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Ann Thorac Surg 1993;55:413-419
© 1993 The Society of Thoracic Surgeons

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Articles

Preimplantation alteration of adenine nucleotides in cryopreserved heart valves

^a Georgetown University School of Medicine, Washington, DC USA
^b Medical College of Virginia, Richmond, Virginia USA
^c Food and Drug Administration, Rockville, Maryland USA

Accepted for publication May 18, 1992.

^_* Address reprint requests to Dr Hopkins, Department of Surgery, 4PHC, Georgetown University, 3800 Reservoir Rd, NW, Washington, DC 20007.

To assess the initial metabolic phase of cellular injury from cardiac valve processing, high-energy phosphate concentrations were analyzed in valve leaflets subsequent to critical processing steps. Using a porcine model, valves were processed in a manner identical to human homografts, with 58 randomly assigned to five groups representing distinct preparation phases. Group I (controls) sustained 40 minutes of warm ischemia concluded by liquid nitrogen immersion. Remaining groups similarly endured 40 minutes of ischemia, but were subsequently prepared according to stepwise design: II, warm ischemia + 24 hours of 4 °C ischemia; III, warm ischemia + 24 hours of 4 °C antibiotic disinfection; IV, warm ischemia + 24 hours at 4 °C (without antibiotics) + cryopreservation (–1 °C/min cryoprotected freezing); and V, warm ischemia + disinfection + cryopreservation. At each regimen's conclusion leaflet extracts were assayed by high-performance liquid chromatography for high-energy adenine nucleotides (adenosine triphosphate, adenosine diphosphate, adenosine monophosphate) and catabolites. A 47% and 86% decrease in cellular adenosine triphosphate level was observed in group III and group V leaflets, respectively. The level of total adenine nucleotides was maintained up to cryopreservation; thereafter a 74% decrease was noted. Catabolite analysis confirmed incomplete degradation of adenine nudeotides indicating cellular metabolic resilience throughout standard homograft preparation in valves previously exposed to 40 minutes of warm ischemia.

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