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Results for “Ventricular septal defect”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

Acute bacterial endocarditis following traumatic ventricular septal defect.

Traumatic ventricular septal defect occur rarely although penetrating wounds of the heart rate are fairly common. The urgency for the surgical correction of traumatic ventricular septal defects has been debated. In life-saving instances where left heart failure or cardiac tamponade occur, the decision is simple. A case report of early bacterial endocarditis complicating traumatic ventricular septal defect in the first 12 hours following injury has been presented. Avoidance of this complication by early surgical correction is advocated.

Acute Disease↗
PubMed1976

Xylose absorption before and after surgical correction of atrial septal defect (asd) and ventricular septal defect (vsd).

The aim of the study was to ascertain whether the acceleration of physical development in children after surgery for ASD or VSD is due to improved intestinal absorption. There were 17 patients with ASD and 9 patients with VSD (aged 5-15 years) examined. Significantly increased values of the xylose test after surgery were found in both groups. The authors suggest that the improvement in intestinal absorption is due to an increase of systemic blood flow after operation. Simultaneously, the stldy confirms, on natural human model, the known dependence between blood flow and the intestinal absorption rate.

Adolescent↗
PubMed1975

Factors influencing survival following postinfarction ventricular septal defects.

Postinfarction ventricular septal defect (VSD) carries a grave prognosis. Surgical closure appears to improve survival. Eighteen patients with postinfarction VSD are reviewed. Nine died before operation could be performed and 9 underwent closure of the VSD; 4 patients are late survivors. Factors which appear to influence survival are: (1) time of surgical intervention after appearance of VSD, (2) presence or absence of cardiogenic shock, (3) location of the infarct, and (4) operative approach to the VSD. Based on these factors, a method of management for postinfarction VSD is outlined.

Aged↗
PubMed1977

Pulmonary arterial pressure-flow characteristics in atrial septal defect: comparative study with ventricular septal defect and patent ductus arteriosus.

Pulmonary arterial pressure-flow relation was studied in 142 patients with artrial septal defect (ASD) and was compared with that of 139 patients with ventricular septal defect (VSD) and was compared with that of ductus arteriosus (PDA). The incidence of pulmonary arterial mean pressure (PAm) over 25 mmHg was 21 percent in ASD, 36 percent in VSD and 43 percent in PDA, and that over 40 mmHg was 3 percent, 23 percent and 19 percent, respectively. Large left to right shunt over 50 percent was found more frequently in ASD (58 percent) than in VSD (22 percent) and PDA (30 percent). When patients were separated into 2 groups at a PAm of 40 mmHg, lower pressure group showed a positive correlation between PAm and left-to-right shunt in each disease, although the correlation was poor in ASD (r equals 0.23) as compared with VSD (r equals 0.49) and PDA (r equals 0.47). The slope of the regression line was less steep in ASD (0.08) than in VSD (0.17) and PDA (0.14). It is considered that pulmonary hypertension in ASD develops on the basis of pulmonary vascular changes caused by prolonged hyperkinetic circulation.

Adolescent↗
PubMed1977

Left ventricular approach to multiple ventricular septal defects.

Multiple muscular ventricular septal defects were closed through an apical left ventriculotomy in 11 patients. The patients were divided into two groups: Group 1, 8 patients who had transposition of the great arteries, and group 2, 3 patients without transposition. There were 4 deaths in Group 1 and non in Group 2. Two of the deaths were caused by a hypoplastic right ventricle, 1 by airway obstruction, and 1 by heart failure and pulmonary edema in a patient who had additional unrecognized muscular defects. An apical left ventriculotomy provides excellent exposure of the septum. The field is not obscured by trabecular bands or papillary muscles. Although 1 patient died because of residual VSDs, this approach, compared with previously described methods, minimizes the risk of unrecognized defects.

Animals↗
PubMed1978

Ventricular septal defect associated with left ventricular outlfow tract obstruction below the defect.

Muscular subaortic stenosis associated with ventricular septal defect (VSD) is a rare but important anomaly. Two types of left ventricular outflow tract (LVOT) obstruction should be distinguished on the basis of morphologic as well as hemodynamic differences, depending on whether the stenosis is localized above (Type I) or below (Type II) the defect. The five cases presented are all in the latter category. In the first two cases the correct diagnosis was not made until after repair of the VSD. Two patients had previously undergone banding of the pulmonary artery (PAB). Marked carotid shudder and a vertical QRS axis in the frontal plane were presented in all cases. For the diagnosis to be established by catheterization, the catheter tip must be maneuvered into the apical part of the left ventricular cavity in order to detect the stenosis on the withdrawal curve. It is difficult to visualize the stenosis by angiography. The surgical approach through the VSD via a right atriotomy is highly recommended for Type II subaortic stenosis.

Angiocardiography↗
PubMed1975

Postinfarction ventricular septal defect with posterior ventricular aneurysm. Result of a single distal right coronary artery obstruction.

A patient with postinfarction ventricular septal defect, posterior aneurysm, severe congestive heart failure, and significant atherosclerosis in the distal right coronary artery only is reported. Closure of the defect resulted in quich recovery of the patient. We demonstrated that a single significant lesion in one coronary artery can cause rupture of the interventricular septum.

Coronary Angiography↗
PubMed1977

Aortic regurgitation associated with ventricular septal defect. Echocardiographic and hemodynamic observations.

Ventricular septal defect is sometimes associated with aortic regurgitation. In this report, an echocardiogram demonstrating dramatic prolapse of the noncoronary cusp into the left ventricular outflow tract and ventricular septal defect in a patient with Down's syndrome and ventricular septal defect, confirmed by angiographic studies, is presented. The echocardiogram supports the concept of anatomic lack of support of the aortic ring due to a deficient septum and hemodynamically significant flow of blood to the right ventricle through the ventricular septal defect, resulting in trauma to aortic cusps and prolapse.

Adult↗
PubMed1977

Traumatic ventricular septal defect and delayed post-pericardiotomy ventricular herniation.

A knife wound of the heart produced a ventricular septal defect. Surgical repair of a myocardial laceration and pericardiotomy for relief of cardiac tamponade were performed. Progressive exercise intolerance developed over an 8-year period. In addition, the patient experienced intermittent partial cardiac herniation resulting in angina-like chest pain. The patient is now asymptomatic after correction of the pericardial defect and closure of the ventricular septal defect.

Adult↗
PubMed1978

Right atrial ultrastructure in congenital heart disease. I. Comparison of ventricular septal defect and endocardial cushion defect.

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.

Basement Membrane↗