Daly/Cost comparison in the management of peripheral arterial disease at 17 Belgian hospitals.

OBJECTIVE: Peripheral arterial disease (PAD) is a manifestation of atherosclerosis that affects the lower extremities and afflicts more than 200 million people worldwide. Because of limited resources, the need to provide quality care associated with cost control is essential for health policies. Our study concerns an interhospital comparison among seventeen Belgian hospitals that integrates the weighting of quality indicators and the costs of care, from the hospital perspective, for a patient with this pathology in 2018. METHODS: The disability-adjusted life years (DALYs) were calculated by adding the number of years of life lost due to premature death and the number of years of life lost due to disability for each in-hospital stay. The DALY impact was interpreted according to patient safety indicators. We compared the hospitals using the adjusted values ​​of costs and DALYs for their case mix index, obtained by relating the observed value to the predicted value obtained by linear regression. RESULTS: We studied 2,437 patients and recorded a total of 560.1 DALYs in hospitals. The in-hospital cost average [standard deviation (SD)] was €8,673 (€10,893). Our model identified the hospitals whose observed values were higher than predicted; six needed to reduce the costs and impacts of DALYs, six needed to improve one of the two factors, and four seemed to have good results. The average cost (SD) for the worst performing hospitals amounted to €27,803 (€28,358). CONCLUSIONS: Studying the costs of treatment according to patient safety indicators permits us to evaluate the entire chain of care using a comparable unit of measurement.

A rare case of aortic endograft infection by Francisella tularensis: A case report.

INTRODUCTION AND IMPORTANCE: endovascular repair is an alternative to open repair for abdominal aortic aneurysms (AAA), which lowers morbidity and mortality but may presents infectious complications. Endograft infection is a rare but serious life-threatening condition with a mortality rate up to 50 %. We reported a case of aortic endograft infection by Francisella tularensis, rare and highly virulent gram-negative coccobacillus known for use in bioterrorism. CASE PRESENTATION: A 79-year-old man presented with asthenia, weight loss, night sweats and one episode of fever. In 2007, he underwent aorto-bi-iliac endograft repair for AAA without any complication. The diagnostic workup showed some signs of inflammation, but negative blood cultures and no sign of infection on CT scan. The combination of positron emission tomography (PET) and white blood cell (WBC) scintigraphy led to the diagnosis of aortic endograft infection. The management was antimicrobial therapy and surgery. Perioperative analysis shows the presence of Francisella Tularensis. DISCUSSION AND CONCLUSIONS: Aortic endograft infection is a serious complication with a high mortality rate. Its diagnosis may be difficult, but the combination of WBC scintigraphy and PET scan may improve identification of the infection, even if blood cultures and CT scan are negative. The gold standard treatment is removal of the endograft, debridement, and in situ reconstruction along with antibacterial therapy.

Beneficial Effects of Tacrolimus on Brain-Death-Associated Right Ventricular Dysfunction in Pigs.

BACKGROUND: Right ventricular (RV) dysfunction remains a major problem after heart transplantation and may be associated with brain death (BD) in a donor. A calcineurin inhibitor tacrolimus was recently found to have beneficial effects on heart function. Here, we examined whether tacrolimus might prevent BD-induced RV dysfunction and the associated pathobiological changes. METHODS: After randomized tacrolimus (n = 8; 0.05 mg·kg-1·day-1) or placebo (n = 9) pretreatment, pigs were assigned to a BD procedure and hemodynamically investigated 1, 3, 5, and 7 h after the Cushing reflex. After euthanasia, myocardial tissue was sampled for pathobiological evaluation. Seven pigs were used as controls. RESULTS: Calcineurin inhibition prevented increases in pulmonary vascular resistance and RV-arterial decoupling induced by BD. BD was associated with an increased RV pro-apoptotic Bax-to-Bcl2 ratio and RV and LV apoptotic rates, which were prevented by tacrolimus. BD induced increased expression of the pro-inflammatory IL-6-to-IL-10 ratio, their related receptors, and vascular cell adhesion molecule-1 in both the RV and LV. These changes were prevented by tacrolimus. RV and LV neutrophil infiltration induced by BD was partly prevented by tacrolimus. BD was associated with decreased RV expression of the ß-1 adrenergic receptor and sarcomere (myosin heavy chain [MYH]7-to-MYH6 ratio) components, while ß-3 adrenergic receptor, nitric oxide-synthase 3, and glucose transporter 1 expression increased. These changes were prevented by tacrolimus. CONCLUSIONS: Brain death was associated with isolated RV dysfunction. Tacrolimus prevented RV dysfunction induced by BD through the inhibition of apoptosis and inflammation activation.

Tacrolimus Prevents Mechanical and Humoral Alterations in Brain Death-induced Lung Injury in Pigs.

Rationale: Donor brain death-induced lung injury may compromise graft function after transplantation. Establishing strategies to attenuate lung damage remains a challenge because the underlying mechanisms remain uncertain. Objectives: The effects of tacrolimus pretreatment were evaluated in an experimental model of brain death-induced lung injury. Methods: Brain death was induced by slow intracranial infusion of blood in anesthetized pigs after randomization to tacrolimus (orally administered at 0.25 mg ⋅ kg-1 twice daily the day before the experiment and intravenously at 0.05 mg ⋅ kg-1 1 h before the experiment; n = 8) or placebo (n = 9) pretreatment. Hemodynamic measurements were performed 1, 3, 5, and 7 hours after brain death. After euthanasia of the animals, lung tissue was sampled for pathobiological and histological analysis, including lung injury score (LIS). Measurements and Main Results: Tacrolimus pretreatment prevented increases in pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary capillary pressure and decreases in systemic arterial pressure and thermodilution cardiac output associated with brain death. After brain death, the ratio of PaO2 to FiO2 decreased, which was prevented by tacrolimus. Tacrolimus pretreatment prevented increases in the ratio of IL-6 to IL-10, VCAM1 (vascular cell adhesion molecule 1), circulating concentrations of IL-1ß, and glycocalyx-derived molecules. Tacrolimus partially decreased apoptosis (Bax [Bcl2-associated X apoptosis regulator]-to-Bcl2 [B-cell lymphoma-2] ratio [P = 0.07] and number of apoptotic cells in the lungs [P < 0.05]) but failed to improve LIS. Conclusions: Immunomodulation through tacrolimus pretreatment prevented pulmonary capillary hypertension as well as the activation of inflammatory and apoptotic processes in the lungs after brain death; however, LIS did not improve.

Intraspinal Iliac Venous Stent Migration with Lumbar Nerve Root Compression.

BACKGROUND: Venous stenting is a common treatment for chronic peripheral venous disease. The most frequent complications caused by this technique are stent misplacement and intracardiac or intravascular stent migration. In this publication, we will describe the first case of an intraspinal stent misplacement leading to lumbar nerve root compression. CASE DESCRIPTION: Our patient was a 20-year-old woman with a bilateral pulmonary embolism caused by a right common iliac vein thrombosis and a severe compression of the left common iliac vein by the right common iliac artery (May-Thurner or Cockett syndrome). She underwent an endovascular stenting of the left iliac vein. A few days later, she reported some pain in the right L5 radicular and showed signs of hypoesthesia of the left leg and of paresis of the left extensor hallucis longus muscle. A lumbar computed tomography scan showed a stent misplacement into the spinal canal through the left L5 foramen with nerve root compression. She underwent a surgical removal of the stent through a unilateral L5-S1 laminarthrectomy. The postoperative follow-up showed a complete clinical recovery and a control lumbar computed tomography scan confirmed the L5 nerve root decompression. CONCLUSIONS: The intraspinal misplacement of a venous stent is a rare complication that may cause nerve root injury. It requires a prompt treatment. Surgically removing the stent by a posterior approach seems to be a simple and safe therapeutic option.

Robotic lymphadenectomy of an internal mammary lymph node metastasis.

A 58-year-old woman was diagnosed with a left-sided lone internal mammary swollen lymph node on a routine follow-up computer tomography, 42 months after a left mastectomy in the context of a ductal carcinoma grade III. The suspected metastasis was successfully removed in toto using a 3-port-da Vinci robotic procedure and the patient was discharged home without any complication on the third postoperative day. Robotically assisted oncological lymph node removal is safe, easily performed and economically affordable.

Mechanical versus humoral determinants of brain death-induced lung injury.

BACKGROUND: The mechanisms of brain death (BD)-induced lung injury remain incompletely understood, as uncertainties persist about time-course and relative importance of mechanical and humoral perturbations. METHODS: Brain death was induced by slow intracranial blood infusion in anesthetized pigs after randomization to placebo (n = 11) or to methylprednisolone (n = 8) to inhibit the expression of pro-inflammatory mediators. Pulmonary artery pressure (PAP), wedged PAP (PAWP), pulmonary vascular resistance (PVR) and effective pulmonary capillary pressure (PCP) were measured 1 and 5 hours after Cushing reflex. Lung tissue was sampled to determine gene expressions of cytokines and oxidative stress molecules, and pathologically score lung injury. RESULTS: Intracranial hypertension caused a transient increase in blood pressure followed, after brain death was diagnosed, by persistent increases in PAP, PCP and the venous component of PVR, while PAWP did not change. Arterial PO2/fraction of inspired O2 (PaO2/FiO2) decreased. Brain death was associated with an accumulation of neutrophils and an increased apoptotic rate in lung tissue together with increased pro-inflammatory interleukin (IL)-6/IL-10 ratio and increased heme oxygenase(HO)-1 and hypoxia inducible factor(HIF)-1 alpha expression. Blood expressions of IL-6 and IL-1ß were also increased. Methylprednisolone pre-treatment was associated with a blunting of increased PCP and PVR venous component, which returned to baseline 5 hours after BD, and partially corrected lung tissue biological perturbations. PaO2/FiO2 was inversely correlated to PCP and lung injury score. CONCLUSIONS: Brain death-induced lung injury may be best explained by an initial excessive increase in pulmonary capillary pressure with increased pulmonary venous resistance, and was associated with lung activation of inflammatory apoptotic processes which were partially prevented by methylprednisolone.

Influence of Donor Lung Surfactant-A and -B Protein Expression on the Development of Primary Graft Dysfunction After Lung Transplantation: A Pilot Study.

BACKGROUND Primary graft dysfunction (PGD) is responsible of high early mortality in lung transplanted patients. We measured the rate of surfactant proteins in the organ donor, and we observed the occurrence of lung PGD in the recipient. The co-relation between these two parameters was evaluated. MATERIAL AND METHODS In this pilot study, we prospectively collected blood samples and lung biopsies in thirteen donors at the time of recovery of organs before preservation. Gene expression of SP-A, SP-B, SP-D, and CC16 was evaluated by real-time quantitative PCR. Surfactant proteins plasma levels were evaluated by ELISA. Post-transplant assessments included hemodynamic, arterial blood gas measurements, and radiographic evaluation to determine PGD and lung biopsies. RESULTS Nine of the thirteen recipients (69%) developed lung infiltrates and four (31%) developed PGD at either stages 2 or 3. SP-A and SP-B expressions were dramatically reduced in lung allografts of these patients, while lung expression of SP-D and CC16 remained unchanged. Plasma levels of SP-A, SP-B, SP-D, and CC16 did not differ. CONCLUSIONS Primary graft dysfunction may be initiated in the donor. Lung allografts with low lung SP-A and SP-B gene expression prior to implantation are associated with increased incidence of lung infiltrates after transplantation.

Giant true aneurysm of superficial femoral artery in patient with multiple atherosclerotic aneurysms: A case report.

True atherosclerotic aneurysms of superficial femoral artery (SFA) are rare and often associated with other peripheral or aortic aneurysms. We report the case of a 84-year-old patient presenting a giant degenerative ruptured aneurysm of the superficial femoral artery. The patient underwent successful aneurysm resection and bypass grafting, with a satisfying long-term follow-up and patency of the graft. The patient was also operated one year before, for a ruptured aneurysm of the abdominal aorta. This case report is rare, because we described a case of patient with multiple atherosclerotic aneurysms, who present, for the second time, a life threating ruptured aneurysm. In this report, we see extreme and rapid evolution of SFA Aneurysm before being symptomatic. Degenerative aneurysms of the lower extremity most commonly involve the popliteal artery, while they are rarely detected in the femoral region (Leon et al., 2008). In this region, aneurysms most frequently involve the common femoral artery (CFA), whereas true aneurysms of the superficial femoral artery (SFA) represent only 15% to 25% of femoral arterial aneurysms [1-5]. Degenerative aneurysms of the SFA display peculiar characteristics (in terms of clinical onset, diagnostic timing, and clinical behavior) so that they differ from other peripheral aneurysms. Because the relative rarity of this location, our case report can be useful to participate to increase the number of reported cases, and define the therapeutic approach for this rare location.

Roles of inflammation and apoptosis in experimental brain death-induced right ventricular failure.

BACKGROUND: Right ventricular (RV) dysfunction remains the leading cause of early death after cardiac transplantation. Methylprednisolone is used to improve graft quality; however, evidence for that remains empirical. We sought to determine whether methylprednisolone, acting on inflammation and apoptosis, might prevent brain death-induced RV dysfunction. METHODS: After randomization to placebo (n = 11) or to methylprednisolone (n = 8; 15 mg/kg), 19 pigs were assigned to a brain-death procedure. The animals underwent hemodynamic evaluation at 1 and 5 hours after Cushing reflex (i.e., hypertension and bradycardia). The animals euthanized, and myocardial tissue was sampled. This was repeated in a control group (n = 8). RESULTS: At 5 hours after the Cushing reflex, brain death resulted in increased pulmonary artery pressure (27 ± 2 vs 18 ± 1 mm Hg) and in a 30% decreased ratio of end-systolic to pulmonary arterial elastances (Ees/Ea). Cardiac output and right atrial pressure did not change. This was prevented by methylprednisolone. Brain death-induced RV dysfunction was associated with increased RV expression of heme oxygenase-1, interleukin (IL)-6, IL-10, IL-1ß, tumor necrosis factor (TNF)-α, IL-1 receptor-like (ST)-2, signal transducer and activator of transcription-3, intercellular adhesion molecules-1 and -2, vascular cell adhesion molecule-1, and neutrophil infiltration, whereas IL-33 expression decreased. RV apoptosis was confirmed by terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling staining. Methylprednisolone pre-treatment prevented RV-arterial uncoupling and decreased RV expression of TNF-α, IL-1 receptor-like-2, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and neutrophil infiltration. RV Ees/Ea was inversely correlated to RV TNF-α and IL-6 expression. CONCLUSIONS: Brain death-induced RV dysfunction is associated with RV activation of inflammation and apoptosis and is partly limited by methylprednisolone.

Bosentan reverses the hypoxia-induced downregulation of the bone morphogenetic protein signaling in pulmonary artery smooth muscle cells.

AIMS: Pulmonary hypertension (PH) is a common complication of chronic hypoxic lung diseases. Bone morphogenetic protein (BMP) and endothelin-1 signaling pathways have been shown to be altered in hypoxic PH and to play crucial roles in the associated pulmonary artery remodeling. We, therefore, aimed to study the potential link between hypoxia and the alteration of BMP and endothelin-1 signaling observed in pulmonary artery smooth muscle cells (PA-SMCs) in hypoxic PH. MATERIALS AND METHODS: Human PA-SMCs were treated with hypoxia-mimetic agent cobalt chloride (CoCl2; 100µM), with or without pretreatment with a dual endothelin receptor antagonist bosentan (10µM). Expressions of preproendothelin-1 (PPET1), BMP type 2 receptor (BMPR-2), and one BMP signaling target gene, the inhibitor of DNA binding 1 (ID1) were evaluated by real time quantitative polymerase chain reaction. BMP2-treated PA-SMCs were assessed for Smad1/5/8 signaling activation by Western Blotting. KEY FINDINGS: Treatment of PA-SMCs with CoCl2 increased PPET1 gene expression, while it did not alter expressions of endothelin converting enzyme, endothelin receptor type A or type B. Hypoxia-mimetic agent CoCl2 decreased the expressions of BMPR-2 and ID1 maximally after 3- and 6-hour treatment respectively, while CoCl2 treatment progressively increased noggin expression. Bosentan pretreatment restored expressions of BMPR-2 and ID1, as well as the activation (by phosphorylation) of Smad1/5/8 signaling induced by BMP2. SIGNIFICANCE: Hypoxia induces the downregulation of the BMP signaling in PA-SMCs, at least, partly through the endothelin system. In hypoxic PH, increased endothelin-1 production might therefore contribute to the altered BMP signaling and subsequent PA-SMC hyperplasia.

Myocardial inflammation in experimental acute right ventricular failure: Effects of prostacyclin therapy.

BACKGROUND: Acute transient pulmonary hypertension may induce a state of persistent right ventricular (RV) failure. We hypothesized that this could be related to an activation of inflammatory processes and reduced by prostacyclin therapy. METHODS: Sixteen dogs were assigned to a 90-minute pulmonary artery banding (n = 8), or to a sham operation (n = 8). Hemodynamic variables were measured 30 minutes after banding release. This was repeated in 7 dogs with pulmonary artery banding-induced RV failure, followed by a 60-minute epoprostenol infusion. After euthanasia of the animals, myocardial tissue was sampled. RESULTS: Persistent RV failure was associated with increased myocardial expression of interleukin (IL)-1ß, IL-6, monocyte chemoattractant protein 1, pro-inflammatory IL-6/IL-10, and neutrophil and macrophage infiltration, whereas heme oxygenase 1 expression was decreased. These changes were observed in RV and to a lesser extent in the left ventricle (LV). In the RV only, expressions of prostacyclin synthase and anti-inflammatory IL-10 and IL-33 decreased and vascular cell adhesion molecule expression increased, whereas macrophage inflammatory protein-1α and intercellular adhesion molecule 1 expressions remained unchanged. After epoprostenol infusion, there was decreased expression of IL-1ß, macrophage inflammatory protein-1α, and vascular cell adhesion molecule 1 and increased IL-10 expression in the RV and the LV, whereas monocyte chemoattractant protein-1 decreased in the RV only. Epoprostenol infusion resulted in decreased RV IL-6/IL-10 and pro-apoptotic Bax/Bcl-2, together with decreased RV neutrophil and RV and LV macrophage infiltration. The RV ratio of end systolic-to-pulmonary arterial elastances was inversely correlated to RV IL-6/IL-10, macrophage, and neutrophil infiltration, and to RV heme oxygenase-1 and IL-33 expression. CONCLUSIONS: Acute afterload-induced persistent RV failure is associated with an activation of inflammatory processes, which are limited by epoprostenol.

Endothelin-Bone morphogenetic protein type 2 receptor interaction induces pulmonary artery smooth muscle cell hyperplasia in pulmonary arterial hypertension.

BACKGROUND: Endothelin receptor antagonists improve pulmonary arterial hypertension (PAH). Mutations in the bone morphogenetic protein (BMP) type 2 receptor (BMPR2) predispose to PAH. Here, we sought to determine whether there might exist interactions between these 2 signaling pathways and their effect on the acquisition of the altered phenotype of pulmonary artery smooth muscle cells (PA-SMCs) observed in PAH. METHODS: Expression of BMPR2, of the BMP agonist BMP4, and of the BMP antagonists gremlin1 and gremlin2 was evaluated in lungs and in PA-SMCs from 6 PAH patients and 14 controls treated with endothelin-1. Endothelin-1 pre-treated PA-SMCs were assessed for proliferation, apoptosis, and downstream signaling activation of Smad1/5/8 and p38 mitogen-activated protein kinase (p38(MAPK)) after BMP2 treatment. RESULTS: In PA-SMCs from PAH patients, expression of BMPR2 and BMP4 decreased, whereas expression of gremlin1 and gremlin2 increased compared with controls. Treatment of control PA-SMCs with endothelin-1 induced a dose-dependent increase in gremlin1 and gremlin2, whereas BMPR2 and BMP4 expression decreased, reaching similar levels as those observed in PAH cells. In control PA-SMCs, endothelin-1 pre-treatment reduced inhibitor of DNA binding 1 (Id1) expression and Smad1/5/8 activation induced by BMP2, whereas it enhanced p38(MAPK) activation. Moreover, BMP2 decreased serum-induced proliferation and increased the pro-apoptotic Bax/Bcl-2 ratio. These effects were attenuated by endothelin-1 pre-treatment. Endothelin-1 did not alter BMPR2 signaling in PA-SMCs from PAH patients. CONCLUSIONS: Endothelin-1 downregulates canonical BMPR2 signaling. This is related to decreased BMPR2 and increased anti-BMP gremlin expression associated with increased activation of p38(MAPK) and results in PA-SMC proliferation.

Vancomycin population pharmacokinetics during extracorporeal membrane oxygenation therapy: a matched cohort study.

INTRODUCTION: The aim of this study was to describe the population pharmacokinetics of vancomycin in critically ill patients treated with and without extracorporeal membrane oxygenation (ECMO). METHODS: We retrospectively reviewed data from critically ill patients treated with ECMO and matched controls who received a continuous infusion of vancomycin (35 mg/kg loading dose over 4 hours followed by a daily infusion adapted to creatinine clearance, CrCl)). The pharmacokinetics of vancomycin were described using non-linear mixed effects modeling. RESULTS: We compared 11 patients treated with ECMO with 11 well-matched controls. Drug dosing was similar between groups. The median interquartile range (IQR) vancomycin concentrations in ECMO and non-ECMO patients were 51 (28 to 71) versus 45 (37 to 71) mg/L at 4 hours; 23 (16 to 38) versus 29 (21 to 35) mg/L at 12 hours; 20 (12 to 36) versus 23 (17-28) mg/L at 24 hours (ANOVA, P = 0.53). Median (ranges) volume of distribution (Vd) was 99.3 (49.1 to 212.3) and 92.3 (22.4 to 149.4) L in ECMO and non-ECMO patients, respectively, and clearance 2.4 (1.7 to 4.9) versus 2.3 (1.8 to 3.6) L/h (not significant). Insufficient drug concentrations (that is drug levels < 20 mg/dL) were more common in the ECMO group. The pharmacokinetic model (non-linear mixed effects modeling) was prospectively validated in five additional ECMO-treated patients over a 6-month period. Linear regression analysis comparing the observed concentrations and those predicted using the model showed good correlation (r(2) of 0.67; P < 0.001). CONCLUSIONS: Vancomycin concentrations were similar between ECMO and non-ECMO patients in the early phase of therapy. ECMO treatment was not associated with significant changes in Vd and drug clearance compared with the control patients.

Heme oxygenase-1 and inflammation in experimental right ventricular failure on prolonged overcirculation-induced pulmonary hypertension.

Heme oxygenase (HO)-1 is a stress response enzyme which presents with cardiovascular protective and anti-inflammatory properties. Six-month chronic overcirculation-induced pulmonary arterial hypertension (PAH) in piglets has been previously reported as a model of right ventricular (RV) failure related to the RV activation of apoptotic and inflammatory processes. We hypothesized that altered HO-1 signalling could be involved in both pulmonary vascular and RV changes. Fifteen growing piglets were assigned to a sham operation (n = 8) or to an anastomosis of the left innominate artery to the pulmonary arterial trunk (n = 7). Six months later, hemodynamics was evaluated after closure of the shunt. After euthanasia of the animals, pulmonary and myocardial tissue was sampled for pathobiological evaluation. Prolonged shunting was associated with a tendency to decreased pulmonary gene and protein expressions of HO-1, while pulmonary gene expressions of interleukin (IL)-33, IL-19, intercellular adhesion molecule (ICAM)-1 and -2 were increased. Pulmonary expressions of constitutive HO-2 and pro-inflammatory tumor necrosis factor (TNF)-α remained unchanged. Pulmonary vascular resistance (evaluated by pressure/flow plots) was inversely correlated to pulmonary HO-1 protein and IL-19 gene expressions, and correlated to pulmonary ICAM-1 gene expression. Pulmonary arteriolar medial thickness and PVR were inversely correlated to pulmonary IL-19 expression. RV expression of HO-1 was decreased, while RV gene expressions TNF-α and ICAM-2 were increased. There was a correlation between RV ratio of end-systolic to pulmonary arterial elastances and RV HO-1 expression. These results suggest that downregulation of HO-1 is associated to PAH and RV failure.

Extracorporeal life support associated with hypothermia and normoxemia in refractory cardiac arrest.

AIM: We describe a 1-year experience with extracorporeal cardiopulmonary resuscitation (ECPR) for in-hospital (IHCA) and out-of-hospital cardiac arrest (OHCA) associated with intra-arrest hypothermia and normoxemia. METHODS: Since January 1st 2012, ECPR has been applied in our hospital to all patients less than 65 years of age and without major co-morbidities who develop refractory cardiac arrest (CA) with bystander CPR. Over a 1-year period of observation, we recorded 28-day survival with intact neurological outcome and the rate of organ donation. RESULTS: During the observational period, 24 patients were treated with ECPR, with a median age of 48 years. Ten patients had IHCA. Acute coronary syndrome and/or major arrhythmias were the main cause of arrest. Intra-arrest cooling was used in 17 patients; temperature on ECMO initiation in these patients was 32.9 °C [32-34]. The time from collapse to ECPR was 58 min [45-70] and was shorter in survivors than in non-survivors (41 min [39-58] vs. 60 min [55-77], p=0.059). Non-survivors were more likely to have coagulopathy and received more blood transfusions. Six patients (25%) survived with good neurological outcome at day 28. Four patients with irreversible brain damage had organ function suitable for donation. CONCLUSION: ECPR provided satisfactory survival rates with good neurologic recovery in refractory CA for both IHCA and OHCA. ECMO may help rapidly stabilise systemic haemodynamic status and restore organ function.

Actual knowledge of systemic inflammation reaction during cardiopulmonary bypass.

Systemic inflammation response is a complex physiopathological host response following aggression. This phenomenon is well described during cardiac surgery under cardiopulmonary bypass but also in the context of off-pump cardiac surhery. The goal of this article is to review the different mechanisms involved in the systemic inflammation response, abusively called "systemic inflammatory response syndrome". The article will describe the different component of this response with a clear definition of different pathways found in this process. The possible relation between systemic inflammation and postoperative outcome will be described. The different therapeutic and prophylactic options evaluated to decrease the systemic inflammation reaction will be summarized.