What is wrong with the right ventricle after surgical closure of a ventricular septal defect?

The outcomes of patients after surgical closure of a ventricular septal defect (VSD) performed during infancy or childhood is considered to be excellent with low long-term morbidity and mortality.1–3 In most congenital heart centres, patients after surgical VSD closure are discharged from follow-up if there are no known significant residual lesions such as a residual VSD, aortic regurgitation, or subaortic stenosis. This probably explains why there are very few long-term follow-up studies on one of the most common indications for congenital heart surgery. The study by Heiberg et al.4 looked at a small group of adult patients who underwent surgical closure of a VSD during infancy or childhood. The authors studied left and right ventricular structure and function using cardiac magnetic resonance imaging (cMRI) in 27 young adult patients (mean age 20.5 years) who underwent surgical VSD closure around 1.9 years of age. All patients were clinically asymptomatic. The authors observed that the RVs in the patients were slightly larger and more hypertrophied (higher RV mass index) when compared with normal controls. They also observed a slightly lower fractional area change suggesting a lower RV ejection fraction. Using feature tracking cMRI analysis, they found a small increase in radial RV strain with normal longitudinal RV strain. The left ventricular dimensions and function were within normal range. These data suggest incomplete right ventricular remodelling in patients after VSD closure with residual RV hypertrophy and dilation associated with increased radial deformation. The clinical significance and long-term implications of these findings are currently unknown, but the residual changes are interesting and require further investigation. The paper can be criticized for the methodology used to analyse RV size and function. The authors did not quantify RV volumes and ejection fraction, arguing that the more prominent RV trabeculations in the VSD group precluded a reliable RV endocardial tracing. This is a missed opportunity as MRI is generally considered to be the best technique for assessing RV volumes and other groups have reported reliable results in the presence of RV hypertrophy and dilatation.5,6 Interestingly the authors decided to measure RV mass index, which theoretically would have the same technical problems as RV volumetric calculations. They also missed the opportunity to obtain detailed echocardiographic data, which could have provided further important information on RV structure and function. Despite these methodological limitations, the findings are interesting and somewhat surprising.

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