ORIGINAL RESEARCH In vitro quality and platelet function of cold and delayed cold storage of apheresis platelet concentrates in platelet additive solution for 21 days Hanne Braathen , 1 Joar Sivertsen, 1 Turid Helen Felli Lunde, 1 Einar Klæboe Kristoffersen, 1,2 Jörg Assmus, 3 Tor Audun Hervig, 1,2 Geir Strandenes, 1,4 and Torunn Oveland Apelseth 1,5 BACKGROUND: Cold storage of platelets may extend shelf life compared to room temperature storage. This study aimed to investigate in vitro platelet quality and function in cold-stored and delayed-cold-stored nonagitated apheresis platelets in platelet additive solution during storage for 21 days. STUDY DESIGN AND METHODS: Ten double apheresis platelet concentrates in 37% plasma/63% PAS-IIIM were split into two groups; nonagitated 2 to 6  C storage (CSPs) and delayed cold storage (DCSPs) with 7 days agitated storage at 20-24  C followed by nonagitated cold storage for 14 additional days. Platelet count, metabolism, viscoelastic properties, and aggregation ability were measured on Days 1, 7, 14, and 21. RESULTS: All platelet units, both CSPs and DCSPs, complied with the EU guidelines throughout storage for 21 days. Swirling was not detectable after cold storage. Cold storage improved platelet function; however, DCSP on Day 7 showed poorer results compared to CSP. Cold storage slowed down metabolism, with lower lactate and higher glucose concentrations in the CSP compared to the DCSP throughout storage for 21 days. CONCLUSION: Cold storage of platelets improved platelet function in in vitro assays, even though delayed cold storage on Day 7 showed poorer results compared to continuous cold storage. This difference could be explained by accelerated metabolism and higher glucose consumption during the period of room temperature storage. Cold storage and delayed cold storage could ease inventory management. Further studies investigating the in vitro and clinical effects of cold-stored and delayed-cold-stored platelets are encouraged. T he introduction of a balanced transfusion approach in treatment of hemorrhagic shock using RBC con- centrates, plasma, and platelet concentrates (PCs) has been associated with improved outcomes. 1–3 The platelet storage lesion and risk of bacterial growth limit the shelf life of room temperature–stored PCs. 4–7 Short shelf life leads to wastage and creates logistical challenges. It also increases pressure to recruit donors, which is a growing prob- lem for blood centers. 8 Studies have shown that cold storage of platelets reduces bacterial growth and preserves mitochondrial function, in vitro aggregation response, and clot formation longer. 9–14 Thus, the shelf life of apheresis PCs could be extended through cold storage. In the past, platelets were routinely stored cold at 4  C. However, this practice was abandoned when studies showed that cold storage led to a reduction in circulation time. 15–17 Slichter et al. 15 reported a reduction of in vivo viability from ABBREVIATIONS: CSPs = cold-stored platelets; DCSPs = delayed- cold-stored platelets; LME = linear mixed-effect; MA = maximum clot strength; MaxA = maximum aggregation; MPV = mean platelet volume; PAS = platelet additive solution; PCs = platelet concentrates; R = time to first clot formation; TEG = thromboelastography; TRAP-6 = thrombin receptor activating peptide 6. From the 1 Department of Immunology and Transfusion Medicine, the 3 Department of Research and Development, and the 5 Department of Medical Biochemistry and Pharmacology, Haukeland University Hospital, the 2 Department of Clinical Sciences, University of Bergen, Bergen and the 4 Medical Services, Norwegian Armed Forces, Sessvollmoen, Norway. Address reprint requests to: Hanne Braathen, Department of Immunology and Transfusion Medicine, Haukeland University Hospital, P.O. box 1400 5021 Bergen, Norway; e-mail: hanne.braathen@ helse-bergen.no. This work was supported by grants from the Norwegian Armed Forces Joint Medical Services. Received for publication January 3, 2019; revision received April 28, 2019, and accepted April 29, 2019. doi:10.1111/trf.15356 © 2019 AABB TRANSFUSION 2019;00;1–10 TRANSFUSION 1