Clarifying the Surgical Morphology of Inlet Ventricular Septal Defects (original) (raw)

Pathophysiology, Investigations, and Management of Ventricular Septal Defect

Zenodo (CERN European Organization for Nuclear Research), 2021

Background: Ventricular septal defects (VSDs) are still one of the most prevalent surgical indications in newborns and children with congenital heart disease. With advances in echocardiography, cardiac catheterization is no longer necessary in the treatment of these individuals. Although perioperative mortality and morbidity for isolated defects are still low, unique scenarios such as surgical care of numerous VSDs and decision-making in patients with pulmonary hypertension remain difficult. This chapter examines both classic and recent evidence that has shaped the management of this condition, as well as the facts underlying developing interventional methods utilized in both the catheterization lab and the operating room. Conclusion: VSD is the most common congenital abnormality at birth. Small flaws should close on their own within the first year of life; however, larger faults can cause serious difficulties. The major interventions for big problems are surgical VSD closure and device closure.

Anatomy of the ventricular septal defect in outflow tract defects: Similarities and differences

The Journal of Thoracic and Cardiovascular Surgery, 2015

Objective: The study objective was to analyze the anatomy of the ventricular septal defect found in various phenotypes of outflow tract defects. Methods: We reviewed 277 heart specimens with isolated outlet ventricular septal defect without subpulmonary stenosis (isolated outlet ventricular septal defect, 19); tetralogy of Fallot (71); tetralogy of Fallot with pulmonary atresia (51); common arterial trunk (54); double outlet right ventricle (65) with subaortic, doubly committed, or subpulmonary ventricular septal defect; and interrupted aortic arch type B (17). Special attention was paid to the rims of the ventricular septal defect viewed from the right ventricular side and the relationships between the tricuspid and aortic valves. Results: The ventricular septal defect was always located in the outlet of the right ventricle, between the 2 limbs of the septal band. There was a fibrous continuity between the tricuspid and aortic valves in 74% of specimens with isolated outlet ventricular septal defect, 66% of specimens with tetralogy of Fallot, 39% of specimens with tetralogy of Fallot with pulmonary atresia, 4.6% of specimens with double outlet right ventricle, 1.8% of specimens with common arterial trunk, and zero of specimens with interrupted aortic arch type B (P<.005). When present, this continuity always involved the anterior tricuspid leaflet. Conclusions: The ventricular septal defect in outflow tract defects is always an outlet ventricular septal defect, cradled between the 2 limbs of the septal band. However, there are some differences regarding the posteroinferior and superior rims of the ventricular septal defect. These differences suggest an anatomic continuum from the isolated outlet ventricular septal defect to the interrupted aortic arch type B rather than distinct physiologic phenotypes, related to various degrees of abnormal rotation of the outflow tract during heart development: minimal in isolated outlet ventricular septal defect; incomplete in tetralogy of Fallot, tetralogy of Fallot with pulmonary atresia, and double outlet right ventricle; absent in common arterial trunk; and excessive in interrupted aortic arch type B.

Device Closure of Congenital Ventricular Septal Defects

Congenital Heart Disease, 2007

Ventricular septal defects (VSD), which cause volume overload, may be closed by interventional method. The success depends on the precise anatomic definition of the defect and its relation to other cardiac structures. We report our first experiences of transcatheter closure of perimembranous and muscular VSD. Between May 2005 and September 2006, transcatheter closure of VSD was attempted in 38 patients. Implantation was successful in 37 patients. In one patient, the procedure failed because of the long sheath kinking. We observed important complications in three patients: severe tricuspid valve regurgitation, residual VSD and tricuspid valve regurgitation and right bundle branch block in the short-term follow-up. Transcatheter device closure with Amplatzer device seems to be effective and safe in the treatment of perimembranous and muscular VSDs. Tricuspid valve incompetence may cause problems. Long-term results are required to determine the efficacy and safety.