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Department of Cardiovascular & Thoracic Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8879
(Email: michael.jessen{at}utsouthwestern.edu).
The inflammatory response to cardiopulmonary bypass (CPB) has been studied extensively, yet it remains incompletely understood. Multiple investigations have established that blood contact with foreign surfaces of the circuit components and with nonendothelialized surfaces in the surgical field contributes to this inflammatory process and ultimately affects patient morbidity and mortality. In this study Fabre and colleagues [1] collected blood samples during cardiac surgery in a manner designed to isolate the effects on blood that is lost from the heart and contacts the pericardial cavity before it is returned to the CPB circuit from the effects on blood due to suction forces applied to decompress the left ventricle (LV) and provide a dry operative field. Their findings demonstrate the greater importance of blood contact with the pericardium in activating the coagulation cascade, releasing pro-inflammatory markers and causing hemolysis. Perhaps not surprisingly, blood suctioned directly from the aorta and LV did not exhibit a great degree of activation as these structures are lined by endothelial cells, which, if not damaged, should not serve as an activating medium. In contrast, the pericardial surface is shown in this study and others to be a potent activator of thrombin, and tissue factor pathway activation seems to play a prominent role in this process. Of interest, suction forces did not seem to affect platelet function as assessed by P-selectin expression, but contact with the pericardium significantly reduced this marker of platelet function.
The study has several limitations. Blood samples drawn from the ascending aortic vent line may be exposed to a great deal more of the cold cardioplegia solution, as all cardioplegia was administered by an antegrade route. We do not know the volume of blood contacting the pericardium or the length of time it was in contact with the pericardium before it was sampled. Also, blood aspirated from the pericardium was analyzed, but then processed through a cell-saver before it was returned to the body. It would have been very instructive to also have sampled blood after processing in the cell-saver to see if the same activation profile exists. If the activation is attenuated, then any relationship to adverse events may be blunted.
The clinical relevance of these findings was not tested in this study. However, one might speculate that avoidance of blood contact with the pericardium or processing this blood before returning it to the CPB circuit may reduce the inflammatory response and decrease platelet dysfunction. Both effects could be beneficial and support the strategy of either discarding or processing through a cell-saver any blood that contacts the pericardium. Indeed, these approaches have been shown effective by other investigators in reducing postoperative bleeding and decreasing neurologic events. Surgeons need to be aware that all blood from the operative field is not equivalent and greater vigilance in managing blood that contacts the pericardium may be an important venue to exploit to improve patient outcomes in cardiac surgery.
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