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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.


Article written by researchers from the Division of Cardiology and Gazes Cardiac Research Institute, Department of Comparative Medicine, and Division of Pediatric Cardiology, Medical University of South Carolina. Published in the Journal of Clinical Investigation, August 1988, volume 82, pages 544-551. Includes abstract, references, tables, and diagrams.