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Biomedical subjects

Robert H Anderson

Publications and source records attributed to Robert H Anderson.

At least 19 recordsLinked to original sources
PubMed2005

Ventricular myocardial architecture as visualised in postmortem swine hearts using magnetic resonance diffusion tensor imaging.

OBJECTIVE: The three-dimensional arrangement of the ventricular myocardial architecture remains controversial, in part because histological assessment is difficult to achieve, while anatomic dissections are, of necessity, destructive. In this study, we describe how the use of magnetic resonance diffusion tensor imaging has permitted us to reconstruct with precision the architecture of the ventricular myocardial fibres in the post-mortem swine heart. METHODS AND RESULTS: We obtained diffusion-weighted spin-echo measurements of autopsied porcine hearts using a whole body MR system. We calculated the diffusion tensor and the corresponding eigenvectors on a voxel-by-voxel basis. This permitted us to colour code the fibres, and reconstruct them by connecting voxels in direction of the largest eigenvector. Such reconstructions show that, in the middle layer of the left ventricle, most of the fibres have a circular orientation, albeit that a far from negligible component runs in a transverse direction. With increasing distance from the epicardium, the orientation of the fibres shows a continuous change in angulation with respect to an axis normal to the epicardium. CONCLUSION: Our data presented here supports the concept that the ventricular mass is arranged as a complex three-dimensional mesh of tangential and intruding fibres. The data offers no support for the concept of a "unique myocardial band". The method has the potential to detecting deviations from this basic normal architecture, being capable of reconstructing the ventricular mass so as to assess the spatial coordinates of any single fibre strand. The technique, therefore, has major potential clinical applications in the setting of the failing or malformed heart, potentially being able to identify either systematic or regional disarray of the myocardial fibres.

Animals↗
PubMed2005

The architecture of the ventricular mass and its functional implications for organ-preserving surgery.

It has generally been accepted that the myocardial fibres within the ventricular mass are arranged in syncytial fashion, precluding the identification of discrete and isolated muscular pathways. Recently, however, an entire hypothesis for surgical treatment has been proposed on the basis of the existence of a 'ventricular myocardial band', suggesting that this arrangement in itself points to detrimental results following partial ventriculectomy. In this review, we re-state the evidence supporting the accepted concept of the ventricular mass being made up of an undefined number of wedge-shaped functional units, each of them exerting its individually programmed contribution to the global activity of the ventricular walls. The wedge-shaped units consist of bundles of individual fibres which are arranged tangentially. An important subset of fibres intrudes into the ventricular wall, thus creating oblique pathways. Their angle of intrusion varies, and can be measured at up to 30 degrees . The steeper the angle of their intrusion, the more efficiently do the fibres counteract the systolic mural thickening. The network of supporting connective tissue, nonetheless, provides the necessary steep angulation towards the endocardium. This fibrous matrix serves as continuous chain for the transmission of forces, including that in the direction from the epicardium towards the endocardium, resulting in a dilating force. We have shown, using needle force probes, that in the hypertrophic heart the dynamic equilibrium of dilating and constricting forces acts at elevated diastolic and systolic levels, because the obliquity of the fibres increases due to the thickening of the wall, and there is a concomitant increase in connective tissue, causing an increase in the forces opposing systolic mural thickening. Then, in a vicious cycle, both populations of myocardial fibres stimulate each other to hypertrophy. Eventually, coronary perfusion becomes critically impaired, with still further deposition of connective tissue. Ultimately, the vector of the dilating force comes to dominate the constricting force, and the ventricle dilates. In this setting, partial left ventriculectomy remains a functionally sound intervention, since it is capable of improving global ventricular function by improving the geometrical state of the remaining anatomic myocardial units.

Biomechanical Phenomena↗
PubMed2004

Normal and abnormal fetal cardiac anatomy.

The heart is often perceived as a difficult organ to understand by ultrasound during fetal life. This is undoubtedly reflected in the low detection rate of cardiac abnormalities as compared to those of most other organ systems in the fetus. In this article we start by updating classical concepts of cardiac embryology, many of which were previously difficult to understand since they were overly simplistic or purely observational. We then lead on to the structure and growth of the fully formed fetal heart where we review the anatomy and ultrasound appearances in detail and provide comparisons with major abnormalities. We emphasise the fact that a solid understanding of cardiac anatomy can enable those involved in fetal medicine to make full use of the views of the heart that are obtained by ultrasound and which are often only transient.

Echocardiography↗
PubMed2004

Reconstruction of the patterns of gene expression in the developing mouse heart reveals an architectural arrangement that facilitates the understanding of atrial malformations and arrhythmias.

Firm knowledge about the formation of the atrial components and of the variations seen in congenital cardiac malformations and abnormal atrial rhythms is fundamental to our understanding of the normal structure of the definitive atrial chambers. The atrial region is relatively inaccessible and has continued to be the source of disagreement. Seeking to resolve these controversies, we made three-dimensional reconstructions of the myocardial components of the developing atrium, identifying domains on the basis of differential expression of myocardial markers, connexin40, and natriuretic precursor peptide A. These reconstructions, made from serial sections of mouse embryos, show that from the outset of atrial development, the systemic and pulmonary veins are directly connected to the atrium. Relative to the systemic junctions, however, the pulmonary venous junction appears later. Our experience shows that three-dimensional reconstructions have three advantages. First, they provide clear access to the combined morphological and molecular data, allowing clarification and verification of morphogenetic concepts for nonmorphological experts and setting the scene for further discussion. Second, they demonstrate that, from the outset, the myocardium surrounding the pulmonary veins is distinct from that clothing the systemic venoatrial junctions. Third, they reveal an anatomical and molecular continuity between the entrance of the systemic venous tributaries, the internodal atrial myocardium, and the atrioventricular region. All these regions are derived from primary myocardium, providing a molecular basis for the observed nonrandom distribution of focal right atrial tachycardias.

Animals↗
PubMed2004

Cited2 controls left-right patterning and heart development through a Nodal-Pitx2c pathway.

Malformations of the septum, outflow tract and aortic arch are the most common congenital cardiovascular defects and occur in mice lacking Cited2, a transcriptional coactivator of TFAP2. Here we show that Cited2(-/-) mice also develop laterality defects, including right isomerism, abnormal cardiac looping and hyposplenia, which are suppressed on a mixed genetic background. Cited2(-/-) mice lack expression of the Nodal target genes Pitx2c, Nodal and Ebaf in the left lateral plate mesoderm, where they are required for establishing laterality and cardiovascular development. CITED2 and TFAP2 were detected at the Pitx2c promoter in embryonic hearts, and they activate Pitx2c transcription in transient transfection assays. We propose that an abnormal Nodal-Pitx2c pathway represents a unifying mechanism for the cardiovascular malformations observed in Cited2(-/-) mice, and that such malformations may be the sole manifestation of a laterality defect.

Animals↗
PubMed2004

Lineage and morphogenetic analysis of the cardiac valves.

We used a genetic lineage-labeling system to establish the material contributions of the progeny of 3 specific cell types to the cardiac valves. Thus, we labeled irreversibly the myocardial (alphaMHC-Cre+), endocardial (Tie2-Cre+), and neural crest (Wnt1-Cre+) cells during development and assessed their eventual contribution to the definitive valvar complexes. The leaflets and tendinous cords of the mitral and tricuspid valves, the atrioventricular fibrous continuity, and the leaflets of the outflow tract valves were all found to be generated from mesenchyme derived from the endocardium, with no substantial contribution from cells of the myocardial and neural crest lineages. Analysis of chicken-quail chimeras revealed absence of any substantial contribution from proepicardially derived cells. Molecular and morphogenetic analysis revealed several new aspects of atrioventricular valvar formation. Marked similarities are seen during the formation of the mural leaflets of the mitral and tricuspid valves. These leaflets form by protrusion and growth of a sheet of atrioventricular myocardium into the ventricular lumen, with subsequent formation of valvar mesenchyme on its surface rather than by delamination of lateral cushions from the ventricular myocardial wall. The myocardial layer is subsequently removed by the process of apoptosis. In contrast, the aortic leaflet of the mitral valve, the septal leaflet of the tricuspid valve, and the atrioventricular fibrous continuity between these valves develop from the mesenchyme of the inferior and superior atrioventricular cushions. The tricuspid septal leaflet then delaminates from the muscular ventricular septum late in development.

Animals↗
PubMed2004

Spatiotemporal analysis of programmed cell death during mouse cardiac septation.

Cell death is thought to play an important role in mammalian cardiogenesis, although a precise map of its distribution during the crucial period of cardiac septation has so far been lacking. In this study, the spatiotemporal distribution of programmed cell death (PCD) during mouse cardiac septation is described between embryonic days 10.5 and 13.5. Two types of foci of cell death can be demonstrated in the developing heart. Those with high-intensity, with a PCD index greater than 1%, are clearly visible on individual TUNEL-assayed sections. Low-intensity foci, with a PCD index of less than 1%, become visible only following summation of data. High-intensity foci occur exclusively within the endocardial cushions of the outflow tract and atrioventricular region, appearing at the 52-54 somite stage (late E11.5), concomitant with the formation of the central mesenchymal mass. Low-intensity foci are present throughout the period of cardiac development from E10.5 to E13.5 and are frequently localized to regions of septation, such as the muscular ventricular septum and the mesenchymal cap of the primary atrial septum. Expression of Fas and FasL corresponds to these low-intensity foci, but not those with high-intensity, suggesting that activation of this death receptor may be specifically involved in molecular control of the low-intensity foci.

Animals↗
PubMed2004

Controversies concerning the anatomical definition of the conduction tissues.

Conduction across the atrioventricular junctions had long been controversial, with arguments raging as to whether such conduction was myogenic or neurogenic. The landmark study of Tawara in 1906 established the existence of an axis of histologically specialized myocardial cells contained within fibrous sheaths as being responsible for rapid conduction from the atrial to the ventricular myocardium. Keith and Flack then demonstrated that the atrial impulse was generated in the sinus node, with subsequent slowing within the atrioventricular node of Tawara. The detailed reviews of Aschoff and Monckeberg then emphasized the morphological features that permit unequivocal recognition of the nodes, along with rapidly conducting tracts. It is now pertinent that we remember these original criteria for anatomical recognition as we discuss the steps involved in the development of these conducting structures from their embryologic primordiums. In this review, we restate the criteria of Aschoff and Monckeberg, then discuss their relevance to the developmental issues, emphasizing that all myocardial cells have the potential to conduct. The important issues, therefore, are the changes that occur as the heart itself changes from a solitary muscular tube, already possessing the capacity t generate an electrocardiogram, to the four-chambered structure we recognize in postnatal life.

Animals↗
PubMed2004

Solitary trunk from the right ventricle with a cleft mitral valve simulating the trifoliate left valve of an atrioventricular septal defect with common atrioventricular junction.

We report a case of a true cleft in the anterior leaflet of the mitral valve. The cleft, however, is directed toward the ventricular septum, and the left ventricular papillary muscles have the same arrangement as seen in the setting of a common atrioventricular orifice. The atrioventricular septum is intact. This appearance reflects the presence, in this patient, of right ventricular origin of a solitary arterial trunk, so that there was no outflow tract within the left ventricle to interpose between the mitral valve and the septum.

Abnormalities, Multiple↗
PubMed2004

Cleft mitral valve in transposition with intact ventricular septum.

We describe two cases of an isolated cleft of the mitral valve in transposition with intact ventricular septum. The cleft is positioned leftward in the pulmonary leaflet, at about 2 o'clock, when viewed from below looking at the cardiac short axis with the right ventricle to one's left hand. Such clefts, when seen in the Taussig-Bing malformation are also positioned leftward. In keeping with our current knowledge of cardiac development, our cases provide further evidence that transposition with an intact ventricular septum is the end-point of the Taussig-Bing spectrum.

Double Outlet Right Ventricle↗
PubMed2004

Cardiac anatomy revisited.

In tomorrow's world of clinical medicine, students will increasingly be confronted by anatomic displays reconstructed from tomographically derived images. These images all display the structure of the various organs in anatomical orientation, this being determined in time-honoured fashion by describing the individual in the 'anatomical position', standing upright and facing the observer. It follows from this approach that all adjectives used to describe the organs should be related to the three orthogonal planes of the body. Unfortunately, at present this convention is not followed for the heart, even though most students are taught that the so-called 'right chambers' are, in reality, in front of their 'left' counterparts. Rigorous analysis of the tomographic images already available, along with comparison with dissected hearts displayed in attitudinally correct orientation, calls into question this continuing tendency to describe the heart in terms of its own orthogonal axes, but with the organ positioned on its apex, so that the chambers can artefactually be visualized with the right atrium and right ventricle in right-sided position. Although adequate for describing functional aspects, such as 'right-to-left' shunting across intracardiac communications, this convention falls short when used to describe the position of the artery that supplies the diaphragmatic surface of the heart. Currently known as the 'posterior descending artery', in reality it is positioned inferiorly, and its blockage produces inferior myocardial infarction. In this review, we extend the concept of describing cardiac structure in attitudinally correct orientation, showing also how access to tomographic images clarifies many aspects of cardiac structure previously considered mysterious and arcane. We use images prepared using new techniques such as magnetic resonance imaging and computerized tomography, and compare them with dissection of the heart made in time-honoured fashion, along with cartoons to illustrate contentious topics. We argue that there is much to gain by describing the components of the heart as seen in the anatomical position, along with all other organs and structures in the body. We recognize, nonetheless, that such changes will take many years to be put into practice, if at all.

Aorta↗