Type Of Ventricular Septal Defect Research Articles

Tetralogy of Fallot Associated with Aortic Insufficiency

Five patients with tetralogy of Fallot associated with aortic insufficiency were studied. They ranged from 6 to 34 years old (mean, 14 years), and 2 patients had a history of subacute bacterial endocarditis. Four patients had a bulboventricular type of ventricular septal defect. Prolapse of the right coronary cusp was the main cause of aortic insufficiency. Deformed valve secondary to subacute bacterial endocarditis and severe dilatation of the aortic annulus were the other causes. In addition to repair of the tetralogy defect, aortic valvuloplasty was performed in 2 patients. In the remaining 3 patients, the ventricular septal defect was closed with a relatively small-sized patch and no aortotomy was made. Four patients survived the operation, and no residual aortic insufficiency was observed in 3 of them. The etiology and the method of operation are discussed.

Straddling and displaced atrioventricular orifices and valves.

This is an anatomic study of 96 hearts with straddling or displaced atrioventricular (AV) valves and orifices. In the complete form, both the annulus and the peripheral connections of either AV valve straddle a ventricular septal defect (VSD) and connect to both ventricles. In the annular form, only the annulus, and in the peripheral type only the peripheral connections of the valve are found in both ventricles. In displaced AV valve, the entire annulus and periphery of one AV valve are displaced into the opposite chamber. These anomalies are commonly seen in complete transposition with or without ventricular inversion, and in double outlet right or left ventricle. Straddling mitral valve is frequently seen in the Taussig-Bing heart. Any type of VSD may be associated with straddling tricuspid valve; however, they usually are of the AV canal type. Straddling and displaced AV valves should be differentiated from criss-cross hearts in which both AV valves are completely connected to oppositely placed ventricles.

Conal anatomy in aortic atresia, ventricular septal defect, and normally developed left ventricle

Although aortic valve atresia is usually associated with severe underdevelopment of the mitral apparatus and left ventricle in rare cases of aortic atresia, the left ventricle may be of normal size, or even enlarged. This occurrence seems related to the presence of a significant ventricular septal defect. We have presented the morphologic findings in seven patients with aortic atresia and normally developed left ventricle, (six necropsied patients, and one studied angiocardiographically). Four autopsied patients had conal type ventricular septal defects, characterized in three by conoventricular malalignment. Subaortic atresia in these patients resulted from leftward deviation of the conal septum. One patient with aortic atresia and well-developed left ventricle had a membranous defect, and one patient had a complete A-V canal. The ventricular septal defect in the patients with conoventricular malalignment are very similar to the conal VSD observed in patients with aortic arch interruptions. Although ultimate survival with these uncommon groupings of anomalies necessitates patency of the ductus arteriosus, clinical recognition rests on (1) awareness of its existence, (2) ultrasonography, and (3) selective biventricular and aortic angiography. It is possible that some of these patients might be candidates for ventriculo-aortic reconstitiution.

Natural history of ventricular septal defect. A study involving 790 cases.

The development of 790 untreated patients affected by ventricular septal defect (VSD) has been the object of a 25-year study. Of these patients, 72% had had at least one catheterization; 13% had several. The mean observation interval is six years, and the average age at the latest data is 19.5 years. This study covers 4717 patient-years. For the entire population, the incidence rate or aortic regurgitation is 6.3% (4.3 for 1000 patient-years) and that of bacterial endocarditis is 3.7% (2.4 for 1000 patient-years). Twenty-five patients died, 15 of them between the ages of one and 39. Of the 499 cases with several clinical examinations, 71% remained stable. In 21%, changes suggesting some level of closure developed; in 7%, infundibular stenosis began to evolve and in 1% pulmonary vascular disease began to appear or became accentuated. These different rates are studied and discussed in relation to patients' age, VSD type, and various follow-up characteristics.

Functional closure of physiologically advantageous ventricular septal defects. Observations in three cases with tricuspid atresia.

Two cases of tricuspid atresia in which spontaneous functional closure of a ventricular septal defect (VSD) was documented are presented. We present a third case to show that the obstruction to pulmonary flow in tricuspid atresia is at the level of the VSD. These VSDs are situated in the muscular portion of the ventricular septum, so that the contraction of the septal muscle could close the VSD. The mechanism of onset of functional closure of this type of VSD is unclear; the mechanism may be similar to that in tetralogy of Fallot. Effective palliation by aortopulmonary and cavopulmonary shunts at intervals of time depending upon the clinical status is suggested. Increasing symptomatology and decreasing intensity of a previously heard murmur in complex congenital heart disease should lead one to suspect functional or anatomic closure of physiologically advantageous VSDs.

Two types of ventricular septal defect in corrected transposition of the great arteries: Reference to surgical approaches

Six autopsied cases of corrected transposition of the great arteries with VSD were examined from the surgical exposure. Two anatomic types concerning the relative height of the two semilunar valves and the position of the VSD were recognized. In four cases (Type I), the two semilunar valves are at the same height viewed from the anteroposterior direction, the parietal band is hypoplastic, and the VSD is located immediately below the aortic and pulmonary valves. In the other two cases (Type II), the aortic valvular level is higher than the pulmonary valvular level and the parietal band in these cases is well-developed. The VSD located beneath the pulmonary valve is clearly separated from the aortic valve by a well-developed parietal band. The first type has an excellent exposure viewed from the left-sided ventricle, while the second has an extremely poor exposure. Therefore, right-sided ventriculotomy is recommended in the latter type. Furthermore, these two anatomic types can be recognized and differentiated in angiocardiographic findings by the relative height of the two semilunar valves and the presence of a filling defect formed by the crista supraventricularis.

Isolated Ventricular Septal Defect: Development Basis for Various Types and Presentation of Classification

A morphologic study was made of 101 specimens of heart containing 112 ventricular septal defects (VSD). Morphogenesis of defects was related to development of the ventricular septum. A classification of VSD based on morphogenesis resulted. VSD's may develop in one of the following components of the ventricular septum: (1) the crista supraventricularis, termed infundibular VSD; (2) pars atrioventriculare of septum membranaceum, termed atrioventricular septal defect or left ventricular-right atrial communication; (3) pars interventriculare of septum membranaceum, termed VSD of septum membranaceum; (4) smooth posterior septum, termed smooth VSD and (5) trabeculated posterior septum, termed trabeculated VSD. Among the 33 examples of infundibular VSD, there were five subtypes. In Type I, the defect lies at the inferior margin of the crista supraventricularis. Type II is a mid-cristal defect. A Type III defect lies in front of the crista. Type IV represents complete absence of the crista; and Type V defects lies at the junction between the crista and the posterior septum. Among the 17 examples of primary VSD's of pars interventriculare of septum membranaceum, there were three subtypes. In Type I the margins of the defect are barren of chordal insertions. In Type II, chordae of the septal leaflet of the tricuspid valve are inserted into the margins of the defect. In Type III, the defect is closed by dense chordae which insert into its margins. There were five subtypes among the 56 examples of smooth VSD's. Type I is a defect of the smooth septum along its junction with the anterior septum and also involves septum membranaceum. Type II denotes complete absence of the smooth septum. Type III is a defect at the junction between the smooth and trabeculated septa. Type IV is a perforationlike defect in the posterior smooth septum proper. Type V is a defect in the smooth septum along its junction with the anterior septum without involvement of the membranous septum. In four specimens, the trabeculated type of VSD was present. Two examples of a defect in pars atrioventriculare of the membranous septum were present.

Venography

A ventricular septal defect (VSD) is one of the most common congenital cardiac lesions. Echocardiography is the primary mode for evaluation of ventricular septal defects. Echocardiographic evaluations of ventricular septal defects are easily reproducible, can be done in a timely fashion, and do not require a complex set up. They give detailed information needed for the diagnosis, treatment and long term follow up. Although diagnosis can now be made prenatally, a more detailed evaluation with confirmation of the diagnosis is not made until after birth with transthoracic echocardiography. With a combination of 2D, color Doppler and spectral Doppler, the VSD location, size, and hemodynamic components can be established. Additionally, sequelae from the VSD and other associated congenital cardiac lesions can also be identified. A review of the standard components of a thorough transthoracic echocardiogram to evaluate the different types of ventricular septal defects will be discussed in this article.

Anatomic types of ventricular septal defect with aortic insufficiency: Diagnostic and surgical considerations

A series of 11 postmortem cases of ventricular septal defect (VSD) with aortic insufficiency (AI) was presented, and an anatomic classification of VSD with AI was proposed. There are two principal anatomic types: VSD beneath the crista supraventricularis (Type I), and VSD beneath the pulmonary valve (Type II). With a subcristal VSD (Type I), there are two subtypes: without pulmonary infundibular stenosis (Type Ia), and with pulmonary infundibular stenosis (Type Ib). Subcristal VSD with AI (Type I) occurred in seven cases. In six of these, the development of AI appeared basically to be related to the underdevelopment of one aortic commissure, usually the right coronary-noncoronary (4:6 cases). A functionally bicuspid aortic valve resulted in five cases. No pulmonary infundibular stenosis (Type Ia) was found in three cases, while four displayed mild to moderate pulmonary infundibular stenosis (Type Ib). The clinical and laboratory picture without pulmonary stenosis was that of AI with a maladie de Roger type of VSD, while the picture with stenosis was that of AI with acyanotic (atypical) tetralogy of Fallot. Subpulmonary VSD with AI (Type II) occurred in four cases. The subpulmonary VSD is a conal septal defect, the conal septal portion of the crista supraventricularis being absent or defective. All four cases had normal aortic commissures. AI resulted from herniation of the right coronary aortic leaflet through the large subpulmonary VSD into the right ventricular outflow tract, resulting in a mild to moderate pulmonary outflow tract gradient in all. Subcristal VSD with AI, with or without pulmonary stenosis, usually was an aortic commissural deficiency problem (in 6:7 cases). Subpulmonary VSD with AI always was a hernia of a basically normal aortic valve into the right ventricular outflow tract (in 4:4 cases). Since the surgical management of the two principal types of VSD with AI is different, their differential diagnosis is of practical clinical importance.

Muscular ventricular septal defects ∗

Ninety-two cases of muscular ventricular septal defect were reviewed. These defects were defined as completely surrounded by muscular septum and consequently did not involve the membranous septum or any valvular ring. They were classified, according to their location in the right side of the muscular ventricular septum, as posterobasal, midseptal, apical, or outflow. Of the 92 cases, 23 were isolated single defects, 14 were isolated multiple defects, and 55 were associated with other major cardiac anomalies. In these 55 cases, the defect was single in 36 cases and multiple in 19. Regardless of the presence or absence of associated cardiac anomalies, when the defect was single, it was posterobasal in about half of the cases. No specific location of multiple defects was apparent. Muscular defects in the outflow tract of the right ventricle were rare. The evidence suggests that muscular ventricular septal defects may cause hemodynamic and clinical syndromes similar to those caused by the usual type of ventricular septal defect. The electrocardiographic features in the 37 cases of isolated defects were analyzed. A possible increased incidence of prominent Q waves in leads reflecting left ventricular potential occurred but, as a generalization, the electrocardiograms were similar to those observed in cases of the usual type of defect.

Supracristal ventricular septal defect

The case of a child with an isolated ventricular septal defect located superior to the crista supraventricularis and immediately below the pulmonary valve is reported. Comment is made on the difficulties attending clinical and laboratory diagnosis of such a lesion. A systolic murmur and thrill located maximally in the pulmonary area in this particular anatomic type of ventricular septal defect emphasizes the direct relation between the site of the murmur and the site of the defect. Surgical considerations concerning this particular variety of septal defect are briefly discussed. It is noted that the supracristal type of ventricular septal defect occurs not only in isolated form but as a component of several other congenital cardiac complexes.

Pulmonary Vascular Resistance Following Thoracotomy

Introduction STUDY of pulmonary vascular resistance following thoracotomy in the human has largely been confined to the late postoperative period. 1 We have measured pulmonary vascular resistance (PVR) preoperatively and in the early postoperative period. A marked elevation at this time is the reason for this presentation. Our interest in the changes in PVR immediately following thoracotomy was stimulated in the early days of open-heart surgery at our institution, when, in error, we operated on a patient with primary pulmonary hypertension. The death of this patient 48 hours later from unrelenting pulmonary hypertension (as gathered by indirect means) in a clinical state of low cardiac output implied an elevation of the PVR. A similar mode of death in the first few postoperative days was experienced in certain patients with high resistance type of ventricular septal defect. Could this be due to an increase in PVR following thoracotomy? If this same

LEFT VENTRICULAR ANGIOCARDIOGRAPHY BY TRANSSEPTAL PUNCTURE OF THE LEFT ATRIUM.

Experiences with 90 left heart angiocardiograms in 170 patients with transseptal left heart catheterizations are discussed. Selective left heart angiocardiograms of patients with aortopulmonary septal defect, patent ductus arteriosus, coarctation of the aorta, different types of ventricular septal defect, and isolated congenital mitral regurgitation are discussed. Examples of valvular, supravalvular, organic subvalvular, and functional hypertrophic subaortic stenosis are shown. The method is also suitable for the demonstration of endocardial fibroelastosis, truncus arteriosus, and hypoplasia of the aorta.

Isolated ventricular septal defect of the persistent common atrioventricular canal type.

Among 60 necropsy specimens of isolated ventricular septal defects and more than 300 cases of ventricular septal defect observed at operation, 15 cases demonstrating unusual anatomic positions of the defect were found. The ventricular defect differed from the ordinary ventricular septal defect in that it usually occupied the position of the ventricular component of the defect in persistent common atrioventricular canal. For this reason it was named ventricular septal defect of the persistent common atrioventricular canal type. Deformities of one or both atrioventricular valves were common (nine of 15 cases). No atrial septal defects of the ostium primum type were present. Anatomic studies of the conduction tissue revealed that this tissue skirted the posterior and inferior aspects of the ventricular septal defect and that, as in persistent common atrioventricular canal, the course taken by the conduction tissue was unusually long, as a result of the peculiar posteroinferior position of the lower edge of the defect. The electrocardiographic features were striking. In all cases the mean electrical axis of the QRS lay above the isoelectric point; the vector loop obtained in the frontal plane from the scalar electrocardiogram was directed counterclockwise, and its main mass was above the zero line. In addition, in all cases there were signs of right ventricular overload, and in some cases of left ventricular overload as well. Electrocardiographic findings of this pattern have been thought by some authors to be diagnostic of persistent common atrioventricular canal, but we observed that they also occurred in each of the cases of isolated ventricular septal defect of the variety described herein. We recognize that in the usual variety of ventricular septal defect this electrocardiographic pattern occurs, but it does so uncommonly. We have not studied its exact incidence. The anatomy, hemodynamics, and surgical considerations are different in cases with this defect from those with persistent common atrioventricular canal. The surgical risk in these cases has been higher than that in the usual type of ventricular septal defect. In the discussion of the electrophysiologic theories that seek to explain the unusual electrocardiographic patterns in this group of cases, a new theory is offered, based on studies of the conduction system. In our opinion, the different orientation of the advancing fronts of depolarization is the result of congenital displacement of the bundle of His in its relation to the ventricular septal defect.

The relation of the aortic root to the ventricular septum in tetralogy of fallot

Three cases of clinically classic tetralogy of Fallot are presented in which angiocardiographic studies demonstrated no overriding of the aorta. These studies indicate that many cases of tetralogy of Fallot should be considered as a type of ventricular septal defect with pulmonic stenosis, in which overriding of the aorta is of no functional or surgical importance.