurate determination of the endocardium even in cases of very poor echogenicity. The resulting contour can be corrected locally by interactive modification using 'rubber banding'. After delineation of the images from different echocardiographic views, volume, ejection fraction, and regional wall motion are determined. Studies using contrast-enhanced echocardiography can be quantified by image intensity analysis in a region of interest in order to determine myocardial perfusion. We evaluated our method by quantifying echocardiographic studies from 12 healthy volunteers. We compared the results with magnetic resonance imaging and concluded that there was no significant difference in volume and ejection fraction calculated from both modalities. Moreover, the image display features and contour correction methods were greatly appreciated by the cardiologists who used the system.

Echocardiography↗
PubMed1982

Experimental production of EVI antibodies.

The production of an antibody which reacts with endocardium, blood vessels, and cardiac interstitial tissue (EVI factor) was experimentally obtained in rabbits immunized either with heterologous heart crude antigen, Trypanosoma cruzi antigen, a mixture of heart and T. cruzi antigens, kidney antigen or lung antigen, and complete Freund's adjuvant. Immunization lasted 2 months, with multiple subcutaneous and foot pad injections being made every 15th day. Preimmunization serum from each animal was used as normal control serum. Rabbit sera were tested by indirect immunofluorescence against mouse heart and skeletal muscle unfixed cryostat sections and revealed by fluoresceinated anti-rabbit globulin diluted 1:80. The highest titers appeared with anti-heart sera (1:192) and with anti-heart/T. cruzi sera (1:96). Incorporation of T. cruzi antigen in heart extract did not increase EVI antibody titers. It is suggested that the EVI factor is an antibody to many antigenic determinants, the majority of which are present in the heart and some of which cross-react with T. cruzi.

Animals↗
PubMed1982

NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations.

The idiopathic hypereosinophilic syndrome (HES) represents a heterogeneous group of disorders with the common features of prolonged eosinophilia of an undetectable cause and organ system dysfunction. Fifty patients with the idiopathic HES were studied over 11 years of the National Institutes of Health. Multiple organ systems were involved; bone marrow hypereosinophilia was common to all patients, but the most severe clinicopathologic involvement was of the heart and nervous system. Postmortem gross pathologic examination of the hearts of patients with idiopathic and nonidiopathic HES suggested that the common mechanism of cardiac disease is the eosinophilia. Endomyocardial biopsy findings showed that the endothelial cells in the endocardium and of the microvasculature were the primary targets of the tissue damage. This damage initiates thrombosis; endocardial fibrosis and restrictive endomyocardopathy may follow. In-vitro culture of circulating eosinophil colony-forming units showed some normal studies, some studies showing increased progenitor cells committed to eosinophil development, and others showing an excess production of eosinophil colony-stimulating factor. Chemotherapy to lower the eosinophil counts has resulted in marked improvement of HES prognosis, as have agressive medical and surgical approaches to cardiovascular complications.

Cardiomyopathies↗
PubMed2000

Vasculogenesis in the day 6.5 to 9.5 mouse embryo.

The process of vasculogenesis was characterized in the 6.5- to 9.5-day mouse embryo and in allantoic culture by analysis of spatial and temporal expression patterns of the endothelial or hematopoietic lineage-associated proteins, TAL1, Flk1, platelet/endothelial cell adhesion molecule (PECAM), CD34, VE-cadherin, and Tie2. The study establishes that: (1) TAL1 and Flk1 are coexpressed in isolated mesodermal cells that give rise to endothelial cells and thus can be defined as angioblasts; (2) hematopoietic cells of blood islands express TAL1, but not Flk1; (3) vasculogenesis in the embryo proper is initiated by mesoderm fated to give rise to the endocardium; (4) the maturation/morphogenesis of blood vessels can be defined in terms of a sequential pattern of expression in which TAL1 and Flk1 are expressed first followed by PECAM, CD34, VE-cadherin, and later Tie2; and (5) TAL1 expression is down-regulated in endothelial cells of mature vessels. (Blood. 2000;95:1671-1679)

Allantois↗