Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Abstract

Children with ventricular septal defect (VSD) often demonstrate failure to thrive (Ff1'). Such patients usually have reduced systemic cardiac output which has been postulated as a cause for their growth retardation. This study was conducted to ascertain the mechanism of the reduced cardiac output in children with VSD and FT1'1 and also in a porcine model of VSD. Forward stroke volume was reduced in VSD-F'IT children, 31±8 ml/m2, compared to normal children, 49±15 ml/m2 (P < 0.05), but was not reduced in children with VSD and normal growth and development (41±16 ml/m2). Forward stroke volume was also reduced in swine with VSD compared to controls. Contractility assessed by mean velocity of circumferential shortening (Vd) corrected for afterload was similar in normals and VSD-FT'I children. Contractile performance was also similar in normal and VSD swine. Afterload assessed as systolic stress was similar in FIT-VSD children and normal subjects. Preload assessed as end-diastolic stress was increased in the VSD-FI' group. End-diastolic volume was not larger in the VSD-FTI' group. We conclude that the reduced stroke volume seen in VSD-FT'I children and VSD-swine was not due to reduced contractility, increased afterload or reduced preload. The reduced stroke volume may have been due to failure of end-diastolic volume to increase adequately.

Bradycardia and the Role of β-Blockade in the Amelioration of Left Ventricular Dysfunction

“…Angiographic volume and LV pressure were varied by use of an inferior vena cava balloon, as done previously. 13,20,21 In turn, loading alterations caused by balloon deflation created the changes in volume, pressure, and stress needed to construct indexes of contractility.…”

“…21 LV wall stress was calculated with the method of Mirsky et al 23 K was determined by fitting the systolic stress and end-systolic wall thickness to the following curvilinear equation:…”

Effects of chronic beta-adrenergic blockade on the left ventricular and cardiocyte abnormalities of chronic canine mitral regurgitation.

“…In vivo contractile function was assessed in these experiments using the mass-corrected slope of the end ejection stress-volume relationship and the end systolic stiffness constant (28,32,33). Although all indexes of in vivo function have their limitations, these two indexes have been investigated extensively by us and by others and their limitations are relatively well known.…”

Right ventricular remodeling in restrictive ventricular septal defect

“…Serial acquisition of myocardium in an asymptomatic rVSD patient is not feasible and there are few animal models to study this important problem. The majority of VSD animal model literature has focused on hemodynamics and/or device testing [23,24], although progress is being made in understanding the genetics behind VSD [2]. Desmin increases in the LV during ischemic HF and is a more robust predictor of cardiac dysfunction than fibrosis and myocyte hypertrophy [14].…”