Stability of an autologous platelet clot in the pericardial sac: An experimental and clinical study

Abstract

Autologous platelet clots serve as slow-release delivery systems for platelet-derived growth factors and cytokines. Their application to the pericardial sac might facilitate salvage and repair of ischemically injured myocardium. However, little is known about platelet clot stability in the pericardial sac. We investigated the stability of platelet clots in vitro and after administration to the pericardial sac in pigs and patients. In 5 Yorkshire-Landrace pigs and 10 patients, in vitro manufactured autologous platelet gel (Medtronic Magellan Platelet Separator) and platelet-rich fibrin (Vivolution Vivostat System) were administered to the pericardial sac for 30 minutes. Two antifibrinolytics (tranexamic acid and aprotinin) were tested for their capacity to stabilize autologous platelet gel. In vitro clots, incubated at 37 degrees C for 48 hours, served as controls. Clot weight was measured before and after administration. In vitro, autologous platelet gel clots of either formula liquefied almost entirely within 60 minutes whereas platelet-rich fibrin clots remained intact. In the pig, platelet clot weight decreased to 16.7% +/- 7.8% (P < .05) and 66.4% +/- 3.2% (P < .05) of initial clot weight for autologous platelet gel and platelet-rich fibrin, respectively. Addition of antifibrinolytics to autologous platelet gel did not reduce clot degradation significantly. In patients, autologous platelet gel and platelet-rich fibrin clot weight remained 9.0% +/- 1.5% (P < .05) and 73.7% +/- 2.6% (P < .05) of initial clot weight, respectively. Autologous platelet gel is unstable both in vitro and in vivo, whereas platelet-rich fibrin remains intact in vitro and, compared with autologous platelet gel, is less subject to degradation in pigs and in patients.