Progress in the Surgical Treatment of Ventricular Septal Defect: An Analysis of a Twelve Years' Experience*

Abstract

Two hundred sixty-seven patients underwent surgical closure of a ventricular septal defect (VSD) over a 12-year period between January 1, 1970 and December 31, 1982. In 152 patients (57%) an associated lesion was present complicating the treatment of the primary lesion: 7 patients had multiple VSDs and among those with single defects, 189 were large (unrestrictive). The median age was 5.2 years ranging from 1 month to 46 years. Sixty-nine were infants under 10 kg of weight. The 30-day operative mortality was 8.6% (23 cases). The main cause of death was a low output syndrome in 16 cases. Thirty-two variables have been collected and their relationship with the death of the patients has been analyzed with univariate and multivariate methods. Logistic analysis has identified the independent significant incremental effect on hospital mortality of low weight (P greater than 0.00001), early operative date (P greater than 0.00001), multiplicity of defects (P = 0.0008), presence of major associated lesions (P = 0.019); the large size of the defect was only probably significant (P = 0.18). Inspection of the nomograms, relating the probability of operative death to weight and age in patients with a large defect, shows that the risk is significantly higher in the 3 kg baby (median age 3.3 months), particularly if major associated lesions are present. In infants with multiple VSDs the risk of operation remains, at the end of 1982, significantly higher than in single defects. However, our data suggest that the risk of open correction in patients over 12 kg of weight approaches that of single VSD if concomitant lesions do not complicate the surgical treatment.

Techniques and results in the management of multiple ventricular septal defects

“…[1][2][3][4] Despite advances in diagnosis and surgical treatment, the morbidity and mortality in patients with multiple VSDs has remained high, primarily resulting from difficulties associated with inadequate exposure and incomplete closure. [5][6][7] Visualization of the VSDs from the right side of the septum often leads to uncertainties in defining the true edges of the VSDs because of the presence of numerous muscular trabeculations. These defects, however, when viewed from the left side of the septum, will generally appear as a discrete, often single, defect with easily discernible margins.…”

Transcatheter closure of ventricular septal defects using the Rashkind device: Initial experience

“…A critical appraisal of our results shows that outcomes are comparable with, and in many cases superior to, those achievable with conventional surgery [1][2][3][4][5][6][7][8]. Some morbidity/mortality and the hemodynamic instability with this procedure may be unavoidable [23] and needs to be viewed in the context of the very significant surgical morbidity/mortality for this very difficult group of patients.…”

“…Before 1970, the reported operative mortality associated with the repair of such defects was 17 to 86 percent [1,2]. As recently as 1983, an operative mortality of 43% was reported for similar patients [7]. Surgical mortality in those patients is most frequently attributed to ventricular dysfunction secondary to left ventriculotomy.…”

“…The identification and surgical closure of apical or multiple muscular ventricular septal defects (VSD) are known to be difficult [1][2][3][4][5][6][7][8]. The presence of additional muscular VSDs in children with otherwise correctable cardiac malformations adversely influences operative risk and timing of definitive surgical intervention.…”

Transcatheter closure of apical ventricular muscular septal defect combined with arterial switch operation in a newborn infant

“…Some of these defects are muscular, which complicates the surgical management of the patients due to difficult defect visualization, high rate of reoperation, and subsequent ventricular dysfunction [1][2][3][4]. Moreover, TGA repair should ideally be performed within the first two weeks of life, when the left ventricle is still able to support the systemic circulation.…”