Leukocyte filtration of blood cardioplegia attenuates myocardial damage and inflammation.
ABSTRACT OBJECTIVES: Leukocyte filtration of blood cardioplegia (cLkF) is postulated to reduce ischaemia-reperfusion myocardial injury. Contradictory results have been published and few studies have addressed perioperative cytokine leakage and haemodynamic status after LkF. METHODS: Thirty patients undergoing isolated aortic valve replacement were randomized to cLkF (cLkF-Group) or to standard cold blood cardioplegia (S-Group). Troponin I (TnI) and lactate were sampled from the coronary sinus at reperfusion. Peripheral TnI and lactate were collected preoperatively at admission, and in the intensive care unit (ICU) at 8, 12, 36 and 60 h postoperatively. Cardiac index (CI), indexed systemic vascular resistances, cardiac cycle efficiency (CCE) and central venous pressure (CVP) were registered preoperatively, at admission to the ICU and at the 6th, 12th, 18th, 24th and 36th postoperative hour. IL-6, IL-8, TNF-alpha and IL-10 were sampled preoperatively, at reperfusion, on admission to the ICU and the 6th, 18th and 24th postoperative hours. RESULTS: The cLkF group showed lower TnI (2.4 ± 0.4 vs. 5.1 ± 0.8 μg/l, P = 0.0001) and lactate (0.9 ± 0.1 vs. 1.6 ± 0.2 mmol/l, P = 0.0001) from the coronary sinus at reperfusion. TnI levels (group-P = 0.0001, group time-P < 0.0001) and lactate (group time-P = 0.001) remained lower postoperatively after cLkF. Ventricular defibrillation at aortic declamping was less common in the cLkF-Group (33.3% vs. S-Group: 93.3%; P = 0.002). Cytokines demonstrated significant postoperative leakage (time-P = 0.0001 in both groups for IL-6, IL-8, TNF-alpha, IL-10), with lower pro-inflammatory (IL-6 group-P = 0.0001, group time-P = 0.0001; IL-8 group-P = 0.0001, group time-P = 0.007; TNF-alpha group-P = 0.0001; group time-P = 0.012) and higher anti-inflammatory cytokine secretion after cLkF (IL-10 group-P = 0.005). Perioperative haemodynamic indices proved to be similar between the two groups (group-P = NS for CI, SVRI, CCE and CVP). CONCLUSIONS: cLkF during blood cardioplegia attenuates myocardial ischaemia/reperfusion injury and reduces perioperative leakage of TnI, lactate and pro-inflammatory cytokines. These data did not result in a better haemodynamic status.
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ABSTRACT: Reperfusion injury can occur after a long period of aortic cross-clamping in patients with left ventricular hypertrophy during open-heart surgery, even with the most up-to-date techniques of myocardial protection. In the present study, we examined whether leukocyte depletion as an adjunct to terminal blood cardioplegia (LDTC) attenuates reperfusion injury in patients with left ventricular hypertrophy (LV mass, >300 g; left ventricular end-systolic volume index, >100 mL/m2) in a group of 30 patients undergoing aortic valve replacement. We used basic cold potassium crystalloid cardioplegic solution. Terminal blood cardioplegic solution (TC) or LDTC was accomplished by mixing a cold potassium crystalloid cardioplegic solution with warm arterial blood obtained through cardiopulmonary bypass and administered to the aortic root for the first 10 minutes of reperfusion. During delivery of LDTC, warm arterial blood was passed through a leukocyte-removal filter. Patients were randomized into one of three groups for reperfusion: whole blood (WB) (n=10), TC (n=10), and LDTC (n=10). Left ventricular biopsies were obtained before ischemia, at the end of ischemia, and 15 minutes after reperfusion. Semiquantitative scoring for ultrastructural alterations indicated that the LDTC group achieved significantly better recoveries of both scores at reperfusion for myocyte damage and for endothelial cell damage of capillaries than did the WB and TC groups. The LDTC group had significantly fewer neutrophils adhering to endothelial cells at reperfusion and a lower level of malondialdehyde derived from myocardium than did the WB and TC groups. Regarding the clinical data, the LDTC group had a lower maximum creatine kinase-MB, a higher percentage of spontaneous defibrillation, a lower pulmonary capillary wedge pressure, and a lower requirement for dopamine that did the WB group, whereas the TC group failed to do better than the WB group. These results demonstrate that leukocyte-depleted reperfusion is potentially beneficial as an adjunct to terminal cardioplegia during cardiac surgery to attenuate reperfusion injury in patients with left ventricular hypertrophy.Circulation 05/1996; 93(9):1640-6. · 15.20 Impact Factor
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ABSTRACT: We tested the hypothesis that controlled reperfusion with leukocyte-depleted blood could improve myocardial protection by reducing the oxidative stress in patients undergoing myocardial revascularization. Thirty-four patients receiving antegrade/retrograde blood cardioplegia were divided into: group A: 11 patients with ejection fractions (EF) less than 35%, treated with leukocyte-depleted controlled blood reperfusion, group B: 11 patients with EF less than 35% in whom no leukocyte depletion was performed, group C: 6 patients with EF more than 45% treated as group A and group D: 6 patients with EF more than 45% without leukocyte depletion. To asses the oxidative stress, we evaluated total, total oxidized (GSSX), and reduced glutathione (GSH) in coronary sinus plasma, immediately before cross-clamping the aorta (T0), and at 0 (T1), 15 (T2) and 30 (T3) min after unclamping it. In groups A and B a significant shift towards oxidation of redox status of glutathione (GSH/GSSX) at T1 vs T0 was observed. Glutathione redox ratio remained low in group B while in group A it returned to the basal value at T2 with a significant difference from group B at T2 and T3. No differences were observed between groups C and D. In conclusion, our data show that leukocyte-depleted reperfusion can afford a better myocardial protection in patients with left ventricular dysfunction, while it seems unnecessary in patients with normal EF.European Journal of Cardio-Thoracic Surgery 02/1995; 9(12):701-6. · 2.67 Impact Factor
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ABSTRACT: Leukocyte depletion during cardiopulmonary bypass has been demonstrated in animal experiments to improve pulmonary function. Conflicting results have been reported, however, with clinical depletion by arterial line filter of leukocytes at the beginning of cardiopulmonary bypass. In this study, we examined whether leukocyte depletion from the residual heart-lung machine blood at the end of cardiopulmonary bypass would improve lung function and reduce the postoperative inflammatory response. Thirty patients undergoing elective heart operations were randomly allocated to a leukocyte-depletion group or a control group. In the leukocyte-depletion group (n = 20), all residual blood (1.2 to 2.1 L) was filtered by leukocyte-removal filters and reinfused after cardiopulmonary bypass, whereas in the control group an identical amount of residual blood after cardiopulmonary bypass was reinfused without filtration (n = 10). Leukocyte depletion removed more than 97% of leukocytes from the retransfused blood (p < 0.01) and significantly reduced circulating leukocytes (p < 0.05) and granulocytes (p < 0.05) compared with the control group. Levels of the inflammatory mediator thromboxane B2 determined at the end of operation (p < 0.05) were significantly lower in the depletion group than in the control group, whereas no statistical differences in interleukin-6 levels were found between the two groups. After operation, pulmonary gas exchange function (arterial oxygen tension at a fraction of inspired oxygen of 0.4) was significantly higher in the leukocyte-depletion group 1 hour after arrival to the intensive care unit (p < 0.05) and after extubation (p < 0.05). There were no statistical differences between the two groups with respect to postoperative circulating platelet levels and blood loss, and no infections were observed during the whole period of hospitalization. These results suggest that leukocyte depletion of the residual heart-lung machine blood improves postoperative lung gas exchange function and is safe for patients who are expected to have a severe inflammatory response after heart operations.Journal of Thoracic and Cardiovascular Surgery 09/1996; 112(2):494-500. · 3.53 Impact Factor