Muscular Septum Research Articles

Observation of root variations in human coronary arteries

In dissection courses conducted from 1999 through to 2003, five specimens were found to have coronary arteries with variant roots and branches, as follows: in specimens 1-4, roots of the right coronary artery (RCA) and right conus branch arose independently from the right aortic sinus (RAS); in specimen 5, the RCA and left coronary artery (LCA) originated from the RAS. The LCA pierced the upper part of the muscular interventricular septum and appeared on the surface, then dividing into the anterior interventricular and the circumflex branches. In the present study, we considered that the right conus arteries in specimens 1-4 were the remnant blood capillaries around the aorta towards the RAS in the embryonic stage. In specimen 5, the vessel near the left aortic sinus was poorly developed as a small thin artery. Instead, the LCA was developed from the anterior and posterior interventricular septal branches.

The Effect of Vascular Endothelial Growth Factor on in vitro Embryonic Heart Development in Rats

In vitro effects of vascular endothelial growth factor (VEGF) on heart development and total embryonic growth were investigated in 84 rat embryos (obtained from nine pregnant females) at 9.5 days of gestation that were cultured in whole rat serum (WRS), in <30 kDa + >50 kDa serum fractions [retenate (R)], and in R + VEGF. After 24-h culture, the embryos from each group were harvested and divided into two groups. One group was analysed morphologically and biochemically to obtain embryo protein content, the second group was serially sectioned and examined by light microscopy. Morphological score, embryo protein content, somite number and crown-rump length of embryos indicated that embryos cultured in R had significant embryonic retardation, whereas the addition of VEGF to R increased embryonic growth and development. The morphological scores for WRS, R and R + VEGF were 57.7 +/- 0.87, 46.6 +/- 1.90 and 52.1 +/- 0.97, somite numbers were 26.5 +/- 0.47, 20.1 +/- 0.63 and 24.4 +/- 0.46, crown-rump lengths were 3 +/- 0.07, 2.4 +/- 0.06 and 2.7 +/- 0.06 mm, and embryo protein contents were 160.5 +/- 7.41, 98.2 +/- 4.81 and 141.1 +/- 10.96 mug per embryo, respectively. The results of histological examination of heart development were similar. The hearts of embryos grown in R were unseptated and tubular. The atrioventricular endocardial cushions were incompletely developed. The addition of VEGF to R improved heart development. There were no gross morphological differences in the cardiac development between embryos grown in WRS and R + VEGF. In both groups, development of the muscular interventricular septum had begun. Development of the atrioventricular cushions was also similar in both groups and had caused narrowing of the atrioventricular canals, but the atrial septation was not observed.

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.

Transcatheter closure of congenital muscular ventricular septal defect.

The success with occlusion devices for the closure of atrial septal defects and patent ductus arteriosus prompted the transcatheter closure of single and multiple muscular ventricular septal defects (VSD). The procedure for VSD was first attempted by Lock et al. in 1988 and devices originally designed for the closure of other intracardiac defects (Rashkind umbrella device, Lock clamshell, Cardioseal, coils, Sideris buttoned device etc.) were used with a variable success rate and a residual shunt. Recently, specially designed Amplatzer muscular VSD occluder and Sideris device are in use. The Amplatzer muscular VSD occluder has been undergoing clinical trial since 1998 after the animal experiments had shown 100% occlusion and complete endothelization at 3 months. The procedure was first attempted in August 1995 using the Rashkind umbrella device and since April 1998 only the Amplatzer muscular VSD occluder has been used. Of the149 patients who underwent transcatheter closure of VSD, 50 had muscular trabecular defects in various locations: mid-muscular, anterior, posterior, or apical. All cases were selected by detailed transthoracic and/or transesophageal echocardiography (TTE) and aneurysm of the muscular septum was observed in three of them. The age range was 3-28 years and the diameter of VSD was 4-11 mm. In all but one patient, the device was deployed from the venous side. Simultaneous TTE was done for proper positioning of the device and continuous electrocardiographic monitoring was also done for any arrhythmia/conduction defects. All patients were followed up every 3 months and received 3-5 mg/kg aspirin for 6 months. The procedure was successful in all patients. The Rashkind umbrella device (17 mm) was used in two and Amplatzer muscular VSD occluder (6-14 mm) in 48 patients. Forty-four devices were delivered by antegrade transvenous approach and six by the transjugular route. None had residual shunt, new aortic regurgitation, or tricuspid regurgitation. Transient complete heart block after 24 hours was noticed in one patient. On a follow-up of 2-90 months, the device was in position in all patients. There was no embolization of the device, and no late-conduction defects, infective endocarditis, or hemolysis. Transcatheter closure of muscular VSD is safe and efficacious, and should be considered as a procedure of choice as an alternative to surgery that avoids cardiopulmonary bypass.

Spontaneous closure of ventricular septal defects followed up from

This study evaluates the incidence and timing of spontaneous closure (SC) of ventricular septal defect (VSD) using Doppler color flow mapping. A total of 225 infants (mean age 30 days) were diagnosed with uncomplicated VSD: 31 (14%) subpulmonary VSD, 159 (70%) perimembranous, and 35 (16%) muscular. The patients were divided into two groups according to the presence or absence of congestive heart failure (CHF). SC was confirmed with color Doppler. Surgical closure was performed in 59 patients (26%). SC occurred in 107 patients (48%); three (10%) of 31 with subpulmonary VSD, 75 (47%) of 159 with perimembranous VSD, and 29 (83%) of 35 with a muscular VSD. Average age at SC was 19 months. In three SC patients with a subpulmonary VSD, there was no aortic valve prolapse and no aortic regurgitation. SC occurred in 96% of SC patients with a perimembranous VSD by the age of 6 years, and in 93% of those with a muscular VSD by the age of 3 years. In patients without CHF, the rate of SC was 72%; 23% in subpulmonary VSD, 74% in perimembranous, and 85% in muscular. SC occurred in only 23% of patients with a perimembranous VSD with CHF. Mean age at the final examination was 6.9 years in 59 patients with a VSD remaining open, and 63% of patients with a perimembranous VSD remaining open had an aneurysm of the ventricular membranous septum. The SC rate of VSD by mean age of 6.9 years was 48%, but it was 72% in patients without CHF. In patients with CHF, SC was seen only in patients with a perimembranous VSD. The rate of SC was 10% in subpulmonary VSD. The authors contend that SC probably occurred by growth of muscular septum surrounding VSD. Muscular VSD spontaneously closed earlier than perimembranous VSD.

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.

DSCR1 gene expression is dependent on NFATc1 during cardiac valve formation and colocalizes with anomalous organ development in trisomy 16 mice

The Down syndrome critical region 1 ( DSCR1) gene is present in the region of human chromosome 21 and the syntenic region of mouse chromosome 16, trisomy of which is associated with congenital heart defects observed in Down syndrome. DSCR1 encodes a regulatory protein in the calcineurin/NFAT signal transduction pathway. During valvuloseptal development in the heart, DSCR1 is expressed in the endocardium of the developing atrioventricular and semilunar valves, the muscular interventricular septum, and the ventricular myocardium. Human DSCR1 contains an NFAT-rich calcineurin-responsive element adjacent to exon 4. Transgenic mice generated with a homologous regulatory region of the mouse DSCR1 gene linked to lacZ ( DSCR1(e4)/lacZ) show gene activation in the endocardium of the developing valves and aorticopulmonary septum of the heart, recapitulating a specific subdomain of endogenous DSCR1 cardiac expression. DSCR1(e4)/lacZ expression in the developing valve endocardium colocalizes with NFATc1 and, endocardial DSCR1(e4)/lacZ, is notably reduced or absent in NFATc1 − /− embryos. Furthermore, expression of the endogenous DSCR1(e4) isoform is decreased in the outflow tract of NFATc1 −/− hearts, and the DSCR1(e4) intragenic element is trans-activated by NFATc1 in cell culture. In trisomy 16 (Ts16) mice, expression of endogenous DSCR1 and DSCR1(e4)/lacZ colocalizes with anomalous valvuloseptal development, and transgenic Ts16 hearts have increased β-galactosidase activity. DSCR1 and DSCR1(e4)/lacZ also are expressed in other organ systems affected by trisomy 16 in mice or trisomy 21 in humans including the brain, eye, ear, face, and limbs. Together, these results show that DSCR1(e4) expression in the developing valve endocardium is dependent on NFATc1 and support a role for DSCR1 in normal cardiac valvuloseptal formation as well as the abnormal development of several organ systems affected in individuals with Down syndrome.

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.

Direct Nail Injury to the Heart Without Functional or Hemodynamic Compromise

A 14-year-old girl was admitted to the emergency room (ER) because of blast injury. On arrival, her blood pressure was 100/70 mm Hg, with a heart rate of 140 bpm. She had superficial facial burns and multiple lacerations on different parts of her body. There was an entry wound in the right posterior axillary line at the level of the eighth intercostal space. On auscultation, she had normal heart sounds and slightly diminished breath sounds in the right lung. A chest radiograph showed a right hydropneumothorax and a nail …

Septation and separation within the outflow tract of the developing heart.

The developmental anatomy of the ventricular outlets and intrapericardial arterial trunks is a source of considerable confusion. First, major problems exist because of the multiple names and definitions used to describe this region of the heart as it develops. Second, there is no agreement on the boundaries of the described components, nor on the number of ridges or cushions to be found dividing the outflow tract, and the pattern of their fusion. Evidence is also lacking concerning the role of the fused cushions relative to that of the so-called aortopulmonary septum in separating the intrapericardial components of the great arterial trunks. In this review, we discuss the existing problems, as we see them, in the context of developmental and postnatal morphology. We concentrate, in particular, on the changes in the nature of the wall of the outflow tract, which is initially myocardial throughout its length. Key features that, thus far, do not seem to have received appropriate attention are the origin, and mode of separation, of the intrapericardial portions of the arterial trunks, and the formation of the walls of the aortic and pulmonary valvar sinuses. Also as yet undetermined is the formation of the free-standing muscular subpulmonary infundibulum, the mechanism of its separation from the aortic valvar sinuses, and its differentiation, if any, from the muscular ventricular outlet septum.

Deficiency of the vestibular spine in atrioventricular septal defects in human fetuses with down syndrome

Data on the morphogenesis of atrioventricular septal defect (AVSD) in Down syndrome are lacking to support molecular studies on Down syndrome heart critical region. Therefore, we studied the development of complete AVSD in human embryos and fetuses with trisomy 21 using 3-dimensional graphic reconstructions and immunohistochemical markers. Eight trisomic hearts with AVSD and 10 normal hearts, ranging from 5 to 16 weeks’ gestation, were examined. In AVSD, the muscular septum primum and venous valves develop normally, and the size and histology of the nonfused endocardial cushions also appear normal. However, the mass of extracardiac mesenchyme (vestibular spine), located at the dorsal mesocardium, is reduced and does not protrude ventrally along the right wall of the common pulmonary vein. As a result of this, the muscular septum primum and the right pulmonary ridge are seen as 2 separate septa that attach to the inferior endocardial cushion. Both the muscular septum primum and the superiorly fused venous valves (septum spurium) converge and are capped by a small rim of mesenchyme, which forms the roof of the persisting ostium primum and connects to cushions and the reduced vestibular spine. At 7 weeks, ventricular septation in AVSD is comparable to 5 to 6 weeks of normal cardiac development. At later stages, the septum spurium forms the anterosuperior limbus of the septum secundum and the mesenchymal cap becomes the bridging tendon that connects the bridging leaflets. Therefore, reduced expansion of the vestibular spine derived from the dorsal mesocardium appears to play an important role in the development of AVSD in Down syndrome.

Cardiac septation: a late contribution of the embryonic primary myocardium to heart morphogenesis.

Heart morphogenesis comprises 2 major consecutive steps, viz. chamber formation followed by septation. Septation is the remodeling of the heart from a single-channel peristaltic pump to a dual-channel, synchronously contracting device with 1-way valves. In the human heart, septation occurs between 4 and 7 weeks of development. Cardiac looping and chamber formation bring the contributing structures into position to engage in septation. Cardiomyocytes that participate in chamber formation do not materially contribute to septation. The (re)discovery of the role of extracardiac mesenchymal tissue in atrioventricular septation, the appreciation that the formation of the right atrioventricular connection is more than a mere rightward expansion of the atrioventricular canal, the awareness that myocardium originating from the so-called anterior heart field regresses after its function as outflow-tract sphincter ceases, and the recent finding that the myocardialized proximal portion of the outflow-tract septum becomes the supraventricular crest have all significantly enhanced our understanding of the morphogenetic processes that contribute to septation. The bifurcation of the ventricular conduction system is the landmark that separates the contribution of the atrioventricular cushions and the outflow-tract ridges to septation and that divides the muscular ventricular septum in inlet, trabecular, and outlet portions.

The morphology of the specialized atrioventricular junctional area: the evolution of understanding.

Although knowledge of its existence has barely exceeded one century, the anatomic pathway for conduction of the cardiac impulse from atria to ventricles has been the source of much controversy, controversy that continues to the present day. This article describes how attention to the original descriptions, along with adherence for sensible definitions for the histological distinction of conduction tissues, could have defused many of these disagreements. One of the problems with the initial descriptions was that they were written in German. Even this is no longer a problem, since the major text devoted to the topic has recently been translated into English, and is now available for all to study. This key work was the monograph produced by Sunao Tawara, a Japanese pathologist who studied in the first decade of the 20th century in the laboratory of Ludwig Aschoff. Tawara showed that the atrial impulse was conducted to the ventricular myocardium by a solitary pathway of specialized myocardium. He likened this pathway to a tree, with its roots in the base of the atrial septum, and its branches straddling the crest of the muscular ventricular septum. Significantly, he showed that the pathway became insulated as it crossed from atrial to ventricular musculatures, and suggested that the point at which the muscle became engulfed in fibrous tissue should be taken as the boundary between the "knoten," or atrioventricular node, and the penetrating bundle described earlier by Wilhelm His. The authors' findings are entirely compatible with the account given by Tawara. Like Tawara, they recognize atrial transitional cells, a compact node, the penetrating bundle, and the ventricular conduction pathways as the segments of the conduction axis which can be considered to represent the specialized atrioventricular junction.

Tetralogy of Fallot: Total Correction

he events that give rise to the c1evelol)iiieiit of the T constellation of lesions that we refer to as tetralogj of Fallot are still micertain. Regardless of the true teleological cause, it is hel1)ful for the surgeon to approach this defect as resulting from anterocephalad deviation of the ventricular outlet septum. "monology with sequellae." The resulting malalignment ventricular septal defect (VSD), aortic override, ancl right ventricular outflow tract ol~struction are thus easily understood. The right ventricular hypertrophy can he appreciated as secondary to the VSD and right ventricular outflow tract ohstructioii. Right ventricular outflow obstruction is increased by hypertrophy of the anterior limb of the septal ]land, anomalous anterior muscular bands, and outlet septum as well as pulmonary valve and arterial anomalies (Fig I). Classically the VSD is circular, juxtaaortic, and nonrestrictive and results from the malalignment of the parietal extension of the infundibular and trabecular septae. As such, the defect lies between the infundibular septum and is cradled by the anterior and posterior limbs of the septal band (Fig 11).

Surgical repair of supposedly multiple defects within the apical part of the muscular ventricular septum

Background. A distinct defect has been described within the apical part of the muscular ventricular septum, which has multiple orifices when seen from its right ventricular aspect. Closure has been suggested using umbrella devices introduced on a catheter. Such an intervention, however, can be technically difficult in small infants. Methods. We have recently seen two examples of this type of complex communication between the apexes of both left and right ventricles. Neither could be closed by catheterization. A surgical approach was used through a modified apical right ventriculotomy. We have also studied two autopsied specimens, which clarify the morphologic arrangement. Results. Both patients were closed successfully, with trivial residual shunt and good biventricular functions. The patients were clinically well at 2-year follow-up. Conclusions. Surgical division of right ventricular trabeculations makes it feasible to identify and repair the septal deficiency, which is a solitary hole. On the basis of our morphologic study, we offer an explanation for the anatomic arrangement that differs from the one proposed by recent previous investigators. If the ventricular incision is appropriately placed, our anatomic studies suggest that it is possible to visualize the solitary opening from its right ventricular aspect, and achieve surgical closure with a single patch.

Fetal myocardial hypertrophy in an experimental model of gestational diabetes

The frequent occurrence of prenatal hypertrophy of the muscular ventricular septum has been widely reported in fetuses of diabetic mothers. This experimental study was carried out to test the hypothesis that the weight of the heart, the ratio of the cardiac weight to that of the body, the thickness of the muscular ventricular septum, and the myocytic profile within the ventricular septum are all increased in fetuses of diabetic rats in comparison to fetuses of normal rats. Diabetes was induced in 5 pregnant Wistar rats, bearing 30 fetuses, on the eighth day after conception, by intraperitoneal injection of 50 mg/kg of streptozotocin. Five normal pregnant Wistar rats, bearing 20 fetuses, made up the control group. Morphometric data were obtained by a computer-assisted method applied to the measurements of the thickness of the ventricular septum, and myocytic nuclear area. Statistical analysis utilized Student's t-test and Kruskal-Wallis test. The mean thickness of the septum was 675.56 microm (+/-159) in the control fetuses, and 904.39 microm (+/-262) in the fetuses carried by diabetic mothers (p < 0.001). The cardiac weight was 0.016 g (+/-0.004) in the control group, and 0.023 g (+/-0.005) in the group of diabetic fetuses (p < 0.001). The ratio of cardiac to body weight was 0.294% (+/-0.079) in the control group, and 0.514% (+/-0.073) in the diabetic group (p < 0.001). The myocytic nuclear area was 14.70 microm2 in the control group, and 21.43 microm2 in the diabetic group (p < 0.001). The presence of cellular and morphologic cardiac hypertrophy in fetuses of diabetic rats was demonstrated by the significant difference between the two groups for each analyzed feature.

Transcatheter closure of subaortic ventricular septal defect (VSD) using a nickel–titanium spiral coil (NitOcclud): animal study and initial clinical results

Transcatheter closure of VSD has been successful in defects of the muscular septum distant from the aortic and mitral valve apparatus. Attempts to close subaortic VSDs have been largely unsuccessful because of device-related aortic insufficiency. The NitOcclud device is a Nitinol spiral coil device which has been evaluated in animals with subaortic VSD. Results of the animal study are promising, and the device has also been implanted in a few humans. This paper describes the device, the implant technique in subaortic VSD, and the results of animal and human implants.

Cross-sectional echocardiographic assessment of atrioventricular septal defect: basic morphology and preoperative risk factors.

Accurate evaluation of an atrioventricular septal defect is readily achieved by echocardiography. A sound understanding of the basic morphology and associated lesions is key to this approach. This article first details the features that are common to all hearts with an atrioventricular septal defect, irrespective of the presence or absence of an interatrial or interventricular communication. These common features are: (1) inlet outlet disproportion; (2) absence of the atrioventricular muscular septum; (3) abnormal position of the left ventricular papillary muscles; (4) abnormal configuration of the atrioventricular valves and, (5) cleft in the left atrioventricular valve. These are all predicated by a sprung atrioventricular junction. Second, is a detailed outline of the associated risk factors that must be identified by the echocardiographer prior to presenting the patient for surgical management, with the most important ones being abnormalities of the left atrioventricular valve and left ventricular outflow tract obstruction. Indeed, in this current era it is rarely necessary to perform other investigations prior to surgical repair.

The anatomy of the septal perforating arteries in normal and congenitally malformed hearts

Background: Many cardiac operations involve incisions and sutures on or near the ventricular septum. These jeopardize the septal perforating arteries. Our aim was to provide guidelines for the surgeon to predict the site of these vessels. Methods and Results: We dissected 50 hearts. In 16 of these we also conducted histologic examination of the area of the septum containing the atrioventricular node, the penetrating bundle (of His), and the branching atrioventricular bundle to elucidate the source of the vascular supply to these structures. The major perforating septal arteries arise from the superior interventricular artery or, in hearts with a rudimentary right ventricle, from the superior delimiting artery. The first is usually the largest. The location of this artery can be predicted relative to the position of the medial papillary muscle. In abnormal hearts, holes within the ventricular septum in the presence of a well-developed muscular outlet septum were found to deviate the path of the septal perforating arteries in a predictable manner. The triangular area bordered by the margin of the ventricular septal defect, the muscular outlet septum, and the medial papillary muscle is free of major perforating arteries. The histologic studies showed that the conduction tissues at the base of the ventricles tend to receive their blood supply from arteries arising from the inferior interventricular artery, except in double-inlet left ventricle, in which the arterial supply is from the right-sided delimiting artery. Conclusion: The location of the first superior septal perforating artery is predictable in many cases. Its course leaves a triangular area on the muscular ventricular septum that is free of major arteries. (J Thorac Cardiovasc Surg 2001;121:1046-52)

Cardiac hydatid cysts with intracavitary expansion

Background. Hydatid cyst disease is a significant health problem for undeveloped and developing countries. Although cardiac involvement is rare, early diagnosis and treatment of this situation is important.Methods. To investigate the long-term outcome of patients who underwent operation for cardiac hydatid cysts with intracavitary expansion, we reviewed 8 patients who had cardiac hydatidosis and who underwent operation in our institution between January 1988 and November 1999. All patients presented with intracavitary protrusion of the cysts. Seven patients were women. The mean age was 33 ± 14.3 years with a range of 17 to 55 years. The cysts were located on the right ventricular outflow tract (2 patients), right midventricular part of the muscular septum, left atrial free wall and apical portions of the right (2), or left (2 patients) ventricle. Standard cardiopulmonary bypass and crystalloid antegrade cardioplegia with aortic cross-clamping were used in all patients. In one, with right ventricular hydatid cyst, we used cardiopulmonary bypass with femoral cannulation and total circulatory arrest at less than 18°C systemic hypothermia. This patient, who was arrested because of pulmonary emboli could not be weaned from cardiopulmonary bypass and died.Results. The cystic cavity was cleaned and closed with multiple pursestring sutures in 4 patients. In 2, cardiac and cystic cavities were united by partially resecting part of the cyst facing the cavity. In another patient, a left ventricular patch plasty was performed after removal of the cystic material in the left ventricle. Mebendazole was used postoperatively in all patients. Except for 1 patient who died, all were discharged without postoperative complications. The mean follow-up was 7.5 ± 5 years. There was no late cardiac mortality or recurrence.Conclusions. Cardiac hydatid cysts with intracavitary expansion should be treated surgically without delay. Gentle handling of the heart during cardiopulmonary bypass minimizes operative risk. All patients should be investigated for systemic cysts.