Elsevier

The Annals of Thoracic Surgery

Volume 56, Issue 5, November 1993, Pages 1014-1019
The Annals of Thoracic Surgery

Original article
Restrictive ventricular septal defect: How small is too small to close?

https://doi.org/10.1016/0003-4975(95)90006-3Get rights and content

Abstract

Historically, indications for ventricular septal defect closure have included congestive heart failure, pulmonary hypertension, aortic insufficiency with or without aortic valve prolapse, and prior bacterial endocarditis. However, controversy exists as to how the lifetime risk of an isolated, nonoperated restrictive ventricular septal defect compares with the risk of surgical closure in an asymptomatic child. Between 1980 and 1991, cardiac catheterization and elective ventricular septal defect closure (age > 1 year, pulmonary to systemic flow ratio < 2.0) were performed in 141 patients aged 1 to 23 years (mean age, 6.1 ± 4.7 years). Mean systolic pulmonary artery pressure was 26.9 ± 13.0 mm Hg, and mean pulmonary to systemic flow ratio was 1.6 ± 0.3. Aortic valve prolapse was present in 63 patients (45%), aortic insufficiency was present in 25 (18%), and 5 (3.5%) had prior bacterial endocarditis. There were no early or late deaths or major morbidity. No patient required a ventriculotomy to accomplish ventricular septal defect closure. Mean postoperative intensive care unit stay was 1.3 ± 0.9 days, and mean hospital stay was 5.5 ± 1.9 days. There were no instances of permanent complete atrioventricular dissociation, reoperations for bleeding, postoperative wound infections, or roperations for residual or recurrent ventricular septal defect. These improved results justify a reevaluation of historic indications for ventricular septal defect closure. Surgical closure of a restrictive ventricular septal defect removes the socioeconomic stigma associated with living with an uncorrected cardiac defect, and the surgical risk as defined by this experience when compared with known natural history studies is less than the lifetime risks of development of bacterial endocarditis or progressive aortic valve prolapse leading to aortic insufficiency.

References (2)

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Presented at the Twenty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 25–27, 1993.

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