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Title	Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive
Alternative Title	Mechanism of decreased forward stroke volume
Author	Corin, William J.;Swindle, M. Michael;Spann, James F., Jr.;Nakano, Kiyoharu;Frankis, Mary;Biederman, Robert W.W.;Smith, Allison;Taylor, Ashby;Carabello, Blase A.
Contributor(s)	Journal of Clinical Investigation (Publisher)
Date	1988-08
Subject.MeSH	Cardiac Catheterization Heart Defects, Congenital Hemodynamics Myocardial Contraction Stroke Volume Heart Septal Defects, Ventricular Failure to Thrive Child Swine Models, Animal
Subject.LCSH	Cardiac catheterization;Cardiac output;Congenital heart disease;Heart--Contraction;Ventricular septal defects;Failure to thrive syndrome;Pediatric cardiology;Children--Research;Swine as laboratory animals;American Society for Clinical Investigation
Description	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.
Collection	MUSC Faculty Journal Articles
Contributing Institution	Waring Historical Library (MUSC)
Date Digital	2015-09
Rights	Copyright 1988, American Society for Clinical Investigation (ASCI).
Language	English
Type	Text
Format	application/pdf
Media Type	Periodicals
Resource Identifier	fja_0019_1988
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.

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

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