The long-term results of closure of ventricular septal defect with pulmonary vascular disease

Background In children, the practice of transcatheter closure of intracristal ventricular septal defect (icVSD) has been limited. Currently, there is a lack of comparison between device closure of perimembranous ventricular septal defect (pmVSD) and icVSD, and long‐term clinical outcomes are rare. Methods and Results This study included a total of 633 children (39 with icVSD and 594 with pmVSD), aged 18 months to 16 years, who underwent transcatheter closure of ventricular septal defect between January 2014 and December 2018. All patients were followed up until September 2020, with a median follow‐up of 46 months in the pmVSD group and 52 months in the icVSD group. The procedural success rate was 96.3% and 84.6% in pmVSD and icVSD groups, respectively ( P =0.002). The median of age, weight, procedure time, fluoroscopic time, and radiation dose were greater in the icVSD group compared with the pmVSD group. More eccentric ventricular septal defect occluders were used in the icVSD group. Most adverse events were minor without any intervention, with cardiac rhythm/conduction abnormalities being the most common. In the pmVSD group, 2 patients experienced complete atrioventricular block, with one implanting a permanent pacemaker and the other dying of cardiac arrest secondary to reversible complete atrioventricular block 40 days postprocedure. Complete left bundle‐branch block occurred in 14 patients, and 12 cases were transient. In the icVSD group, no complete atrioventricular block or death occurred, and one patient developed transient complete left bundle‐branch block. Conclusions In selected patients, transcatheter device closure of pmVSD and icVSD can be performed safely and successfully, with excellent medium‐ and long‐term results in children.

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Operable ventricular septal defect despite severe pulmonary hypertension and cyanosis!

Cardiology in the Young ◽

10.1017/s1047951119001057 ◽

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.

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

PEDIATRICS ◽

10.1542/peds.38.2.220 ◽

1966 ◽

Vol 38 (2) ◽

pp. 220-230 ◽

Cited By ~ 2

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.

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