INCREASING PULMONARY VASCULAR RESISTANCE DURING INFANCY IN ASSOCIATION WITH VENTRICULAR SEPTAL DEFECT

PEDIATRICS ◽  
1966 ◽  
Vol 38 (2) ◽  
pp. 220-230 ◽  
Author(s):  
Julien I. E. Hoffman ◽  
Abraham M. Rudolph
Keyword(s):  
Ventricular Septal Defect ◽  
Vascular Disease ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Septal Defect ◽  
The Other ◽  
Pulmonary Vascular Disease ◽  
Ventricular Septal Defects ◽  
Septal Defects ◽  
Pulmonary Arterial

Three children with big ventricular septal defects, large pulmonary blood flows, and pulmonary hypertension were catheterized at the ages of 3, 6, and 6 months. Pulmonary vascular resistance was low in two and slightly raised in the other. Recatheterization at the ages of 9, 16, and 26 months, respectively, showed increases of pulmonary vascular resistance in all, and the ventricular septal defects were successfully closed by open-heart operation soon thereafter. In the one child who was recatheterized only after there was clinical evidence of a raised pulmonary vascular resistance, postoperative catheterization showed a progressive rise in pulmonary vascular resistance indicating progressive pulmonary vascular disease. The other two children who were clinically well were recatheterized specifically to try and detect early pulmonary vascular changes and, in contrast, in both of these children pulmonary arterial pressures and vascular resistances have returned to normal after operation. These patients demonstrate that in those at risk of developing pulmonary vascular disease (big ventricular septal defect with high pressures and flows), pulmonary vascular resistance can rise rapidly in early life. In these patients progressive pulmonary vascular disease could be prevented if surgery to lower pulmonary arterial pressure and blood flow is done early enough. Even in patients who appear to be improving, recatheterization is necessary to demonstrate a moderate rise in pulmonary vascular resistance, since a moderate rise is not detectable by current clinical techniques.

Operable ventricular septal defect despite severe pulmonary hypertension and cyanosis!

2019 ◽  
Vol 29 (7) ◽  
pp. 986-988
Author(s):  
Shyam S. Kothari ◽  
Jay Relan ◽  
Velayoudam Devagourou
Keyword(s):  
Pulmonary Hypertension ◽  
Ventricular Septal Defect ◽  
Vascular Disease ◽  
Mitral Stenosis ◽  
Septal Defect ◽  
The Other ◽  
Pulmonary Vascular Disease ◽  
Early Age ◽  
Eisenmenger Syndrome ◽  
Severe Pulmonary Hypertension

AbstractPatients with a significant left-to-right shunt at ventricular level may become inoperable at an early age due to irreversible pulmonary vascular disease. On the other hand, even suprasystemic pulmonary hypertension due to mitral stenosis remains treatable. We report a 24-year-old patient with large ventricular septal defect, severe mitral stenosis and cyanosis who improved after surgical correction of both the lesions. This emphasises the importance of additional post-capillary pulmonary hypertension in Eisenmenger syndrome.

The Eisenmenger malformation: a morphologic study

2015 ◽  
Vol 26 (2) ◽  
pp. 269-279 ◽  
Author(s):  
Angelo Restivo ◽  
Cira R. T. di Gioia ◽  
Robert H. Anderson ◽  
Raffaella Carletti ◽  
Pietro Gallo
Keyword(s):  
Aortic Valve ◽  
Ventricular Septal Defect ◽  
Septal Defect ◽  
The Other ◽  
Ventricular Septal Defects ◽  
Free Standing ◽  
Morphologic Study ◽  
Marked Individual ◽  
Septal Defects ◽  
The Right

AbstractWe studied 11 autopsied cases of the Eisenmenger malformation, comparing the findings with 11 hearts with intact ventricular septal structures, and nine hearts having perimembranous ventricular septal defects in the absence of aortic overriding. We found variable lengths for the subpulmonary infundibulum in the hearts with Eisenmenger defects. It was well developed in three hearts, of intermediate length in seven, and very short in one of the specimens. The muscular outlet septum was also of variable length compared with the free-standing subpulmonary infundibular sleeve. Except for one, all hearts had fibrous continuity between the aortic and tricuspid valvar leaflets, such that the ventricular septal defect was then perimembranous. In the remaining case, there was a completely subaortic muscular infundibulum, with the ventricular septal defect showing only muscular borders. The medial papillary muscle was absent in the majority of cases, but was well formed in three hearts, all with relatively short muscular outlet septums. We identified mild, intermediate, and severe degrees of rightward rotation of the aortic valve, and these findings correlated with the extent of aortic valvar overriding. In nine of the 11 hearts, the ventriculo-arterial connections were concordant, but there was double-outlet from the right ventricle in the other two specimens. Based on our anatomic and morphometric observations, we conclude that the hearts we have defined as having Eisenmenger defects show marked individual variation in their specific phenotypic anatomy.

Use of pulmonary arterial unifocalization into cryopreserved homograft pulmonary arterial bifurcation grafts to facilitate complete correction of pulmonary atresia with ventricular septal defect, nonconfluent (absent) central pulmonary arteries and multiple major aortopulmonary collateral arteries

1995 ◽  
Vol 5 (3) ◽  
pp. 217-224 ◽  
Author(s):  
Richard A. Hopkins ◽  
Deborah A. Imperato ◽  
John T. Cockerham ◽  
Stephen R. Shapiro
Keyword(s):  
Ventricular Septal Defect ◽  
Vascular Disease ◽  
Septal Defect ◽  
Pulmonary Arteries ◽  
Pulmonary Atresia ◽  
Pulmonary Vascular Disease ◽  
Major Aortopulmonary Collateral Arteries ◽  
Collateral Arteries ◽  
Pulmonary Arterial ◽  
Aortopulmonary Collateral

AbstractThree children with pulmonary atresia and ventricular septal defect with absent central pulmonary arteries underwent successful complete correction following preliminary staging procedures for unifocalization and deletion of multiple major aortopulmonary collateral arteries. The unifocalization procedures were accomplished using valveless pulmonary arterial cryopreserved allografts. This technique was found to facilitate and simplify the final repair. All patients survived the complete correction. The patients have been followed for 1½-4 years following the final surgery. One child died two years after repair from pneumonia complicated by asthma. One patient appears to have progression of pulmonary vascular disease despite the complete repair, and one patient continues to do well both symptomatically and hemodynamically. The results suggest that this method of unifocalization solves many of the problems inherent to more classical techniques, but the overall prognosis of patients in this diagnostic entity has yet to be completely defined.

Increased Prevalence of Ventricular Septal Defect: Epidemic or Improved Diagnosis

PEDIATRICS ◽  
1989 ◽  
Vol 83 (2) ◽  
pp. 200-203
Author(s):  
Gerard R. Martin ◽  
Lowell W. Perry ◽  
Charlotte Ferencz
Keyword(s):  
Ventricular Septal Defect ◽  
Septal Defect ◽  
Ductus Arteriosus ◽  
Coarctation Of The Aorta ◽  
Cardiovascular Malformations ◽  
Ventricular Septal Defects ◽  
Live Births ◽  
Septal Defects ◽  
Clinical Diagnoses ◽  
Control Study

The Baltimore-Washington Infant Study is an ongoing case-control study of congenital cardiovascular malformations in infants in whom the clinical diagnoses have been confirmed by echocardiography, catheterization, surgery, or autopsy. An increase in the prevalence of ventricular septal defects was detected in 1,494 infants with congenital cardiovascular malformations between 1981 and 1984. The prevalence of congenital cardiovascular malformations increased from 3.6 to 4.5 per 1,000 live births (P<.025) and the prevalence of ventricular septal defect increased from 1.0 to 1.6 per 1,000 live births (P< .001). The increase in ventricular septal defects accounted for the total increase in congenital cardiovascular malformations. The prevalence of isolated ventricular septal defect increased from 0.67 to 1.17 per 1,000 live births (P<.001). The prevalence of ventricular septal defect with associated coarctation of the aorta, patent ductus arteriosus, atrial septal defect, and pulmonic stenosis did not change. The prevalence of ventricular septal defect diagnosed by catheterization, surgery, and autopsy did not change; however, defects diagnosed by echocardiography increased from 0.30 to 0.70 per 1,000 live births (P<.001). It is concluded that the reported increase in prevalence of ventricular septal defect is due to improved detection of small, isolated ventricular septal defects and that there is no evidence of an "epidemic."

scholarly journals Percutaneous-perventricular device closure of ventricular septal defect: mid-term follow-up.

2020 ◽  
Author(s):  
Long Wang ◽  
Lin Xie ◽  
Weiqiang Ruan ◽  
Tao Li ◽  
Changping Gan ◽  
...  
Keyword(s):  
Ventricular Septal Defect ◽  
Septal Defect ◽  
Close Monitoring ◽  
The Novel ◽  
Ventricular Septal Defects ◽  
Device Closure ◽  
Residual Shunt ◽  
Septal Defects ◽  
Perventricular Device Closure

Abstract Background: This report presents updated data and mid-term follow-up information to a former study introducing the novel technique of percutaneous-perventricular device closure of doubly committed subarterial ventricular septal defect. Methods: Thirty-eight patients were added to the former series. There were 54 patients in total who had isolated doubly committed subarterial ventricular septal defects and underwent percutaneous-perventricular device closure. Closure outcomes and possible complications were measured in the hospital and during the 2.5-year follow-up. Results: Surgery was successful in 53 patients (98.1%). There was no death, residual shunt, new valve regurgitation or arrhythmia either perioperatively or during the entire follow-up period. Only one patient developed pericardial effusion and tamponade in the former series. The mean hospital stay was 3.2±0.6 days (range, 3.0 to 6.0 days), and only one unsuccessful case needed blood transfusion (1.9%). Conclusions: The percutaneous-perventricular device closure of isolated doubly committed subarterial ventricular septal defects appeared to be safe. Close monitoring for bleeding is essential postoperatively, especially in younger patients. This technique is generally safe with acceptable mid-term follow-up.

Assessment and follow-up of patients with ventricular septal defect and elevated pulmonary vascular resistance

1989 ◽  
Vol 63 (5) ◽  
pp. 327-331 ◽  
Author(s):  
John M. Neutze ◽  
Tatsuo Ishikawa ◽  
Patricia M. Clarkson ◽  
A.Louise Calder ◽  
Brian G. Barratt-Boyes ◽  
...  
Keyword(s):  
Ventricular Septal Defect ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Septal Defect

Clinical course in children and adolescents with ventricular septal defect

2019 ◽  
Vol 27 (7) ◽  
pp. 529-534
Author(s):  
Noor Mohammad Noori ◽  
Alireza Teimouri
Keyword(s):  
Pulmonary Hypertension ◽  
Ventricular Septal Defect ◽  
Septal Defect ◽  
Clinical Course ◽  
Defect Size ◽  
Eisenmenger Syndrome ◽  
Ventricular Septal Defects ◽  
Laboratory Findings ◽  
Septal Defects

Background Ventricular septal defect, the most common congenital heart defect, is characterized by an opening between the ventricles. This study aimed to evaluate the clinical course and associations between the characteristics of ventricular septal defect. Methods This cross-sectional study was conducted on 1498 children with ventricular septal defects, aged <19 years, who were referred to our center between 2003 and 2018. The diagnosis was suspected from a combination of clinical and laboratory findings, and confirmed by transthoracic echocardiography. Results Of the 1498 children, 54.9% were boys, 78.4% of defects were perimembranous, 30.4% of patients had pulmonary hypertension, 67.5% had regular follow-up, and 76 (5.1%) had complications including 28 (1.9%) with Eisenmenger syndrome; 10 died due to Eisenmenger syndrome during follow-up. The defects closed spontaneously in 38.9% and after surgery in 20.9%. Boys tended to have more perimembranous, inlet, and outlet forms (56.40%, 50.60%, 51.90%, respectively), whereas girls had more muscular types (51.80%). Most patients with pulmonary hypertension had perimembranous defects (83.10%). The majority of patients with pulmonary hypertension had large (63.40%) or moderate (36.60%) defects. Pulmonary hypertension had a significant association with defect size ( p < 0.001). After surgery, residual defects were found mostly in cases of large defects (84.60%). Most patients with spontaneous closure were younger than 4 years. Conclusion Almost four-fifths of children with ventricular septal defects had perimembranous types, and almost one-third had pulmonary hypertension which was associated with defect size. Two-fifths of the defects closed spontaneously. There was a low incidence of complications after surgery.

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