Prevention of ischemic myocardial contracture through hemodynamically controlled DCD

Ylva Wahlquist, Kristian Soltesz, Qiuming Liao, Xiaofei Liu, Harry Pigot, Trygve Sjöberg, Stig Steen

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Abstract

Purpose—Ischemic myocardial contracture (IMC) or ‘‘stoneheart’’ is a condition with rapid onset following circulatory death. It inhibits transplantability of hearts donated uponcirculatory death (DCD). We investigate the effectiveness of hemodynamic normalization upon withdrawal of life-sustaining therapy (WLST) in a large-animal controlled DCD model, with the hypothesis that reduction in cardiac work delays the onset of IMC. Methods—A large-animal study was conducted comprising of a control group (n = 6) receiving no therapy upon WLST, and a test group (n = 6) subjected to a protocol for fully automated computer-controlled hemodynamic drug administration. Onset of IMC within 1 h following circulatory death defined the primary end-point. Cardiac work estimates based on pressure-volume loop concepts were developed and used to provide insight into the effectiveness of the proposed computer-controlled therapy. Results—No test group individual developed IMC within 1 h, whereas all control group individuals did (4/6 within30 min). Conclusion—Automatic dosing of hemodynamic drugs in the controlled DCD context has the potential to prevent onset of IMC up to 1 h, enabling ethical and medically safe organ procurement. This has the potential to increase the use of DCD heart transplantation, which has been widely recognized as a means of meeting the growing demand for donor hearts.
Original languageEnglish
Pages (from-to)485-493
JournalCardiovascular Engineering and Technology
Volume12
Issue number5
DOIs
Publication statusPublished - 2021

Subject classification (UKÄ)

  • Control Engineering

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  • Ex Vivo Working Porcine Heart Model

    Pigot, H., Soltesz, K. & Steen, S., 2024 Apr 28, Experimental Models of Cardiovascular Diseases: Methods and Protocols. Ishikawa, K. (ed.). 2 ed. New York, NY: Humana Press, p. 87-107 20 p. (Methods in Molecular Biology; vol. 2803).

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