[Surgery of ventricular septal defects, and heart defects associated with ventricular septal defects].
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Traumatic heart block remains a major concern after ventricular septal defect (VSD) closure in patients with atrioventricular discordance. A technique of closing the VSD, placing the suture line on the morphologically right side of the septum without opening the systemic ventricle, is described. This was used in 13 consecutive patients. The VSD was closed through the right atrium in eight patients, the left ventricle in three patients, the right atrium and the left ventricle in one patient, and through the right ventricle in one patient with atrioventricular disordance and ventriculo-arterial concordance. All patients were in sinus rhythm preoperatively, two exhibited atrioventricular dissociation before intracardiac manipulation began, and 11 patients were in sinus rhythm postoperatively. No major arrhythmia could be attributed to the closure of the VSD.
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Left ventricular and left atrial volume, left ventricular ejection fraction, and left ventricular muscle mass were determined preoperatively and postoperatively in 13 patients who underwent surgical closure of ventricular septal defects in the first two years of life. Left ventricular end-diastolic volume and systolic output averaged 255 +/- 19% (+/- SEM) and 240 +/- 19% of normal, respectively, before operation but fell to within normal limits postoperatively. Left ventricular ejection fraction was normal preoperatively (100 +/- 4% of normal) and remained so after correction (106 +/- 3%, NS). Left ventricular mass was mildly elevated at the preoperative catheterization (271 +/- 21%) and decreased significantly following repair (P less than 0.001). However, the postoperative left atrial volume (147 +/- 14%) remained abnormal (P greater than 0.05). These data suggest that when early surgical closure of a ventricular septal defect is necessary because of failure of medical management, good results with regard to postoperative left ventricular size and function can be expected.
Controversies remain concerning the nomenclature, nature and pathogenesis of the various forms of univentricular heart. Common ventricle may well represent a very large ventricular septal defect while the nature of the indeterminate or nonspecific form of univentricular heart remains in doubt. Univentricular heart, right ventricular type, could be ascribed to overshift of the embryonic atrioventricular canal to the right, resulting in both atrioventricular ostia entering a large ventricular chamber which has the morphological characteristics of a right ventricle. In univentricular heart, left ventricular type on the other hand, the rightward shift of the atrioventricular canal appears to have failed or remained incomplete, possibly due to an abnormal position of the atrioventricular canal relative to the bulboventricular septum. Normal septation of the atrioventricular canal results in both atrioventricular ostia giving access to a large ventricle which in the main has the morphological features of a left ventricle.
Complications of myocardial infarction in the form of aneurysm of the heart, mitral incompetence and ventricular septal defect cause considerable changes in intracardiac hemodynamics which lead to severe disturbances in the circulation system in different periods after myocardial infarction. The timely and properly made diagnosis allows the prognostic severity of the complication to be appraised and the optimum therapeutic tactics determined. The given classifications of this pathological conditions promote a differential approach in considering the indications and contraindications in each case. Analysis of 312 operations shows that correction of the abnormality under conditions of extra-corporeal circulation in combination with direct myocardial revascularization is the most adequate intervention.
The authors report their experience with two-stage surgical treatment of severe ventricular septal defects in babies: initial banding of the pulmonary artery, followed by closure of the ventricular septal defect and removal of the band by an open-heart technique. Out of 162 operations to band the pulmonary artery, 90 were for cases of ventricular septal defect. The mortality was low (9.1%) when there was a ventricular septal defect with or without a patent ductus. It is considerably higher (31.4%) when there is a coincident coarctation of the aortic isthmus. So far 38 children have had the second operation, with 2 deaths. The authors have studied the surgical problems and the long-term results (6 months to 3 years follow-up) in the first 29 patients undergoing surgery. Although the results from this two-stage operation are good, when the authors take into account their current experience with one-stage closure of ventricular septal defects in the babies, they feel that this latter technique is to be preferred. Reservations must, however, be expressed when the child is very young (Weighing 3.5 kg or less), when there are multiple defects between the ventricles, and when the defect is severe, with a combination of VSD, patent ductus and coarctation of the aorta, and sometimes when the opertion must be carried out as an emergency.
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Patients with double outlet right ventricle can be separated into four distinct groups. In the largest (Group III), patients have a subaortic ventricular septal defect and pulmonary stenosis and clinically resemble patients with tetralogy of Fallot. In the next largest group (Group I), patients have a subpulmonry ventricular septal defect and no pulmonary stenosis and clinically resemble children with D-transposition of the great arteries and a ventricular septal defect. These patients have a high rate of coarctation of the aorta leading to early congestive heart failure, and their overall prognosis is poor. In the next largest group (Group II), patients have a subaortic ventricular septal defect and no pulmonary stenosis. Their presentation is similar to that of children with a large ventricular septal defect and pulmonary hypertension. In the smallest group (Group IV), the ventricular septal defect is uncommitted. Survivors in this group also clinically resemble children with a large ventricular septal defect and pulmonary hypertension. When present, coarctation of the aorta and severe mitral valve abnormalities greatly influence the prognosis in double outlet right ventricle. Although the prevalence of associated cardiac abnormalities is large, asplenia, polysplenia, chromosomal abnormalities and other congenital noncardiac abnormalities occur in only 12.5% of patients with double outlet right ventricle.
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Ultrastructural studies were performed on portions of the operatively resected right atrium from six patients with a ventricular septal defect and six patients with an endocardial cushion defect. The six patients with a ventricular septal defect had normal right atrial mean pressure and no evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients appeared normal and measured 6 to 12 mu in diameter. The six patients with an endocardial cushion defect had elevated right atrial mean pressure and evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients were generally larger than 12 mu in diameter. The cells were irregular and had multiple and occasionally widened intercalated discs. In addition, there were degenerative changes in two patients with markedly increased atrial pressure. These changes included extensive loss of contractile elements, aggregation of small irregular mitochondria and proliferation of tubules of the sarcoplasmic reticulum. The structural changes suggest that hypertrophy of the right atrium may be secondary to volume overload of the atrium, whereas degenerative changes may be secondary to increased right atrial pressure.
It is often difficult to make the clinical distinction between acute mitral regurgitation caused by papillary muscle dysfunction or rupture and ventricular septal defect complicating an acute myocardial infarction. A case of a patient with rapidly progressive congestive heart failure and a loud murmur is presented. Echocardiography strongly suggested the presence of a flail posterior mitral leaflet. However, the patient was subsequently found to have rupture of the interventricular septum. This diagnosis was made with bedside right heart catheterization and was later confirmed by left ventriculography and direct inspection at the time of surgery. The mitral valve apparatus was completely normal. Thus this case demonstrates the apparent lack of specificity of the accepted echocardiographic criteria for flail mitral leaflet and acutely ruptured interventricular septum, and the potential necessity of cardiac catheterization to distinguish between these entities.
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Extensive surgery for all of the mechanical complications of ischemic heart disease is feasible with early diagnosis, catheterization, and aggressive medical and surgical therapy. A patient is report who, after recovering from cardiogenic shock, required a coronary bypass, closure of ventricular septal defects, mitral valve replacement, aneurysmectomy, and temporary pacemaker wires. The outcome was successful.
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Report on two girls with an obstruction within the right ventricle beneath the infundibulum. A muscular band - probabaly the abnormally situated moderator band - emerges at right angles from the ventricular septum, crosses the lumen and ends at the anterior wall of the right ventricle, thus separating a high-pressure inflow chamber from a low-pressure out-flow chamber. The latter compartment is distinctly larger than the infundibular chamber in Fallot's tetralogy. In bt connecting the left ventricle with the hig-pressure compartment. In one patient an increase of severity of the obstruction could be documented; this child showed a subvalvular membranous aortic stenosis. The diagnosis has to be established by meticulous pressure recording between pulmonary and tricuspid valve and by dye injection into the right ventricle. Ventricular septum defect (in 80%), subvalvular aortic stenosis (in about 10%), pulmonary valvular and peripheric stenosis and open Ductus Botalli are the most important accompanying lesions. The malformation - not diagnosed prior to surgery - causes serious trouble during operation. The investigator thus has to be aware of this condition in every pulmonary valvular ahd subvalvular stenosis especially when accompanied by a ventricular septum defect.