Optimizing Donor Heart Outcome After Prolonged Storage With Endothelial Function Analysis and Continuous Perfusion

• Published in: The Annals of thoracic surgery Vol. 78; no. 4; pp. 1362 - 1370
• Main Authors: Poston, Robert S., Gu, Junyan, Prastein, Deyanira, Gage, Fred, Hoffman, John W., Kwon, Michael, Azimzadeh, Agnes, Pierson, Richard N., Griffith, Bartley P.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01.10.2004
• Subjects: Aerobiosis; Animals; Coronary Vessels - physiology; Cryopreservation - methods; Cryopreservation - statistics & numerical data; Diastole; Dogs; Endothelium, Vascular - physiology; Energy Metabolism; Heart - physiology; Heart Transplantation; Lactates - metabolism; Myocardial Reperfusion; Myocardium - metabolism; Organ Preservation - methods; Organ Preservation - statistics & numerical data; Organ Preservation Solutions - pharmacology; Organ Size; Oxygen Consumption; Peroxidase - analysis; Systole; Time Factors; Tissue Donors; Ventricular Function, Left; 34
• ISSN: 0003-4975; 1552-6259
• DOI: 10.1016/j.athoracsur.2004.02.143

By minimizing tissue ischemia, continuous perfusion (CP) during organ transport may increase the safety of “marginal donors.” My colleagues and I investigated whether an analysis of donor heart viability predicts recovery of grafts challenged with a 24-hour preservation interval. Dog hearts underwent cold static storage (CS) for 8 hours (n = 8) or 24 hours (n = 2) or CP for 24 hours with cold asanguinous, oxygenated solution (n = 8). Myocardial systolic and diastolic function and oxygen and lactate consumption were assessed at base line, during CP, and after Langendorff blood reperfusion. Base line endothelial function was evaluated by the percentage transcoronary change ([coronary sinus − aorta]/aorta) in myeloperoxidase and by platelet function and coronary flow reserve after 20 seconds of coronary artery occlusion. During CP, the endothelium was assessed by transcoronary protein release and coronary resistance. Edema was assessed by weight gain and histology. Base line systolic and metabolic functions showed no relation to post-Langendorff function. Compared with CS, CP resulted in a greater recovery in systolic function (87% ± 35% vs 65% ± 15% of baseline; p = 0.05) and a shorter interval required for lactate consumption to exceed production (7.0 ± 6.8 minutes vs 15.0 ± 8.9 minutes; p = 0.06). Endothelial function was heterogeneous: coronary flow reserve, 2.7 ± 0.7; percentage change in myeloperoxidase, −8.4% ± 6.8%; and change in platelet function, 4.3% ± 3.5%, as determined by thromboelastography angle at base line. Protein release during CP for 24 hours was 8.3 ± 7.1 g. Two factors predicted more than 75% systolic pressure generation recovery: use of CP and normal endothelial function ( p = 0.05; Fisher's exact test). However, CP led to edema according to histology, weight gain (72 ± 29 g), and impaired diastolic function versus CS (end-diastolic pressure-volume relationship, 1.4 ± 0.4 mm Hg/mL vs 0.8 ± 0.3 mm Hg/mL; p = 0.08). Better systolic function despite 16 hours' more preservation than cold storage corroborates the idea that CP supports aerobic metabolism at physiologically important levels. Viability analysis focused on endothelial function and identified organs that were able to tolerate this 24-hour preservation interval.