Effects of leukocyte depletion on cardiopulmonary protection and inflammation after valve surgery.
ABSTRACT To evaluate the effects of leukocyte-depleting filtration on myocardial and pulmonary protection and the inflammatory response in patients undergoing valve surgery.
Fifty-two patients who underwent mitral valve or mitral and aortic valve replacement were randomized into two groups with or without a leukocyte-depleting filter during surgery. The filter was used from 10 minutes before the release of the aortic cross-clamp to the end of cardiopulmonary bypass.
Total leukocyte and neutrophil counts showed a short-term reduction in patients undergoing leukocyte filtration, but there was no significant difference between the two groups during the study. Serum levels of cardiac troponin I were lower than that of the control group (p=0.030). Leukocyte depletion resulted in a significantly higher oxygenation index (p=0.002) and a lower respiratory index (p=0.003) compared with the control group. Serum levels of interleukin-8 were significantly elevated in patients undergoing leukocyte filtration compared with patients without leukocyte filtration (p=0.001). There were no statistically significant differences between the two groups with regards to the concentration of interleukin-6 and TNFα, or the duration of intensive care and hospital stay.
Leukocyte depletion is associated with improved myocardial and lung protection but does not appear to attenuate the inflammatory response in valve surgery.
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ABSTRACT: Acute kidney injury (AKI) after cardiac operations is a serious complication associated with postoperative mortality. Multiple factors contribute to AKI development, principally ischemia-reperfusion injury and inflammatory response. It is well proven that glucocorticoid administration, leukocyte filter application, and miniaturized extracorporeal circuits (MECC) modulate inflammatory response. We conducted a systematic review of randomized controlled trials (RCTs) in which one of these inflammatory system modulation strategies was used, with the aim to evaluate the effects on postoperative AKI. MEDLINE and Cochrane Library were screened through November 2011 for RCTs in which an inflammatory system modulation strategy was adopted. Included were trials that reported data about postoperative renal outcomes. Because AKI was defined by different criteria, including biochemical determinations, urine output, or dialysis requirement, we unified renal outcome as worsening renal function (WRF). We identified 14 trials for steroids administration (931 patients, WRF incidence [treatment vs. placebo]: 2.7% vs. 2.4%; OR: 1.13; 95% CI: 0.53-2.43; P = 0.79), 9 trials for MECC (947 patients, WRF incidence: 2.4% vs. 0.9%; OR: 0.47; 95% CI: 0.18-1.25; P = 0.13), 6 trials for leukocyte filters (374 patients, WRF incidence: 1.1% vs. 7.5%; OR: 0.18; 95% CI: 0.05-0.64; P = 0.008). Only leukocyte filters effectively reduced WRF incidence. Not all cardiopulmonary bypass-related anti-inflammatory strategies analyzed reduced renal damage after cardiac operations. In adult patients, probably other factors are predominant on inflammation in determining AKI, and only leukocyte filters were effective. Large multicenter RCTs are needed in order to better evaluate the role of inflammation in AKI development after cardiac operations.Artificial Organs 07/2013; 38(2). DOI:10.1111/aor.12127 · 1.87 Impact Factor
Journal of cardiothoracic and vascular anesthesia 12/2012; 27(5). DOI:10.1053/j.jvca.2012.09.013 · 1.48 Impact Factor
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ABSTRACT: CONTEXT: Cardiopulmonary bypass (CPB) is a commonly used technique in cardiac surgery but is associated with acute, transient, renal dysfunction that has a negative impact on long-term survival. OBJECTIVE: To unravel the molecular pathogenesis of renal injury following CPB. DESIGN: To obtain insight into the pathogenesis of renal dysfunction following CPB, we performed a microarray analysis of renal gene expression in the rat. SETTING: University Medical Centre Groningen. INTERVENTION: Rats underwent CPB or a sham procedure for 60 min and were sacrificed at 60 min, 1 and 5 days after the procedure. MAIN OUTCOME MEASURES: Renal gene expression profile as determined by microarray analysis. RESULTS: Expression of 420 genes was significantly altered in CPB compared to the sham procedure, and in 407 genes, this was evident in the acute phase (60 min) following CPB. Gene ontology analysis revealed 28 of these genes were involved in inflammatory responses, with high expression of genes downstream of mitogen-activated protein-kinase (MAP-kinase) signalling pathways. Potent inducers identified are from the interleukin-6 cytokine family that consists of interleukin-6 and oncostatin M (OSM), which signal through the gp130-cytokine receptor complex. The plasma concentration of interleukin-6 was hugely increased by CPB as measured by ELISA. Expression of genes downstream of these signalling pathways that lead to production of chemokines, adhesion molecules and molecules involved in coagulative pathways, was upregulated. CONCLUSION: CPB induces an acute and local inflammatory response in the kidney, which might contribute to renal injury. The signalling pathways involved identified by gene expression analysis may represent pharmacological targets to limit renal injury following CPB.European Journal of Anaesthesiology 01/2013; DOI:10.1097/EJA.0b013e32835ce530 · 3.01 Impact Factor