TY - JOUR
T1 - Leukocyte filtration and aprotinin
T2 - Synergistic anti-inflammatory protection
AU - Olivencia-Yurvati, Albert H.
AU - Wallace, Neil
AU - Ford, Sheila
AU - Mallet, Robert T.
PY - 2004
Y1 - 2004
N2 - Cardiopulmonary bypass activates an array of cellular and humoral inflammatory mechanisms that culminate in diverse or organ-specific injury. A manifestation of inflammatory injury to the heart, atrial fibrillation ranks among the most frequent and potentially life-threatening postsurgical complications. Pulmonary manifestations of the inflammatory response are also of major concern. Neutrophils activated by passage through the extracorporeal circuit inflict local injury and provoke the inflammatory cascade by producing oxyradicals and proinflammatory factors. This study tested if a combination of leukocyte depletion and aprotinin suppression of neutrophils could minimize postbypass atrial fibrillation and pulmonary dysfunction. In part one, two randomized groups of 90 patients undergoing primary coronary artery bypass grafting received full Hammersmith aprotinin alone (control group) or combined with leukofiltration (study group) and were prospectively examined. The dual treatment decreased the incidence of postoperative atrial fibrillation (7 of 90, 7.8%) by 67% versus aprotinin alone (21 of 90, 23.3%). Respiratory gas exchange in these patients was assessed from pulmonary shunt fraction. In the first two hours postbypass, pulmonary shunt fraction in the dual treatment group increased 40% less than in the group receiving aprotinin alone (p = 0.002), and subsided more quickly and completely over the next six hours. In part two, the cardiopulmonary bypass group receiving aprotinin+leukofiltration was retrospectively compared with 45 patients undergoing off-pump coronary revascularization. A strong, albeit not statistically significant trend (p = 0.08) toward a lower incidence of atrial fibrillation was found in the dual treatment group versus the off-pump group (8 of 45, 17.8%). These findings suggest that combining mechanical and pharmacologic suppression of the systemic inflammatory response could mitigate its deleterious arrhythmic and pulmonary complication.
AB - Cardiopulmonary bypass activates an array of cellular and humoral inflammatory mechanisms that culminate in diverse or organ-specific injury. A manifestation of inflammatory injury to the heart, atrial fibrillation ranks among the most frequent and potentially life-threatening postsurgical complications. Pulmonary manifestations of the inflammatory response are also of major concern. Neutrophils activated by passage through the extracorporeal circuit inflict local injury and provoke the inflammatory cascade by producing oxyradicals and proinflammatory factors. This study tested if a combination of leukocyte depletion and aprotinin suppression of neutrophils could minimize postbypass atrial fibrillation and pulmonary dysfunction. In part one, two randomized groups of 90 patients undergoing primary coronary artery bypass grafting received full Hammersmith aprotinin alone (control group) or combined with leukofiltration (study group) and were prospectively examined. The dual treatment decreased the incidence of postoperative atrial fibrillation (7 of 90, 7.8%) by 67% versus aprotinin alone (21 of 90, 23.3%). Respiratory gas exchange in these patients was assessed from pulmonary shunt fraction. In the first two hours postbypass, pulmonary shunt fraction in the dual treatment group increased 40% less than in the group receiving aprotinin alone (p = 0.002), and subsided more quickly and completely over the next six hours. In part two, the cardiopulmonary bypass group receiving aprotinin+leukofiltration was retrospectively compared with 45 patients undergoing off-pump coronary revascularization. A strong, albeit not statistically significant trend (p = 0.08) toward a lower incidence of atrial fibrillation was found in the dual treatment group versus the off-pump group (8 of 45, 17.8%). These findings suggest that combining mechanical and pharmacologic suppression of the systemic inflammatory response could mitigate its deleterious arrhythmic and pulmonary complication.
UR - http://www.scopus.com/inward/record.url?scp=2342555174&partnerID=8YFLogxK
U2 - 10.1191/0267659104pf714oa
DO - 10.1191/0267659104pf714oa
M3 - Article
C2 - 15161060
AN - SCOPUS:2342555174
SN - 0267-6591
VL - 19
SP - S13-S19
JO - Perfusion
JF - Perfusion
IS - SUPPL. 1
ER -