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PubMed1997

Effects of lidocaine and diltiazem on ventricular tachyarrhythmia and dispersion of conduction during severe myocardial ischemia in canine hearts.

The purpose of this study was to investigate the effects of lidocaine and diltiazem on ventricular tachyarrhythmia and dispersion of conduction during severe myocardial ischemia in dogs. Myocardial ischemia was produced by a 10-min occlusion of the left anterior descending artery by the retrograde blood flow technique. Saline, lidocaine, and diltiazem were infused intravenously before and during occlusion in groups A (n = 16), B (n = 22) and C (n = 13), respectively. The incidence of ventricular tachycardia (VT) consisting of ten or more VPC was 19% in group A, 73% in group B and 31% in group C (A vs. B, P < 0.01), and that of ventricular fibrillation (VF) was 31%, 64%, and 15%, respectively (A vs. B, P < 0.05). The time of the onset of VT preceding VF was shorter in group B than in group A (207.9 +/- 13.9 vs. 353.2 +/- 70.7 sec, P < 0.05). The time taken to reach maximal dispersion of conduction delay in the epicardium was shorter in group B than in group A (192.1 +/- 11.9 vs. 337.5 +/- 38.2 sec, P < 0.01), and the dispersion of conduction delay in the intramyocardial layers was smaller in group B than in group A (229.9 +/- 24.5 vs. 360.0 +/- 35.6 sec, P < 0.01). The time taken to reach maximal dispersion of conduction delay in the endocardium was greater in group C than in group A (400.8 +/- 38.8 vs. 274.4 +/- 23.9 sec, P < 0.01). However, there were no significant differences among the three groups with regard to the maximal dispersion of conduction delay in the epicardium, in the endocardium, or intramyocardial layer. These results suggest that lidocaine increased ventricular tachyarrhythmia due to an acute increase in dispersion of conduction in the epicardium and intramural layer, and that diltiazem was not effective in preventing ventricular tachyarrhythmia and did not affect the dispersion of conduction in the epicardium or intramural layer despite improvement in the endocardium.

Animals↗
PubMed2004

[Effects of Evan Blue on perfused dimension display and rabbit left ventricular action potential].

OBJECTIVE: Simultaneous recording of transmembrane action potential at endocardium, midcardium and epicardium and transmural ECG in arterially perfused left ventricular preparation is a new method for researching into the mechanism about ventricular arrhythmia, and in this connection, how to distinguish the perfused area plays a key role in keeping preparations under normal condition. This study is aimed to evaluate the effects of Evan Blue on the displaying of the perfused area and on the characters of transmembrane action potential of the arterially perfused left ventricular preparations. METHODS: Rabbit left ventricular wedge preparations were perfused with Tyrode solution continuously via left circumflex, and the action potential of endocardium, midmyocardium, epicardium or transmural electrocardiogram were recorded simultaneously. The action poatential duration (APD), transmural dispersion of repolarization (TDR) or QT intervals were compared and the color variation of the preparations were studied before and 30 min after perfusion with Evan Blue. RESULTS: Under the basic stimulatory cycle length of 1000, 2000, 4000 ms, there was no significant difference of APD in the same transmural layer or TDR before and after Evan Blue perfusion (P<0.01), but APD or TDR stimulated at basic cycle length of 1000-4000 ms were all higher than those recorded at 500 ms (P<0.01); APDs of endocardium were much longer than those of epicardium or midmyocardium (P<0.01); there was no significant difference in APD, TDR and QT intervals before and after Evan Blue perfusion (P>0.05). No premature ventricular contractions and ventricular tachycardia happened during the experiments. CONCLUSION: Evan Blue can be used as a marker to identify the perfused area.

Action Potentials↗
PubMed1991

Protective effect of selenium and vitamin E against changes induced in heart vessels of rabbits fed chronically on a high-fat diet.

The effect of selenium and vitamin E on lipid level in the blood serum, on the oxygen free radicals generation and on morphology of heart was tested after separate and combined administration to mongrel male rabbits fed on a high-fat diet (HFD). The lipid level and oxygen free radical generation was depressed markedly in animals fed on a HFD and receiving simultaneously selenium and vitamin E. In animals on a HFD the walls of the heart vessels were thickened, always to their complete obliteration. The presence of lipid droplets in endocardium could be observed as well. The hearts of the rabbits receiving selenium showed markedly fewer atheromatously changed vessels. Moreover, no accumulation of lipid droplets was seen in the endocardium of these animals. The least atherosclerotic alterations were observed in the myocardium of rabbits given HFD with addition of selenium and vitamin E in combination, no accumulation of lipids was shown in endocardium of these rabbits. An important finding of this study is, that the combination of selenium and vitamin E results in an intensified protective effect against changes evoked in the heart muscle of rabbits fed on a HFD.

Animals↗
PubMed1990

Mechanical myocardial actuation during ventricular fibrillation improves tolerance to ischemia compared with cardiopulmonary bypass.

Direct mechanical ventricular actuation (DMVA) is a unique non-blood-contacting biventricular assist device that provides circulatory support during ventricular fibrillation without demonstrating adverse effects on the myocardium. The purpose of this study was to assess the preservation of myocardial energy stores and myocardial responses to ischemia after circulatory support during ventricular fibrillation with direct mechanical ventricular actuation versus cardiopulmonary bypass. Twenty adult mongrel dogs were randomized to receive circulatory support with either cardiopulmonary bypass or direct mechanical ventricular actuation. After 4 hours of ventricular fibrillation, hearts were defibrillated and left ventricular transmural biopsies were obtained. Hearts were then excised and subjected to 90 minutes of normothermic total ischemia. Serial biopsies were obtained at 15-minute intervals to determine regional depletion of high energy phosphates. The time-to-peak ischemic contracture was recorded by using needle-tipped Millar catheters placed in the left ventricular endocardium, epicardium, septum, and right ventricle. Time-to-peak ischemic contracture of the endocardium (62.6 +/- 1.4 vs. 58.8 +/- 1.0 minutes, p less than 0.05) and septum (61.1 +/- 6.9 vs. 46.9 +/- 6.2 minutes, p less than 0.004) were significantly prolonged after direct mechanical ventricular actuation versus cardiopulmonary bypass, respectively. Similar trends were noted in the epicardium and right ventricular regions; however, these differences were not statistically significant. Left ventricular adenosine triphosphate (ATP) levels were better preserved after direct mechanical ventricular actuation (22 +/- 1.5 mumols/g dry wt) compared with cardiopulmonary bypass (17 +/- 1.9 mumols/g dry wt). The depletion of left ventricular endocardium ATP during normothermic ischemia was significantly delayed after direct mechanical ventricular actuation compared with cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

Spatial and temporal characteristics of the transmural distribution of collateral flow and energy metabolism during regional myocardial ischemia in the dog.

To characterize the temporal and spatial characteristics of transmural gradients of flow, ATP and CP, dogs (n = 17) were subjected to coronary artery ligation for either 30 minutes or 24 hours. Different radioactive microspheres were given at the onset and end of the ischemic period. Simultaneous multiple transmural biopsies (up to 20 per heart) were obtained (in situ freezing) from central ischemic and surrounding normal tissue after either 30 minutes or 24 hours of elapsed ischemia. After lyophilization each biopsy was divided into up to 6 transmural sub-fragments, each of which was analysed for flow, ATP and CP. At the onset of ischemia flow declined to less than 15% throughout the ischemic zone and there was a slight transmural gradient of flow from epi- to endocardium (12.4 +/- 1.6, 13.5 +/- 2.0, 11.0 +/- 1.8, 10.3 +/- 1.7, 8.5 +/- 1.9 and 8.3 +/- 3.1% of non-ischemic tissue). After 30 minutes of ischemia, collateral flow to the epicardial tissue had increased substantially but endocardial flow remained unchanged, the epi- to endo- gradient was 20.8 +/- 2.5, 18.9 +/- 2.4, 13.7 +/- 2.1, 10.8 +/- 1.5, 8.5 +/- 1.2, 7.6 +/- 1.7. After 24 hours there were further increases in the epi- and mid- myocardial regions but the endocardial flow remained severely depressed, the epi- to endo- gradient was 23.9 +/- 3.2, 24.5 +/- 3.0, 23.6 +/- 4.8, 16.4 +/- 3.3, 9.8 +/- 2.9, 5.8 +/- 2.9%. ATP and CP were severely depressed after 30 minutes of ischemia and reflected flow closely with sharp linear epi- to endo- gradients (17.5 to 10.9 muMol/g dry wt for ATP and 7.4 to 3.1 muMol/g dry wt for CP). After 24 hours, the decline in ATP had been slowed and there was a striking recovery of CP in the epi- and mid- myocardial regions which had experienced increasing collateral flow. CP in the endocardium remained severely depressed. Progressive supplementation of collateral flow early and throughout a 24 hour period of regional myocardial ischemia and the selective delivery of this flow to subepi- and mid- myocardial tissue accounts in part for the natural salvage of this tissue and the deterioration of the endocardium to necrosis. Gradients of flow and metabolism further influence these events and account for the "wave front" of cell death.

Adenosine Triphosphate↗
PubMed1996

[Valve replacement concomitant with anulus reconstruction].

It is important that surgical treatment of infective endocarditis involves complete debridement of the affected tissue. In case of abscess formation in the mitral anulus and/or aortic root, disruption of the anulus occurs because of radical resection of the abscess. David et al. reported a new technique for mitral and aortic anulus reconstruction. The novel part of the technique was the endocardial repair, i.e., suturing of a pericardial patch to the endocardium of the left ventricle. We were surprised to learn that the left ventricular endocardium and muscle are capable of tolerating the stress induced by the prosthetic ring, especially in the mitral position. Since 1992, we treated eight cases of anulus disruption using this technique ; 5 cases involved the mitral anulus, 1 involved the aortic, and 2 involved both. We used a slightly different technique involving suturing of a patch not only to the left ventricular endocardium but also to left atrial wall for reinforcement. Two patients died in the perioperative period. One had a brain abscess ; the other had methicillin-resistant Staphylococcus aureus sepsis and mediastinitis. There was 1 late (sudden, unknown) death 3 years after the operation. No perivalvular leakage, dehiscence of the patch, hemolysis, prosthetic valve endocarditis, or thromboembolism have been observed in the other 5 patients.

Abscess↗
PubMed2000

Mechanisms involved in valvuloseptal endocardial cushion formation in early cardiogenesis: roles of transforming growth factor (TGF)-beta and bone morphogenetic protein (BMP).

Endothelial-mesenchymal transformation (EMT) is a critical event in the generation of the endocardial cushion, the primordia of the valves and septa of the adult heart. This embryonic phenomenon occurs in the outflow tract (OT) and atrioventricular (AV) canal of the embryonic heart in a spatiotemporally restricted manner, and is initiated by putative myocardially derived inductive signals (adherons) which are transferred to the endocardium across the cardiac jelly. Abnormal development of endocardial cushion tissue is linked to many congenital heart diseases. At the onset of EMT in chick cardiogenesis, transforming growth factor (TGFbeta)-3 is expressed in transforming endothelial and invading mesenchymal cells, while bone morphogenetic protein (BMP)-2 is expressed in the subjacent myocardium. Three-dimensional collagen gel culture experiments of the AV endocardium show that 1) myocardially derived inductive signals upregulate the expression of AV endothelial TGFbeta3 at the onset of EMT, 2) TGFbeta3 needs to be expressed by these endothelial cells to trigger the initial phenotypic changes of EMT, and 3) myocardial BMP2 acts synergistically with TGFbeta3 in the initiation of EMT.

Animals↗
PubMed1979

Differences in regional capillary distribution and myocyte sizes in normal and hypertrophic rat hearts.

Data are reported which show significant regional capillary differences in left ventricular endocardium and epicardium of normal rats and of rats with hyperthyroid-induced cardiac hypertrophy. The epicardial region of control rats has 38% more capillaries than the endocardial region. Control endocardial myocytes are 62% larger in cross-sectional area than epicardial myocytes. Hypertrophic hearts exhibit regional differences in capillary density similar to those in the normal hearts, but there is an overall reduction of 12 and 17.5% in capillary density in both regions. The average cross-sectional area of myocytes increases 34.5% in the epicardium and 22.5% in the endocardium.

Animals↗
PubMed1990

Spatial differences of endogenous lectin expression within the cellular organization of the human heart: a glycohistochemical, immunohistochemical, and glycobiochemical study.

Protein-carbohydrate recognition may be involved in an array of molecular interactions on the cellular and subcellular levels. To gain insight into the role of proteins in this type of interaction, surgically removed specimens of human endomyocardial tissue were processed for histochemical and biochemical analysis. The inherent capacity of these sections to bind individual sugar moieties, which are constituents of the carbohydrate part of cellular glycoconjugates, was assessed using a panel of biotinylated neoglycoproteins according to a standardized procedure. Together with appropriate controls, it primarily allowed localization of endogenous lectins. Differences in lectin expression were observed between layers of endocardial tissue, myocardial cell constituents, connective-tissue elements, and vascular structures. The endocardium proved to be positive with beta-galactoside-bearing probes; with neoglycoproteins carrying beta-xylosides, alpha-fucosides, and galactose-6-phosphate moieties; and with probes containing a carboxyl group within the carbohydrate structure, namely sialic acid and glucuronic acid. In contrast, only fucose-and maltose-specific receptors were apparent in the elastic layers of the endocardium. Aside from ascertaining the specificity of the protein-carbohydrate interaction by controls, i.e., lack of binding of the probe in the presence of the unlabelled neoglycoprotein and lack of binding of the labelled sugar-free carrier protein, respective sugar receptors were isolated from heart extracts by using histochemically effective carbohydrates as immobilized affinity ligand. Moreover, affinity chromatography using immobilized lactose as affinity ligand as well as the use of polyclonal antibodies against the predominant beta-galactoside-specific lectin of heart demonstrated that the lactose-specific neoglycoprotein binding was due to this lectin. Remarkably, the labelled endogenous lectin, preferred to plant lectins for detecting ligands of the endogenous lectin, localized ligands in tissue parts where the lectin itself was detected glycohistochemically as well as immunohistologically. This demonstration of receptor-ligand presence in the same system is a further step toward functional assignment of the recorded protein-carbohydrate interaction. Overall, the observed patterns of lectin expression may serve as a guideline to elucidate the precise physiological relevance of lectins and to analyze pathological conditions comparatively.

Endocardium↗
PubMed1995

Relationship between fibronectin expression during gastrulation and heart formation in the rat embryo.

By utilizing myosin immunostaining, we were able to identify early rat myocardium as a thin epithelial sheet and realized that its cohesive movement toward the midline leads to the straight heart tube formation. Localization study of fibronectin mRNA and protein was, therefore, carried out to investigate its tissue origin and possible roles in facilitating mesoderm migration and heart formation. Fibronectin mRNAs were first detected throughout the mesoderm during the early primitive streak stage, suggesting that the mesoderm is the source of fibronectin. By pre-head fold (pre-somite) and head fold (early somite) stages, the mesoderm became largely down-regulated for fibronectin mRNAs, while it was also at these stages when myosin-positive myocardium formed itself into the epithelium and was subsequently folding toward the midline. Thus, there appears to be little fibronectin synthesis during and directly relevant to early heart tube formation. Later, during the early straight heart tube stage (5 somite and older), endocardium became highly positive for fibronectin mRNAs, suggesting that the endocardium is the major source of fibronectin for the cardiac jelly. Based on the results, we present a map for the early mammalian heart in which the heart is a single crescentic band lying in front of the prechordal plate. We also suggest a process for heart tube formation based on the cohesive movement of the myocardial epithelium. During heart tube formation, fibronectin protein had been deposited previously by the mesoderm and was found uniformly in the ECM and not newly produced by any adjacent tissue. The data contradict the endodermal guidance of heart migration by fibronectin gradient and suggest, instead, a permissive role for the fibronectin substrate.

Animals↗
PubMed2002

Structure of the conus arteriosus of the sturgeon (Acipenser naccarii) heart. I: the conus valves and the subendocardium.

Sturgeons are bony fish that retain structural traits typical of the more primitive Chondrostei. From an evolutionary viewpoint, sturgeons are considered relic fish. However, they show remarkable ecological plasticity and are well adapted to contemporary environmental conditions. Although development of the cardiovascular system is critical for all organs and systems, and is affected by evolutionary changes, the structure of the sturgeon heart has been mostly overlooked. This is also true for the conus arteriosus, which, as in Chondrostei, is endowed with several rows of valves and a layer of contractile myocardium. This work reports on the structure of the valves, the endocardium, and the subendocardium of the conus arteriosus of the sturgeon (Acipenser naccarii) heart. It is part of a broader study that aims to cover the entire structure of the sturgeon heart. The conus arteriosus of 15 A. naccarii hearts, ranging in age from juveniles to sexually-differentiated adults, has been studied by conventional light, transmission (TEM), and scanning electron microscopy (SEM). In addition, maceration of the soft tissues with NaOH, and actin localization by fluorescent phalloidin has been used. The conus is a tubular chamber that arises from the right ventricular side and presents two constrictions at the conus-ventricle and conus-aorta junctions. The conus is endowed with three rows of valves: one distal and two proximal. The segment of the conus located between the distal and the two proximal rows is devoid of valvular structures. The distal row has four leaflets, while the two proximal rows show the greatest variation in leaflet number, size, and shape. All leaflets have collagenous chordae tendineae arising from the free border and from the parietal side of the leaflets. The endocardium is a flat endothelium which shows a thick, irregular basement membrane. The leaflet body is formed by a loose connective tissue which blends with the subendocardium. The subendocardium is a connective tissue consisting of myofibroblasts, collagen, and elastin. It is divided into two distinct areas: one proximal, which shows little elastin and poorly organized collagen; and one distal, which is rich in elastin, with cells and extracellular fibers organized into layers that are oriented in alternative circumferential and longitudinal directions. The present report is the first systematic analysis of the structure of the sturgeon conus. Descriptions of the conus valves should recognize the existence of three valve rows only. The variability in valve morphology, and the loose structure of the leaflet tissue make it unlikely that the valves play an effective role in preventing blood backflow. In this regard, the ventricle-conus constriction may act as a sphincter. The subendocardium is an elastic coat capable of actively sustaining the tissue deformation that accompanies the heart contractile cycle. Further comparative studies are needed to provide deeper insight into the structural changes that accompany phyletic diversification.

Animals↗
PubMed1981

The origin of the epicardium and the embryonic myocardial circulation in the mouse.

The origin of the epicardium and the formation of the early blood vessels of the heart prior to the opening of the coronary arteries from the aorta have been studied in the 9-13.5 day post coitum (dpc) mouse embryo heart. The epicardium begins to appear by 9 dpc. The majority of the epicardial cells derive from the somatopleural investment of the septum transversum, from where they migrate, associated to form vesicles, to the dorsal aspect of the ventricles and atria. The epicardial cells then migrate over the lateral surfaces and the AV sulcus to the ventral aspect of the heart. In the subepicardial space around the sulci, the proliferating epithelial tissue is found, also in vesicular form, for a time. The ventrally migrating primordial epicardial tissue ensheaths lastly the truncus arteriosus, while the sinus venosus is coated with epicardium ab initio, where (and also in the SA sulcus) the epicardial cells derive in part from the cuboidal cells of the pleuroperitoneal canal and in part from the somatopleural cells. The early blood vessel formation follows in space and time the development of the epicardium. The first blood vessels appear by dpc by the invagination of the endocardium into the early sinus muscle, and at the same time in the ventricular chamber by the encasing of the endocardium, as the trabeculae become consolidated into the myocardial walls. By this process sinusoids are formed, some of which penetrate through the myocardium and which, by rapid proliferation, form an interconnected subepicardial plexus. These capillaries proliferate ventrally in the wide subepicardial space, reaching the septating truncus, in which the aorta and pulmonary artery are developing. The definitive coronary artery openings appear by 13 dpc, allowing the high pressure blood from the aorta to flow into a preexisting vascular bed.

Animals↗
PubMed2006

Three-dimensional architecture of the left ventricular myocardium.

Concepts for ventricular function tend to assume that the majority of the myocardial cells are aligned with their long axes parallel to the epicardial ventricular surface. We aimed to validate the existence of aggregates of myocardial cells orientated with their long axis intruding obliquely between the ventricular epicardial and endocardial surfaces and to quantitate their amount and angulation. To compensate for the changing angle of the long axis of the myocytes relative to the equatorial plane of the ventricles with varying depths within the ventricular walls, the so-called helical angle, we used pairs of cylindrical knives of different diameters to punch semicircular slices from the left ventricular wall of pigs, the slices extending from the epicardium to the endocardium. The slices were pinned flat, fixed in formaldehyde, embedded in paraffin, sectioned, stained with azan or hematoxilin and eosin, and analyzed by a new semiautomatic procedure. We made use of new techniques in informatics to determine the number and angulation of the aggregates of myocardial cells cut in their long axis. The alignment of the myocytes cut longitudinally varied markedly between the epicardium and the endocardium. Populations of myocytes, arranged in strands, diverge by varying angles from the epicardial surface. When paired knives of decreasing diameter were used to cut the slices, the inclination of the diagonal created by the arrays increases, while the lengths of the array of cells cut axially decreases. The visualization of the size, shape, and alignment of the myocytic arrays at any side of the ventricular wall is determined by the radius of the knives used, the range of helical angles subtended by the alignment of the myocytes throughout the thickness of the wall, and their angulation relative to the epicardial surface. Far from the majority of the ventricular myocytes being aligned at angles more or less tangential to the epicardial lining, we found that three-fifths of the myocardial cells had their long axes diverging at angles between 7.5 and 37.5 degrees from an alignment parallel to the epicardium. This arrangement, with the individual myocytes supported by connective tissue, might control the cyclic rearrangement of the myocardial fibers. This could serve as an important control of both ventricular mural thickening and intracavitary shape.

Animals↗
PubMed1987

Laser-assisted endocardiectomy for refractory ventricular tachyarrhythmias: preliminary intraoperative experience.

Previous in vitro investigations utilizing necropsy specimens have suggested a potential role for laser irradiation in the treatment of refractory ventricular tachyarrhythmias associated with pathologically thickened endocardium. In the patient described in the present report, findings of these previous in vitro studies were applied intraoperatively to a patient undergoing surgery for ischemic heart disease associated with ventricular tachyarrhythmias. Aneurysm resection and manual subendocardial resection were performed using standard techniques. Laser irradiation was used to ablate pathologically thickened endocardium involving the papillary muscle and thereby avoid mitral valve replacement. Postoperatively, there was no auscultatory evidence of mitral regurgitation, and ventricular tachycardia could not be induced by electrophysiologic provocative testing. This preliminary experience confirms that laser irradiation is both a feasible and potentially advantageous means of accomplishing endocardial debridement in patients undergoing arrhythmia-ablation procedures.

Cardiomegaly↗
PubMed2003

Expression patterns of Tgfbeta1-3 associate with myocardialisation of the outflow tract and the development of the epicardium and the fibrous heart skeleton.

Transforming growth factor-beta (Tgfbeta) is essential for normal embryogenesis. The cardiac phenotypes obtained after knockout of each of the three mammalian isoforms suggest different roles during morphogenesis. We studied cardiovascular expression of Tgfbeta1-3 in parallel tissue sections of normal mouse embryos from 9.5 to 15.5 days post coitum (dpc) by using radioactive in situ hybridisation. The Tgfbeta isoforms are differentially expressed in unique and in overlapping patterns during cardiovascular development. In the vessels, Tgfbeta1 is found in the intima, whereas Tgfbeta2 and -beta3 are mainly present in the media and adventitia of the great arteries. Tgfbeta1 is present in the endocardium at all stages examined. The Tgfbeta2 signal in the endocardium of the atrioventricular canal and outflow tract (9.5 dpc) shifts during epithelial-mesenchymal transformation toward the mesenchymal cushions (10.5-11.5 dpc) after which it exhibits a marked spatiotemporal expression pattern as the cushion differentiation progresses (11.5-15.5 dpc). The myocardium underlying the endocardial cushions and the atrial muscular septum are intensely positive for Tgfbeta2 at early stages (9.5-11.5 dpc) and expression decreases at 12.5 days. In contrast to earlier reports, we find marked overlap of Tgfbeta2 and -beta3 expression. Tgfbeta3 expression shows a characteristic distribution in the mesenchymal cushions, suggesting a role in cushion differentiation, possibly additional to Tgfbeta2. From 14.5 dpc onward, a strong Tgfbeta3 signal is found in the fibrous septum primum of the atrium and in the fibrous skeleton of the heart. Special attention was paid to the proepicardial organ and its derivatives. The proepicardial organ strongly expresses Tgfbeta2 as early as 9.5 days, and all isoforms are present in the epicardium from 12.5 dpc onward. The spatiotemporal cardiovascular expression of Tgfbeta1-3 supports both specific and complementary functions during cardiovascular development that might explain functional redundancy between the Tgfbeta-isoforms. The information provided favors novel roles of Tgfbeta1-3 in epicardial development, of Tgfbeta2 in myocardialisation, and of Tgfbeta3 in differentiation of the fibrous structures of the heart.

Actins↗
PubMedDate not supplied

Automated myocardial edge detection on MR images: accuracy in consecutive subjects.

The authors previously demonstrated the feasibility of graph-searching-based automated edge detection in cardiac magnetic resonance (MR) imaging. To further assess the clinical utility of this method, unselected images from 11 consecutive subjects undergoing clinically indicated (except for one healthy volunteer) short-axis spin-echo MR imaging were analyzed. A total of 142 images from the 11 subjects, encompassing the left ventricle from apex to outflow tract, were analyzed. The computer algorithm correctly identified complete endocardial and epicardial contours in 121 of 142 images (85%). Correlations between observer-traced and computer-derived epicardial areas for all images were good (r = .71 for epicardium, r = .83 for endocardium); they improved for a subset of higher-quality images (r = .82 for epicardium, r = .92 for endocardium). The authors conclude that the current data further support the usefulness of computer digital image processing in geometric analysis of cardiac MR image data.

Adolescent↗
PubMed1996

The fate diversity of mesodermal cells within the heart field during chicken early embryogenesis.

In gastrulation stage embryos of birds and mammals, the heart field is established as mesodermal crescents flanking the area rostrolateral to Hensen's node. Subsequent fusion of the bilateral heart primordia gives rise to a single tubular heart consisting of two epithelial layers: an outer myocardium and an inner endocardium. To date, it is uncertain whether these two distinct cell types of the heart arise from common or separate progenitor populations of mesodermal cells within the heart field. By retroviral single cell marking and tracking, we examined the diversity of cell populations present in the heart field of stage 4 chicken embryos. Here we demonstrate that individual mesodermal cells in the heart field gave rise to a clone consisting only of one cell type, either endocardial or myocardial cells; i.e., 95.1% of the mesoderm-derived clones were localized in the myocardium, while 4.9% of them were found in endocardium. No clones containing both of these two cell types were detected. The results suggest that the heart field mesoderm at stage 4 consists of at least two distinct subpopulations, containing more premyocardial cells than preendocardial cells. If there exists a common precursor of both myocardial and endocardial cells, the lineage diversification must occur at or prior to the arrival of mesodermal cells to the heart field.

Animals↗
PubMed1998

Trabecular myocytes of the embryonic heart require N-cadherin for migratory unit identity.

The myocardial wall of the vertebrate heart changes from a simple epithelium to a trabeculated structure during embryogenesis. This process occurs when epithelioid cardiomyocytes migrate toward the endocardium, which we show is coincident with up-regulation of the cell adhesion molecule, N-cadherin. To study the role of N-cadherin expressed at the trabeculation stage, a replication-defective retrovirus expressing a dominant negative mutant of N-cadherin (delta N-cadherin) was engineered. Control viruses were designed to express beta-galactosidase or a full-length N-cadherin. Viruses were introduced into epithelioid presumptive myocytes at the time they initiate the epithelial-mesenchymal transformation. Individual cells infected with control viruses generated daughter myocytes which migrated toward endocardium as a tight cluster, thereby generating a clone that forms a single or at most two trabeculae. In contrast, myocytes expressing delta N-cadherin were sparsely distributed within the myocardium and failed to form the ridge-shaped clone. Thus, in addition to its known roles in myocyte epithelialization and intercalated disc formation, N-cadherin appears to play a role in homotypic interactions between nonepithelial migratory myocytes during trabecular formation of the embryonic heart.

Animals↗