Ventricular Wall Stress and Pump Function of Ventricular Septal Defect of Congenital Heart Defects

About 36,000 infants are born each year with a congenital heart defect (CHD) and charges for treatment surpass $2.2 billion for inpatient surgery alone. Of many different types of CHDs, ventricular septal defect (VSD) is the most common class (∼1/3 of CHDs) of heart deformity present at birth. Though many close spontaneously and rarely require treatment, VSD still accounts for ∼15% of defects requiring an invasive procedure within the first year of life [1]. Generally, the ventricular performance is indexed by geometry, shape, diastolic and systolic function, and myocardial contractility [2]. Ejection fraction (EF) and end-systolic (ES) wall stress also used to assess the ventricular function [3–5]. Ratcliffe and Guy suggested that the assessment of LV function focusing on indices of systolic function, such as EF and contractility (E_ES), is misleading because the shift of end-systolic pressure-volume relationship (ESPVR) and increase/decrease in E_ES and coincident shift of end-diastolic pressure-volume relationship (EDPVR) may result in pseudo increase/decrease of EF even though there may not be any significant change in true LV function (i.e., Starling relationship) [6]. Though Sagawa and associates proposed the ESPVR as a reliable index of intrinsic systolic function [7], it requires derivation of the pressure-volume relationship at different loading conditions by using a noninotropic vasoconstrictor or vasodilator. This may consequently enforce a significant burden on infants with a failing heart. Moreover, irreversible complication of muscle structure can be generated [8–10]. Thus, rigorous quantification of the pump function associated with mechanics has been hindered especially for infants.