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We present a case of antegrade cerebral perfusion based on a circuit with a centrifugal pump for general open-heart surgery to achieving cerebral protection during a challenging hybrid aortic arch repair. [ABSTRACT FROM AUTHOR]

OBJECTIVES To evaluate if pulsatile cardiopulmonary bypass (CPB) has any protective influence on renal function in elderly patients undergoing aortic valve replacement (AVR). METHODS Forty-six patients (≥75 years old) with aortic valve stenosis underwent AVR with either pulsatile perfusion (PP) or non-pulsatile perfusion (NP) during CPB. Haemodynamic efficacy of the blood pump during either type of perfusion was described in terms of the energy equivalent pressure and the surplus haemodynamic energy. Urine samples were collected before surgery, at sternum closure, and at 2 and 18 h of intensive care unit stay to detect acute kidney injury markers. Perioperative urine levels of N-acetyl-β-d-glucosaminidase (NAG), kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin (NGAL) were assessed together with plasma creatinine, creatinine clearance (CCr) and 24-h haemodynamic monitoring. Normally distributed continuous variables were described as mean ± standard deviation and non-normally distributed data were presented as the median [25th–75th percentiles]. RESULTS PP was characterized by a significantly higher amount of surplus haemodynamic energy transferred to the patients (P < 0.001), with lower mean systemic vascular resistance during CPB (P = 0.020) and during 18 h postoperatively (group-P = 0.018). No difference was found between pre- and postoperative CCr in the PP group (71 ± 23 vs 60 ± 35 ml/min, P = 0.27), while its statistically significant perioperative decrement was observed in the NP group (67 ± 24 vs 45 ± 15 ml/min, P < 0.001). The PP group showed significantly lower urinary levels of NAG at 18 h postoperatively (P = 0.008), and NGAL at sternum closure (P = 0.010), 2 h (P < 0.001) and 18 h (P = 0.015) postoperatively. CONCLUSIONS Short-term PP in elderly patients showed higher safety for renal physiology than NP, resulting in better maintenance of glomerular filtration and lower renal tissue injury. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

OBJECTIVE Improved respiratory outcome has been shown after selective pulsatile pulmonary perfusion (sPPP) during cardiopulmonary bypass (CPB). No contemporary study has analysed the impact of sPPP on alveolar and systemic inflammatory response in humans. METHODS Sixty-four patients undergoing a coronary artery bypass graft (CABG) were randomized to sPPP or standard CPB (32 patients each). An alveolar–arterial oxygen gradient (A-aDO2) was measured preoperatively (T0), at ICU arrival (T1), 3 h postoperatively (T2) and postextubation (T3). The bronchoalveolar lavage (BAL) was collected at T0, T1 and T2. White blood cells (WBCs), neutrophils, mononucleates and lymphocytes in BAL infiltrates were compared between the two groups. A cytokine assay for interleukin-1 (IL-1), IL-8, tumour necrosis factor alpha (TNF-α), monocyte chemotactic protein-1 (MCP-1), growth regulated oncogene-alpha (GRO-α) and interferon (IFN)-γ was collected from the BAL and peripheral blood at the same time-points. Repeated-measure analysis of variance and non-parametric statistics were used to assess the between-group and during time differences. RESULTS The two groups proved comparable for perioperative variables. A-aDO2 proved better after sPPP (group-P = 0.0001; group × time-P < 0.0001). BAL infiltrates after sPPP showed lower WBCs, neutrophils and lymphocytes (group-P = 0.0001, group × time-P = 0.0001 for all) together with higher mononucleates (group-P = 0.0001, group × time-P = 0.0001). Proinflammatory cytokines and chemokine MCP-1 were lower in BAL after sPPP (group-P = 0.005, 0.034, 0.036 and 0.005, and group × time-P = 0.001, 0.009, 0.001 and 0.0001 for IL-1, IL-8, TNF-α and MCP-1, respectively), whereas the immune modulator IFN-γ significantly augmented after sPPP (time-P = 0.0001) but remained stable after the standard CPB (time-P = 0.101, group-P = 001, group × time-P = 0.0001). Indeed, serum cytokines were not different in the two groups during the study (P = NS at single time-points and as a function of time). CONCLUSIONS sPPP attenuates alveolar inflammation, as demonstrated by the lower neutrophilic/lymphocytic alveolar infiltration, and the secretion of anti-inflammatory rather than proinflammatory mediators. [ABSTRACT FROM AUTHOR]