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This Article Full Text Full Text (PDF) All Versions of this Article: 295/6/H2427    most recent 00628.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sundareswaran, K. S. Articles by Yoganathan, A. P. Search for Related Content PubMed PubMed Citation Articles by Sundareswaran, K. S. Articles by Yoganathan, A. P.

The total cavopulmonary connection resistance: a significant impact on single ventricle hemodynamics at rest and exercise

¹Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, Georgia; ²Department of Biomedical Engineering, Carnegie Mellon University, Pittsburgh; ³Division of Cardiology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania; ⁴Pediatric Cardiology Services, Atlanta; and ⁵Division of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, Georgia

Submitted 15 June 2008 ; accepted in final form 11 October 2008

Little is known about the impact of the total cavopulmonary connection (TCPC) on resting and exercise hemodynamics in a single ventricle (SV) circulation. The aim of this study was to elucidate this mechanism using a lumped parameter model of the SV circulation. Pulmonary vascular resistance (1.96 ± 0.80 WU) and systemic vascular resistances (18.4 ± 7.2 WU) were obtained from catheterization data on 40 patients with a TCPC. TCPC resistances (0.39 ± 0.26 WU) were established using computational fluid dynamic simulations conducted on anatomically accurate three-dimensional models reconstructed from MRI (n = 16). These parameters were used in a lumped parameter model of the SV circulation to investigate the impact of TCPC resistance on SV hemodynamics under resting and exercise conditions. A biventricular model was used for comparison. For a biventricular circulation, the cardiac output (CO) dependence on TCPC resistance was negligible (sensitivity = –0.064 l·min^–1·WU^–1) but not for the SV circulation (sensitivity = –0.88 l·min^–1·WU^–1). The capacity to increase CO with heart rate was also severely reduced for the SV. At a simulated heart rate of 150 beats/min, the SV patient with the highest resistance (1.08 WU) had a significantly lower increase in CO (20.5%) compared with the SV patient with the lowest resistance (50%) and normal circulation (119%). This was due to the increased afterload (+35%) and decreased preload (–12%) associated with the SV circulation. In conclusion, TCPC resistance has a significant impact on resting hemodynamics and the exercise capacity of patients with a SV physiology.

mathematical modeling; cardiac function; congenital heart defects; magnetic resonance imaging