Key result
Leukocyte filtration of blood cardioplegia reduced Troponin I at reperfusion compared to standard cold blood cardioplegia (2.4 vs. 5.1 μg/l, P=0.0001) without improving hemodynamics.
Why the study?
Does leukocyte filtration of blood cardioplegia reduce myocardial injury and inflammation in patients undergoing isolated aortic valve replacement?
RCT (n=30)
Does leukocyte filtration of blood cardioplegia reduce myocardial injury and inflammation in patients undergoing isolated aortic valve replacement?
Absolute Event Rate: 2.4% vs 5.1%
p-value: p=0.0001
Leukocyte filtration of blood cardioplegia attenuates myocardial ischemia/reperfusion injury and inflammation during aortic valve replacement, though without improving perioperative hemodynamics.
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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Onorati et al. (2012) conducted an RCT in isolated aortic valve replacement (n=30). Leukocyte filtration of blood cardioplegia vs. Standard cold blood cardioplegia was evaluated on Troponin I (TnI) from the coronary sinus at reperfusion (p=0.0001). Leukocyte filtration of blood cardioplegia reduced Troponin I at reperfusion compared to standard cold blood cardioplegia (2.4 vs. 5.1 μg/l, P=0.0001) without improving hemodynamics.
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