Septomarginal Trabecula Research Articles

The conduction bundle at the atrioventricular junction. An anatomical study.

The variability in the topographical anatomy of the conduction bundle at the site of the atrioventricular junction has been studied in four normal human hearts. The junctional area has been removed en bloc and serially sectioned. The conduction bundle and adjacent structures such as the posterior limb of the trabecula septomarginalis and the membranous septum have been reconstructed based on calculations from the histological sections. The study reveals marked variability particularly in the extent of the posterior limb of the trabecula septomarginalis. In one instance, the muscle was almost totally absent so that the branching bundle was located in a midline position and subendocardial both to the right and the left ventricular septal surface. In two hearts, the posterior limb of the trabecula septomarginalis had ramified so that only a small segment of the conduction bundle was covered by muscle. In the remaining case, a well-developed posterior limb of the trabecula septomarginalis completely covered the conduction axis thus accounting for the left-sided position of the bundle. The variability encountered may render the conduction bundle vulnerable to the tensile strain of the tricuspid valve apparatus, enhancing the natural process of wear and tear which may lead to disruption of conduction fibres and heart block, particularly in the elderly. Since the detailed topographical anatomy of the conduction bundle in the atrioventricular junctional area appears to be highly variable from one individual to another, meticulous inspection is mandatory once the area is manipulated at surgery.

Double outlet right ventricle associated with common atrioventricular canal: Report of nine anatomic specimens

Double outlet right ventricle associated with complete atrioventricular (AV) canal is a rare malformation. Nine cases are reported. In this abnormality the anterior AV leaflet is undivided and free floating and the aortic and pulmonary orifices are in the same frontal plane. In four of the nine cases, the conus was bilateral, but it was slightly hypoplastic in two. In five cases there was no subaortic conus and there was mitral-aortic continuity through the ventricular septal defect. Pulmonary stenosis was present in eight cases. Radiograms may best demonstrate the anatomy of the ventricular septal defect; it extends far anteriorly below the aortic valve, and its inferior rim is deviated by the trabecula septomarginalis.

A Histological Study of Surgical Landmarks for the Specialized Atrioventricular Conduction System, with Particular Reference to the Papillary Muscle

Surgical landmarks of the conduction system were histologically evaluated in 29 cardiac specimens. The distribution of the system was grossly inherent to the type of ventricular septal defect as classified by Soto and co-workers, although it varied individually. The relationship of the right bundle branch (RBB) to the papillary muscles was of surgical interest. In defects unrelated to maldevelopment of the septum of the conus, the RBB passed beneath or slightly anterior to upper accessory papillary muscles (AcPMs) and posterior to the medial papillary muscle (MPM), regardless of the subtype of defect. In defects caused by maldevelopment, such as tetralogy of Fallot, it passed anterior to the MPM. Such data support the hypothesis that the RBB descends beneath or anterior to embryological upper AcPMs, whatever the morphological role may be, because of the supposedly independent developmental origin of the MPM and AcPMs. The relationship between the RBB and upper AcPMs appeared further modified by the attitude of the trabecula septomarginalis. Our improved clinical results have demonstrated that such information offers a gross but practical guide for prevention of conduction disturbances.

Abnormal architecture of the ventricles in hearts with an overriding aortic valve and a perimembranous ventricular septal defect (“Eisenmenger VSD”)

Among 111 hearts with so-called “isolated” ventricular septal defect, 18 specimens were found to have a subaortic perimembranous defect with an overriding aortic valve but without pulmonary stenosis. The ventricular architecture was characterized by several abnormalities. A constant finding was the wide right ventricular outflow tract. The outlet septum had its normal continuity with the septomarginal trabecula, but its parietal extension was located relatively far anteriorly. Part of the aortic valve thus inserted to the right ventricular component of the ventriculo-infundibular fold in the gap between the outlet septum and the tricuspid valve. Left ventricular abnormalities comprised mitral valve anomalies in all cases. There was an anteroseptal twist (leftward thickening of the anterior part of the ventricular septum) in 16 cases. A bicuspid aortic valve and/or malformed cusps were observed in 4 cases. Because of the linking phenomenon of aortic override, we also examined 10 hearts with tetralogy of Fallot and, in the latter, such abnormalities were not found. Our observations indicate that this seemingly simple type of defect is part of a complex malformation involving both septation and valve formation. Awareness of the existence of the architectural abnormalities might make them accessible for echocardiographic diagnosis. It was noteworthy that 11 of the 18 patients had chromosomal abnormalities, 9 of them presenting with trisomy-18.

Assessment of right ventricular outflow tract in children by two-dimensional echocardiography using a new subcostal view Angiocardiographic and morphologic correlative study

Evaluation of the right ventricular (RV) outflow tract in congenital heart disease is extremely important for surgical management. Therefore, the value of 2-dimensional echocardiography (2-D echo) to assess the RV outflow tract was studied using a new approach: the subcostal elongated right oblique view. Twenty normal children and 49 children with congenital heart disease, aged 1 day to 11 years, were studied. Significant pulmonary infundibular obstruction was present in 22 patients with conotruncal malformations. To obtain the subcostal elongated right oblique view from the short-axis view at the aortic valve level, the transducer was slightly rotated clockwise with an anterior angulation of about 30° so that the ascending aorta was seen in its long axis, providing an image similar to that obtained by a right ventriculogram in the elongated right anterior oblique view. The deviation of infundibular septum was appreciated by measurement of the angle α, defined by the long axis of the infundibular septum and the plane of aortic cusps. This view could be obtained in 64 patients (92%). In correlation with angiographic or anatomic data, the subcostal elongated right oblique view permitted recognition of several types of RV outflow tract: type I—normally formed RV outflow tract; type II—disorganized RV outflow tract with obstruction (α <90°); type III and IV—disorganized RV outflow tract with obstruction (α >90°). This view could visualize the crista supraventricularis in type I, but also the anatomic components of RV outflow tract that may contribute to obstruction in the other types: infundibular septum, septoparietal trabeculations and trabecula septomarginalis. The subcostal elongated right oblique view was superior to standard 2-D echo views in imaging the RV outflow tract anatomy and defining the severity and type of infundibular obstruction. Thus, 2-D echo using the subcostal elongated right oblique view provides a safe, noninvasive technique for the serial evaluation of RV outflow tract in children both before and after surgical correction.

DPI 201-106, a novel cardioactive agent. Combination of cAMP-independent positive inotropic, negative chronotropic, action potential prolonging and coronary dilatory properties.

The in vitro cardiac effects of DPI 201-106, a novel piperazinyl-indole, were investigated. DPI 201-106 produced concentration-dependent positive inotropic effects in guinea-pig and rat left atria, kitten, rabbit and guinea-pig papillary muscles and Langendorff perfused hearts of rabbits between 10(-7) and 3 X 10(-6) mol/l. During isometric twitches, contraction and relaxation phases were prolonged in guinea-pig left atria and right ventricular papillary muscles from kitten and guinea-pigs. Spontaneous sinus rate was decreased in right atria of guinea-pigs and rats. Coronary flow increased in rabbit isolated hearts. Functional refractory period was increased in left atria from guinea-pigs and rats with EC50 values of 1.7 and 0.24 mumol/l respectively. In electrophysiological measurements, DPI 201-106 prolonged the action potential duration (APD70) in guinea-pig papillary muscles up to 70% and in rabbit atria up to 120% at 3 mumol/l. Other action potential characteristics were not changed in guinea-pig papillary muscles but Vmax was decreased in rabbit left atria. The electrophysiological as well as the positive inotropic effects were stereoselective with the activity residing in the S-enantiomer. DPI 201-106 increased the Ca2+-sensitivity of skinned fibres from porcine trabecula septomarginalis with an EC50 of 0.2 nmol/l. DPI 201-106 dit not change cAMP levels in guinea-pig atria and rabbit papillary muscles. Slow action potentials were not induced by DPI 201-106 in partially depolarized guinea-pig papillary muscles. Phosphodiesterase activity of rat hearts was not inhibited by DPI 201-106 at pharmacologically relevant concentrations. The presence of propranolol did not influence the inotropic potency of DPI 201-106 in guinea-pig atria. In conclusion, DPI 201-106 represents a novel type of positive inotropic agents with a synergistic sarcolemmal and intracellular mechanism of action.

Modification of the precise relationship of the atrioventricular conduction bundle to the margins of the ventricular septal defects by the trabecula septomarginalis

There is a widely recognized relationship between the atrioventricular conduction bundle and the margins of the ventricular septal defects according to whether the defect is perimembranous or muscular. We have shown that this relationship may in turn be markedly influenced by the precise topography of the trabecula septomarginalis. Fifteen hearts, each with a ventricular septal defect, were studied by serial sectioning. Four hearts had an isolated ventricular septal defect in the setting of normal chamber connections and relations. One heart had a truncus arteriosus, seven hearts had Fallot's tetralogy, and three hearts exhibited complete transposition. In those hearts with outlet defects in which a bar of muscle separated the rim of the defect from the position of the conduction bundle, deficiency of the posterior limb of the trabecula septomarginalis permitted the right-sided margin of the conduction axis to "surface" in directly subendocardial position. Moreover, in some of these outlet defects, the conduction axis in the region of the branching bundle was exposed directly upon the crest of the muscular septum. The position of the medial papillary muscle complex was the best landmark to this potential danger area. In some of the examples of Fallot's tetralogy, we observed a firm muscle bar overlying the posteroinferior margin of the defect, which nonetheless was perimembranous. This protected the nonbranching component of the conduction axis in the anticipated danger area. Paradoxically, a deficiency in the trabecula septomarginatis then permitted the branching bundle to sit directly astride the septum along the inferior rim of the defect. We noted particularly marked variability of the atrioventricular conduction axis among the hearts with tetralogy. Our results suggest that close inspection during the operation may reveal whether or not a well-developed trabecula septomarginalis is present and permit conclusions to be drawn concerning the precise position of the atrioventricular conduction axis.

Anatomic obstruction of the right ventricular outflow tract in transposition of the great arteries

In 126 hearts with transposition of the great arteries (TGA), morphologic features of the right ventricular (RV) outflow tract were analyzed. Distinct anatomic outflow tract obstruction was found in 15 of the 55 hearts with a ventricular septal defect (VSD) (27%): 12 had a perimembranous defect (predominantly extending into the infundibulum), 2 had an inlet, and 1 had an infundibular defect. In 12 hearts, outflow tract obstruction was caused by anterior displacement of infundibular septum and ventriculoinfundibular fold; in 3 hearts, it was caused by bulging of the trabecula septomarginalis or ventriculoinfundibular fold, or both. Of 71 hearts with an intact ventricular septum, only 2 (3%) had RV outflow tract obstruction: 1 had a trabecula in front of the aortic ostium and in the other an aberrant hypertrophic muscle bundle crossed the RV cavity, obstructing the entrance to the infundibulum. Associated malformations included aortic arch malformations (6 cases) and tricuspid valve anomalies (6 cases). Thus, anatomic RV outflow tract obstruction may constitute a complicating factor in TGA, notably in cases with VSD. A systemic RV blood pressure may trigger hypertrophy, resulting in progression of the obstruction; establishing normal RV pressure by a “switch” procedure might prevent this progression.

Surgical anatomy of tetralogy of Fallot

On the basis of previous experience, we have analyzed the anatomy of a series of 53 hearts catalogued as having tetralogy of Fallot in the museum of the Children's Hospital of Pittsburgh. All hearts had a ventricular septal defect, aortic overriding, infundibular pulmonary obstruction, and right ventricular hypertrophy. None of the hearts had been operated upon during life. We paid particular attention to features of surgical importance. Thus the ventricular septal defect was found to be of variable form. It was perimembranous in 42 hearts. In 11 hearts it had entirely muscular rims and in the remaining heart it was roofed by the conjoined aortic and pulmonary valve rings (subarterial). From our previous histologic experience, it was evident that this varying morphology significantly affected the surgical anatomy of the atrioventricular conduction tissues. We endeavored to display this disposition as might be viewed by the surgeon. The degree of aortic override was variable, the aortic valve being connected by 15% to 95% to the right ventricle. In 17 hearts more than half the aortic valve was attached to right ventricular musculature. The nature of the infundibular obstruction also varied markedly. In all cases (except the one with absent infundibular septum) the infundibular septum was deviated in cephalad and anterior direction so as to produce obstruction. In the majority of hearts further anatomic structures also contributed to the obstruction. In some hearts there was hypertrophy of the infundibular septum, particularly at its junction with the trabecular septum. In others there was hypertrophy of the trabecula septomarginalis, and in many hearts there was hypertrophy of additional anterior infundibular trabeculations. The pulmonary valve was the narrowest point of the outflow tract in only six hearts, but in many of the others, it was abnormal. The results emphasize that while hearts may exhibit the classical features of tetralogy of Fallot, there is usually considerable individual variation in each of these features which is of major surgical significance.

Embryology of the ventricular septum. Separate origin of its components.

The formation of the ventricular septum was studied in human embryos ranging from 3.6 to 25 mm CR-length. Before septation, two distinct chambers are present which will contribute to the adult ventricles. They are called the bulbus and the ventricle. The circular constriction between these chambers is the bulboventricular fold. The anterior portion of the ventricular septum develops from this bulboventricular fold. Posteriorly, it fuses with a second septum, which is of purely ventricular origin. This is the inlet septum. Another portion of the bulboventricular fold persists as the trabecula septomarginalis. The trabecula septomarginalis divides the normal right ventricle into an inlet portion, stemming from the embryonic ventricle, and an outlet portion which derives from the bulbus.

Histopathological Study on the Conduction System of Complete Right Bundle Branch Block

Eleven autopsy cases (average of 71 years) with complete right bundle branch block were examined histologically with serial sectioning of the conduction system. The results were as follows: 1) moderate to severe reduction of conducting cells in the right bundle branch (RBB) by fibrous replacement in all 11 cases, 2) a preponderance of main lesions in the first portion of the RBB in cases with R configuration in leads V1 and V2, and in the second to the third portion without significant lesion of the Purkinje cell network in the right ventricle in cases with rsR', and RSR' configuration in these leads, 3) as to the etiology, 1 case was assumed to have had rheumatic myocarditis and an another case, 1 chronic ischemia. In cases in which the cause could not be clearly established, reduction of the conducting cells in the first portion of the RBB was thought to be due to fibrosis of the upper ventricular septum. Lesions in the second portion of the RBB may be due to mechanical strain effected by muscle crossing of the trabecula septomarginalis and RBB.

The conducting tissues in primitive ventricle with outlet chamber: Two different possibilities

The conducting tissues have been studied in two cases of primitive ventricle with outlet chamber. In one case the outlet chamber was to the right and in the other, to the left. In both cases there was an anterior node related to the anterior part of the right atrioventricular anulus. In the specimen with a left-sided outlet chamber (l-loop), the bundle passed through the atrioventricular-semilunar fibrous continuity and was intimately related to the posterior artery. Such a relation was absent in the specimen with a right-sided outlet chamber (d-loop), wherein the bundle directly descended on the posterior part of the septum between the main and outlet chambers. The septum is not considered to be the true ventricular septum but rather a hypertrophied trabecula septomarginalis.

What should we call the 'crista'?

Review of published work concerning congenital cardiac anomalies reveals that at least four different structures have been described as the crista supraventricular, in addition to the structure which in the normally formed right ventricle separates pulmonary and tricuspid valves. Possibility of further confusion arises since at least two different structures have been described under the name 'septal band'. We suggest that this potentially confusing situation will be best resolved by reserving the term 'crista' for description of the muscle mass between inflow and outflow portions of the right ventricle when there are no additional outflow tract anomalies. We then suggest that at least three separate structures warrant description in hearts with outflow tract anomalies. The first separates the semilunar valves, the second separates a semilunar valve from an atrioventricular valve, and the third is an extensive septal trabeculation of the right ventricle. Our suggested terms for these structures are the infundibular septum, ventriculo-infundibular fold, and trabecula septomarginalis, respectively. However, we believe that such terms would be better decided and agreed upon within an internationally formulated 'Nomina Cardiologica', a terminology as yet lacking in congenital heart disease.

Right ventricular obstruction resulting from anomalous muscle bundles

Summary Significant right ventricular outflow obstruction may result from large anomalous muscle bundles traversing the right ventricular cavity. These bundles are located below the infundibulum and are distinct from the trabecula septomarginalis and the moderator band. This type of obstruction may occur independently and is anatomically distinguishable from the more common types of infundibular stenosis. Eleven patients with intact septa and anomalous muscle bundle obstruction to right ventricular outflow are presented. In 5 patients, these bundles represented the only cardiac abnormality and were the sole cause of obstruction to blood flow; while in the remaining 6 patients there was an associated pulmonary valvular stenosis. Cardiac catheterization and angiocardiography provided the correct diagnosis in all cases. Eight patients have undergone operation and all have since been asymptomatic. The authors acknowledge with appreciation Dr. James H. Moller’s courtesy in providing us the opportunity to review Case 11.