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Ann Thorac Surg 2005;79:2094-2102
© 2005 The Society of Thoracic Surgeons


Original article: Cardiovascular

In Vitro Flow Analysis of a Patient-Specific Intraatrial Total Cavopulmonary Connection

Diane A. de Zélicourt, MSa, Kerem Pekkan, PhDa, Lisa Wills, BSa, Kirk Kanter, MDb, Joseph Forbess, MDb, Shiva Sharma, MDc, Mark Fogel, MDd, Ajit P. Yoganathan, PhDa,*

a Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia
b Department of Surgery, Emory University, Atlanta, Georgia
c Department of Pediatric Cardiology, Emory University, Atlanta, Georgia
d Division of Cardiology, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania

Accepted for publication December 28, 2004.

* Address reprint requests to Dr Yoganathan, Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Room 2119 U.A. Whitaker Building, 313 Ferst Dr, Atlanta, GA30332-0535 (E-mail: ajit.yoganathan{at}bme.gatech.edu).

BACKGROUND: Understanding the hemodynamics of the total cavopulmonary connection may lead to further optimization of the connection design and surgical planning, which in turn may lead to improved surgical outcome. Although most experimental and numerical investigations have mainly focused on somewhat simplified geometries, investigation of the flow field of true anatomic configurations is necessary for a true understanding.

METHODS: An intraatrial connection was reconstructed from patient magnetic resonance images and manufactured using transparent stereolithography. Power loss, flow visualization, and digital particle image velocimetry as well as computational fluid dynamics simulations were performed to characterize the anatomic flow structure. Given the complexity of the anatomic flow, two simplified versions of the geometry were manufactured and run through power loss and flow visualization studies.

RESULTS: Experimental measurements revealed complex, unsteady, and highly three-dimensional flow structures within the anatomic model, leading to high pressure drops and power losses. The small vessel diameters were the primary cause of these losses. Numerical simulations demonstrated that most of the dissipation occurred in the pulmonary arteries. Finally, asymmetric pulmonary diameters together with the bulgy intraatrial connection favored the rise of flow unsteadiness and unbalanced lung perfusion.

CONCLUSIONS: The technique developed in this study enabled a deeper understanding of the hemodynamics behind an intraatrial connection. Future endeavors would be to study variation among differing surgical techniques, comparing intraatrial and extracardiac approaches.




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