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High-dose remifentanil (1-5 microg kg-1 min-1), commonly used for cardiac surgery, has been associated with muscle rigidity, hypotension, bradycardia, and reduced cardiac output. The aim of this study was to determine an optimal lower remifentanil dose, which should be accompanied by fewer adverse events, that still effectively suppresses haemodynamic responses to typical stressful stimuli (i.e. intubation, skin incision, and sternotomy).Total i.v. anaesthesia consisted of a target-controlled propofol (2 microg ml-1) and a remifentanil infusion. Forty patients were allocated to receive either a constant infusion of remifentanil at 0.1 microg kg-1 min-1 or up-titrations to 0.2, 0.3, or 0.4 microg kg-1 min-1, respectively, 5 min before each stimulus. Subsequently, changes in heart rate and mean arterial blood pressure were recorded for 8 min. Increases exceeding 20% of baseline were considered to be of clinical relevance. Patients who exhibited these alterations were termed responders.The number of responders was less with the two higher remifentanil dosages (P0.05) while propofol target doses could either be kept at the same level or even be reduced without affecting the plane of anaesthesia. Although single phenylephrine bolus had to be applied more frequently in these two groups (P0.05), no severe haemodynamic depression was observed.Remifentanil at 0.3 and 0.4 microg kg-1 min-1 in combination with a target-controlled propofol infusion in the pre-bypass period is well tolerated. It appears to mitigate potentially hazardous haemodynamic responses from stressful stimuli equally well as higher doses when compared with data from the literature.

To determine the degree of neurocognitive dysfunction after placement of internal cardioverter defibrillators (ICD) and its relationship to the extent of neuronal injury, we studied 42 patients undergoing ICD (n = 21) or pacemaker (PM) insertion (control patients, n = 21). The Mini Mental State Examination, the Trailmaking A test and the forward and backward Digit Span tests were used and P300 latencies were determined preoperatively and postoperatively. Serum neuron-specific enolase (NSE) was determined before and at the end of, as well as 2, 6, and 24 h after surgery. Preoperatively, PM patients scored worse in the Digit Span backward and the Trailmaking tests and showed prolonged P300 latencies. Postoperatively, the Digit Span backward scores declined and NSE levels increased only in the ICD group (P < or = 0.05). The difference between preoperative and postoperative Digit Span backward scores correlated with the increase in serum NSE levels (r2 = 0.3, P < or = 0.05). Moreover, P300 latencies increased in 13 of 17 ICD patients, but decreased in 7 of 10 PM patients (P < or = 0.05). PM patients even improved in the Trailmaking test (P < or = 0.05). Neuronal injury from even brief periods of global brain ischemia seems to be associated with deteriorating neurocognitive function.

Magnesium is a calcium and an NMDA-receptor antagonist and can modify important mechanisms of nociception. We evaluated the co-analgesic effect of magnesium in the postoperative setting after on-pump cardiac surgery.Forty patients randomly received either magnesium gluconate as an i.v. bolus of 0.21 mmol kg(-1) (86.5 mg kg(-1)) followed by a continuous infusion of 0.03 mmol(-1) kg(-1) h(-1) (13.8 mg kg(-1) h(-1)) or placebo for 12 h after tracheal extubation. After surgery, remifentanil was decreased to 0.05 microg kg(-1) min(-1) and titrated according to a pain intensity score (PIS, range 1-6) in the intubated, awake patient and a VAS scale (range 1-100) after extubation. If PIS wasor =3 or VASor =30, the infusion was increased by 0.01 microg kg(-1) min(-1); if ventilatory frequency wasor =10 min(-1) it was decreased by the same magnitude.Magnesium lowered the cumulative remifentanil requirement after surgery (P0.05). PISor =3 was more frequent in the placebo group (P0.05). Despite increased remifentanil demand, VAS scores were also higher in the placebo group at 8 (2 vs 8) and 9 h after extubation (2 vs 7) (P0.05). Dose reductions attributable to a ventilatory frequencyor =10 min(-1) occurred more often in the magnesium group (17 vs 6; P0.05). However, time to tracheal extubation was not prolonged.Magnesium gluconate moderately reduced the remifentanil consumption without serious side-effects. The opioid-sparing effect of magnesium may be greater at higher pain intensities and with increased dosages.

In contrast to pretreatment with isoflurane its benefit when applied during reperfusion in rat hearts was only modest. As cellular injury during reoxygenation is greatly determined by sarcoplasmic reticulum (SR) calcium [Ca2+] handling we investigated the effect of isoflurane after simulated ischemia in rat ventricular myocytes. Hypoxic metabolic inhibition was induced by exposure to an acidic medium (pH: 6.3) containing deoxyglucose. Ambient pO2 was reduced to

Although hypercholesterolemia is a strong risk factor for cardiovascular disease, it has in some instances paradoxically been associated with reduced infarct size and preserved contractile function in isolated hearts after ischemia and reperfusion. To elucidate potential cellular protective mechanisms, myocytes of hypercholesterolemic apolipoprotein E-deficient (ApoE−/−) and wild-type mice were subjected to hypoxic metabolic inhibition (I) with subsequent reoxygenation (R). Intracellular Ca2+concentration ([Ca2+]i) and pH (pHi) were monitored as well as cell length and arrhythmic events. Force measurements in papillary muscles were also recorded, and myocardial expression of Na+/H+exchanger 1 (NHE1) and three Ca2+handling proteins [sarco(endo)plasmic reticulum Ca2+-ATPase, Na+/Ca2+exchanger, and plasma membrane Ca2+-ATPase] was quantified. After 30 min of I and 35 min of R, Ca2+overload was more pronounced in wild-type cells ( P < 0.05). In these myocytes, pHialso dropped faster and remained below those values determined in ApoE−/−cells ( P < 0.05). Furthermore, more wild-type myocytes remained in a contracted state ( P < 0.05). This group also showed a higher incidence of arrhythmic events during R ( P < 0.05). No group difference was found in the expression of the Ca2+handling proteins. However, NHE1 protein was downregulated in hearts of ApoE−/−mice ( P < 0.05). Histological results depict hyperplasia in ApoE−/−hearts without atherosclerosis of the coronaries. Contractile dysfunction was not observed in papillary muscles from ApoE−/−hearts. Our results suggest that downregulated myocardial NHE1 expression in hypercholesterolemic ApoE−/−mice could have contributed to increased tolerance to I/R. It remains to be elucidated whether NHE1 downregulation is a unique feature of these genetically altered animals.

Remifentanil, a short-acting opioid, is commonly used in cardiac anesthesia. In this study we sought to demonstrate the feasibility of pain treatment and to determine the remifentanil dose necessary for adequate analgesia in tracheally extubated patients after cardiac surgery. Thirty patients undergoing elective cardiac surgery were included in this study. After surgery, the intraoperatively administered remifentanil was initially continued at 0.05 microg . kg(-1) . min(-1). Before tracheal extubation, a nonsteroidal antiinflammatory drug was administered and remifentanil was reduced to 0.035 microg . kg(-1) . min(-1). Pain assessment using a visual analog scale (VAS) was performed after tracheal extubation, in 2-min intervals for 10 min, every 10 min until the end of the first hour and every 30 min during the ensuing 5 h. A VAS score > or =30 or a respiratory rate

We conducted a Medline search for controlled studies evaluating currently available drugs for pharmacological neuroprotection. They had to be administered prior to transient global cerebral ischaemia without further non-pharmacological measures. We deliberately excluded focal ischaemia since its pathophysiology is substantially different from global ischaemia. A total of 45 articles conducted exclusively in laboratory animals met these criteria. The following classes of agents were evaluated: anaesthetics, GABAergic drugs, calcium-antagonists, anticonvulsives, sodium-channel blockers, potassium-channel activators, NMDA-receptor antagonists, hormones, vasodilators, dopamineand 2-agonists, magnesium, xanthine oxidase- and cyclooxygenase inhibitors, a nootropic, a protease inhibitor, and immunosuppressants. Some of them were applied chronically and others administered via clinically impracticable routes. The available literature favours isoflurane, phenytoin, lamotrigine, magnesium, and potentially, nimodipine, and flunarizine. If factors like costs, toxicity, side effects, route and mode of application are considered, isoflurane and MgSO 4 that have also been safely applied to patients with compromised left ventricular pump function are advantageous but their true role in human neuroprotection remains unclear. © 2004 Elsevier Ireland Ltd. All rights reserved.

OBJECTIVE Repeated induction of ventricular fibrillation with ensuing alterations in electroencephalogram and jugular venous oxygen saturation is common practice during insertion of transvenous implantable cardioverters/defibrillators. We investigated whether these functional changes are also associated with cerebral injury. DESIGN Prospective study. SETTING University hospital. PATIENTS We studied 45 patients undergoing implantable cardioverter/defibrillator insertion. Eleven patients with cardiac pacemaker implantation, which was performed in the same manner yet without the necessity to induce ventricular fibrillation, served as controls. MEASUREMENTS AND MAIN RESULTS Serum neuron-specific enolase and S100 were determined before, immediately postoperatively, and 2 hrs postoperatively. In a randomly composed subgroup, neuron-specific enolase was also determined 6 and 24 hrs after surgery. Implantable cardioverter/defibrillator patients only showed an increase of both markers postoperatively. Median neuron-specific enolase values climbed from a preoperative 9.9 to 12.3 and 14.4 microg/L at 2 and 24 hrs after surgery, respectively. This increase was associated with the number of shocks and the cumulative time in circulatory arrest. The highest median S100 level (0.075 microg/L) was reached 2 hrs after the procedure. Neuron-specific enolase and S100 were extremely elevated (13.7 and 0.970 microg/L, respectively) in one patient after an extended episode of ventricular fibrillation. Plasma hemoglobin levels were in the normal range in implantable cardioverter/defibrillator patients throughout the observation period. CONCLUSIONS Apparently, even brief successive periods of global cerebral ischemia cause neuronal damage without obvious severe neurologic deficits. However, they may be related to subtle postoperative neurologic or cognitive dysfunctions that a number of implantable cardioverter/defibrillator patients exhibit after implantation.

Asymptomatic carotid artery stenosis (CAS) may result in neurological injury after coronary artery bypass surgery, but routine preoperative carotid screening is not undisputed. We studied whether routinely determined carotid duplex results, beyond detecting high-risk patients, additionally influence intraoperative course. One hundred and eight patients without new signs of impaired cerebral circulation were investigated. Anesthesiology, perfusionist records, and patient files were reviewed for patient characteristics, intraoperative variables and postoperative neurological sequelae. There was a higher incidence of prior cerebrovascular events and peripheral artery disease in CAS patients (p B /0.05). Pulsatile flow was employed more frequently in this group (p B /0.05). Severe hyperventilation, hyperglycemia, hemodilution, hyperthermia, and lactacidosis were avoided in both groups. However, labile hemodynamics of CAS patients required more corrective interventions (p B /0.05). There was also a tendency toward greater mortality. Stroke and transient ischemic attack (TIA) occurred in two patients without CAS. Since CAS was associated with a greater degree of cardiovascular instability requiring frequent measures to control hemodynamics, positive duplex results should heighten vigilance. Although CAS does not appear to be the major source of cerebral ischemia, it involves significant comorbidity.

Impaired heart rate variability (HRV) has been described postoperatively. Diminished HRV may be related to myocardial ischemia and potentially causes circulatory instability. Cardiac ischemic events and a compromised cardiovascular function are not uncommon after aortic surgery. Circadian variation of HRV seems to be a prognostically more important parameter than HRV itself with respect to the development of cardiac dysfunction. We therefore investigated whether the diurnal rhythm of HRV is simultaneously altered postoperatively and the potential contribution of myocardial ischemia. After approval by the hospital ethics committee and having obtained informed consent, we studied 11 consecutive male patients undergoing elective aortic surgery. Patients were monitored with a Holter-ECG perioperatively. Spectral HRV measures (total, low, and high frequency power) were determined and night/day ratios calculated. Ischemic ECG changes were recorded and serum was sampled for troponin T analysis. A remarkable decline in circadian variation accompanied the decrease in all HRV parameters postoperatively. Five patients showed ECG changes suggestive of myocardial ischemia and two had increased levels of troponin T. These two patients showed greatly diminished HRV postoperatively with a similarly reduced circadian rhythm. We have demonstrated that the circadian rhythm of HRV is not preserved after aortic surgery. Diminished diurnal variability seems to be a general manifestation and myocardial ischemia may just be one contributing factor. An altered biorhythm in combination with stress related changes in the neuroendocrine system after surgery most likely have a more significant influence on the circadian rhythm of HRV.

Jean-Luc Diehl The French Intensive Care Society organized on 5th and 6th June 2014 its 4th “Paris International Conference in Intensive Care”, whose principle is to bring together the best international experts on a hot topic in critical care medicine. The 2014 theme was “Breakthrough in cardiac arrest”, with many high-quality updates on epidemiology, public health data, pre-hospital and in-ICU cares. The present review includes short summaries of the major presentations, classified into six main chapters:Epidemiology of CAPre-hospital managementPost-resuscitation management: targeted temperature managementPost-resuscitation management: optimizing organ perfusion and metabolic parametersNeurological assessment of brain damagesPublic healthcare, SCOPUS: re.j, info:eu-repo/semantics/published

Summary Reparixin, a CXCR 1/2 antagonist, has been shown to mitigate ischaemia–reperfusion injury (IRI) in various organ systems in animals, but data in humans are scarce. The aim of this double-blinded, placebo-controlled pilot study was to evaluate the safety and efficacy of reparixin to suppress IRI and inflammation in patients undergoing on-pump coronary artery bypass grafting (CABG). Patients received either reparixin or placebo (n = 16 in each group) after induction of anaesthesia until 8 h after cardiopulmonary bypass (CPB). We compared markers of systemic and pulmonary inflammation, surrogates of myocardial IRI and clinical outcomes using Mann–Whitney U- and Fisher's exact tests. Thirty- and 90-day mortality was 0% in both groups. No side effects were observed in the treatment group. Surgical revision, pleural and pericardial effusion, infection and atrial fibrillation rates were not different between groups. Reparixin significantly reduced the proportion of neutrophil granulocytes in blood at the beginning [49%, interquartile range (IQR) = 45–57 versus 58%, IQR = 53–66, P = 0·035], end (71%, IQR = 67–76 versus 79%, IQR = 71–83, P = 0·023) and 1 h after CPB (73%, IQR = 71–75 versus 77%, IQR = 72–80, P = 0·035). Reparixin patients required a lesser positive fluid balance during surgery (2575 ml, IQR = 2027–3080 versus 3200 ml, IQR = 2928–3778, P = 0·029) and during ICU stay (2603 ml, IQR = 1023–4288 versus 4200 ml, IQR = 2313–8160, P = 0·021). Numerically, more control patients required noradrenaline ≥ 0·11 μg/kg/min (50 versus 19%, P = 0·063) and dobutamine (50 versus 25%, P = 0·14). Therefore, administration of reparixin in CABG patients appears to be feasible and safe. It concurrently attenuated postoperative granulocytosis in peripheral blood.

As known from patients with pulsatile ventricular assist devices (VADs), early mobilization, physical exercise, and return to normal life are essential for optimal recovery. Recently, implantable rotary pumps became available for extended left ventricular support as bridges to transplantation. Modified procedures are essential for patient training and hospital discharge. The MicroMed-DeBakey VAD was implanted in 10 patients with end-stage heart disease. After recovery, regular ergometer training was performed with loads adapted to the patient's condition. Procedures for patient observation under outdoor conditions and a blood pressure measuring device for low pulse pressure conditions were developed. Improvement of physical condition was achieved in 8 patients. In the first 2 patients, exercise capacity was limited due to flow obstruction. In the following patients, an increase of workload on the ergometer up to 120 W was observed. Correlated with training, lactate/load relationship and heart rate decreased. Three patients were discharged from the hospital during support. The DeBakey-VAD system can support patients for extended time periods and is suitable for recovery and exercise. Under optimal patient and environmental conditions, discharge from the hospital can be obtained.

OBJECTIVES: Cardiopulmonary bypass (CPB) is known to induce a short pro- and long-lasting anti-inflammatory immune response. The anti-inflammatory protein soluble ST2 (sST2) may be involved in the pathogenesis of postoperative immune dysfunction. We investigated whether continued mechanical ventilation during CPB has an impact on postoperative serum sST2 and cytokine release. METHODS: Thirty patients undergoing conventional coronary artery bypass graft (CABG) operation were randomized into a ventilated on CPB (VG; n = 15) and non-ventilated on CPB group (NVG; n = 15). Blood samples were drawn at the beginning and at the end of surgery, and at the 5 consecutive days. sST2, IL-4, IL-10, IgM, IgG, IL-6 and endotoxin were measured by ELISA. Data are given as mean standard deviation (SD). A Mann–Whitney U-test was used for statistical analysis. RESULTS: Serum levels of sST2 and IL-10 were significantly higher in the NVG when compared with the VG at the first postoperative day (POD-1) [sST2 pg/ml: 1366.4 (433) (VG) vs 2296.3 (1795.5) (NVG) P = 0.029; IL-10 pg/ml: 10.7 (4.0) (VG) vs 15.4 (6.8) (NVG) P = 0.038]. In addition, the secretion of proinflammatory IL-6 was slightly reduced in the VG at POD-1 [IL-6 pg/ml: 83.1 (52.5) (VG) vs 110.2 (42.3) (NVG) P = 0.033]. IL-4, endotoxin, IgM and IgG showed no differences between groups. CONCLUSION: These data suggest that continued mechanical ventilation during CABG attenuates inflammatory and anti-inflammatory immune responses after CPB. Continued mechanical ventilation may have beneficial effects in the attenuation of the CPB-induced immune activation.

We report a case of a child with familial cardiomyopathy who contracted H1N1 influenza followed by cardiovascular collapse requiring immediate arteriovenous ECMO support. Despite the lack of experience with heart transplantation (HTx) soon after H1N1 infection, HTx was considered as an exit strategy since restoration of cardiac function was considered unlikely. In contrast to the most common indication for ECMO use in patients with H1N1 infection, early ECMO support in cases with infection-induced myocardial decompensation may be lifesaving. Additionally, this report shows that urgent heart transplantation in a patient on ECMO support can be performed safely after recent H1N1 infection and simultaneous heparin-induced thrombocytopenia, which has not been reported before. This case also indicates that H1N1 vaccination should be considered for potential transplantation candidates to prevent severe infection.

To study the cause of myocardial injury after elective transvenous insertion of a cardioverter/defibrillator, we measured troponin T (TnT) release in 27 patients. Five patients needing only replacement of the generator with threshold testing served as controls. Compared to the control group, a significant increase in TnT occurred in the patients undergoing insertion, which was greatest in the group receiving screw-in electrodes. There was no correlation between TnT and the number and energy of the shocks and the time in fibrillation. Duration of surgery and TnT release were positively associated. Cardiac injury therefore mainly results from mechanical trauma during insertion of the electrodes and only to a lesser degree from electrical and ischemic lesions.

We describe an instructive case of a 79-year-old patient with a giant coronary aneurysm and a second smaller aneurysm with an uncommon symptomatology. Giant coronary artery aneurysms (>2 cm diameter) are rare pathologic entities with a prevalence of 0.02%. They either can be congenital malformations or are atherosclerotic in origin. Although spontaneous rupture of giant coronary artery aneurysms has been reported, they generally remain silent or induce myocardial ischemia. Our patient, however, showed no signs of myocardial malperfusion but transient position-dependent pre-syncope. The cardiologic work-up and the intraoperative considerations regarding patient management are described. During surgery, manipulation of the giant coronary artery aneurysm caused impairment of right ventricular function and regional wall hypokinesia, as assessed by transesophageal echocardiography. Venous cannulation of the right atrium was thus abandoned and extracorporeal circulation was established via the femoral vein. Subsequent dissection and surgical repair were uneventful and further recovery of the elderly patient was uncomplicated. This case underlines that once the diagnosis is established, proper perioperative management enables successful surgical treatment even of patients of advanced age.

Introduction: Chronic obstructive pulmonary disease (COPD) is a worldwide burden and a major cause of death. The disease is accompanied by chronic inflammation and increased cellular turnover that is partly due to an overwhelming induction of apoptosis. In this study, we hypothesized that systemic markers of apoptosis are altered in patients with mild‐to‐severe COPD. Materials and Methods: A total number of 64 patients and controls were enrolled in the study. Lung function parameters of all groups (nonsmoker, healthy smoker, COPD GOLD I&II, COPD GOLD III&IV) were evaluated at the time of inclusion. Enzyme‐linked immunosorbent assays were used to quantify protein levels in serum samples. Results: Serum contents of apoptotic end‐products caspase‐cleaved cytokeratin‐18 and histone‐associated‐DNA‐fragments were increased in patients with COPD, whereas anti‐inflammatory soluble ST2 showed a peak in patients with COPD I&II (P=0.031) compared to healthy smokers. Levels of pro‐inflammatory caspase‐1/ ICE correlated significantly with the number of pack years (R=0.337; P=0.007). Discussion: Our results indicate a systemic release of apoptosis‐specific proteins as markers for increased cellular turnover accompanied by progression of COPD. Furthermore, soluble ST2 seems to have a critical role in the anti‐inflammatory regulatory mechanism at early stages of the disease. J. Clin. Lab. Anal. 23:372–379, 2009. © 2009 Wiley‐Liss, Inc.

BACKGROUND Cardiopulmonary bypass is known to affect cytokine release leading to a generalized endogenous immune reaction similar to that described in sepsis, without having been explored in great detail. Therefore we evaluated the anti- and pro-inflammatory cytokine responses after heart surgery. METHODS 16 patients who underwent coronary artery bypass graft (CABG) surgery with extracorporeal circulation were included. ST2, IL-4 and IL-10 served as markers for TH2 cytokine response; IL-6, IL-8 and IFN-gamma as TH1 markers. Furthermore, total immunoglobulin subtype analysis (IgM, IgG, IgE) was performed. RESULTS Serum levels of soluble ST2 started to climb at 60 minutes (from 38 +/- 14 preoperatively to 1 480 +/- 890 pg/ml) and peaked 24 hours after surgery (13 360 +/- 2 840 pg/ml, P < 0.001). IL-10 reached a maximum at 60 minutes and returned to baseline levels 24 hours later. IL-6 and IL-8 levels peaked 60 minutes after surgery. IL-4 and IFN-gamma did not change. Only IgM showed a significant peak on day eight ( P < 0.001). CONCLUSION Our results demonstrate that CABG surgery induces a massive long-lasting secretion of ST2, a protein related to immune suppression.

Thromboembolic and bleeding complications in outpatients with a left ventricular assist device are common and can be detrimental. A meticulous balance between anticoagulant and procoagulant factors is therefore crucial. However, in contrast to routinely performed plasmatic coagulation tests, platelet function is hardly ever monitored although recent reports indicated platelet dysfunction. We therefore differentially evaluated platelet function with four commonly used point-of-care devices.In a cross-sectional design platelet function was assessed in 12 outpatients and 12 healthy matched volunteers using thrombelastography platelet mapping, thromboelastometry, platelet function analyzer, and a new whole blood aggregometer (Multiplate).Phenprocoumon produced an international normalized ratio of 3.5. It was associated with a twofold prolongation in the thromboelastometry clotting time (p0.001). Platelet function under high shear was severely compromised: collagen adenosine diphosphate closure times were 2.5-fold longer in patients than in volunteers (p0.001), and 50% of patients had maximal collagen adenosine diphosphate closure time values. Although antigen levels of von Willebrand factor were 80% higher in patients (p0.001), von Willebrand factor-ristocetin was subnormal in 5 of 12 patients. Ristocetin-induced aggregation was also threefold higher in volunteers (p0.001), indicating an additional functional defect of platelets affecting the glycoprotein Ib-von Willebrand factor axis. The von Willebrand factor multimer pattern in patients also appeared abnormal.Multimodal antiplatelet monitoring showed markedly impaired platelet function in patients with a left ventricular assist device. Platelet dysfunction under high shear rates and abnormal ristocetin-induced aggregation is only partly attributable to low von Willebrand factor activity. These findings resemble the acquired von Willebrand syndrome that is associated with microaggregate formation and enhanced bleeding.

The secretion of heat shock protein (HSP) 27, HSP60, HSP70, HSP90alpha, 20S proteasome, and their correlations to proinflammatory cytokine interleukin-6 is unknown in patients undergoing on-pump versus off-pump coronary artery bypass graft (CABG) operation.Forty patients were included in this explorative study (on- versus off-pump CABG, each n = 20). Serum samples were obtained before and 30 minutes, 60 minutes, and 24 hours after CABG operation. Enzyme-linked immunosorbent assay technique was utilized to determine soluble HSP27, 60, 70, and 90alpha, 20S proteasome, and levels of interleukin-6.Serum levels of HSP are increased in patients undergoing on-pump CABG operation as compared with off-pump CABG technique. These differences were highly significant for HSP27, 70, and 90alpha at 60 minutes after initiation of cardiopulmonary bypass (all, p0.001). Concentrations of soluble 20S proteasome were increased 24 hours after operation in on- and off-pump CABG patients (p0.001) and correlated significantly with the serum content of HSP 27, 70, and 90alpha at 60 minutes after initiation of cardiopulmonary bypass (p0.001). No correlation was found when comparing interleukin-6 levels with intravascular leakage of HSP and 20S proteasome after CABG operation.We conclude from our data that the innate immune system is activated owing to spillage of known immune modulatory and apoptosis-associated proteins after CABG operation.

Some of isoflurane's cellular actions, such as interference with intracellular Ca(2+) handling, inhibition of the respiratory chain, and the capability to produce oxygen radicals, could result in impaired cellular function during ischemia/reoxygenation (I/R). We investigated the effects of isoflurane applied during I/R on intracellular Ca(2+), oxygen radical formation, arrhythmic events, and contractile function in rat cardiomyocytes. Single ventricular myocytes were subjected to 30 min of simulated ischemia followed by 30 min of reoxygenation. After baseline measurements, isoflurane-treated cells were exposed to 1 minimum alveolar concentration of isoflurane in air, whereas control cells were exposed to air only. Cytosolic Ca(2+) overload was observed in the isoflurane group (P < 0.05). During ischemia, systolic cell shortening decreased in both groups. In the isoflurane group, arrhythmic events and hypercontracture occurred more often during I/R, and the recovery of contractility during reoxygenation was less marked (P < 0.05). Furthermore, increased oxygen radical generation was detected in isoflurane-treated myocytes during reoxygenation (P < 0.05). Isoflurane given during I/R in this study induced intracellular Ca(2+) accumulation and impaired cell function. These potentially harmful effects were associated with a diminished Ca(2+) clearance and an accelerated oxygen radical production.

BACKGROUND The potentially harmful effects of normothermia on neurological outcome during cardiopulmonary bypass (CPB) are controversial. METHODS In this study, we compared the early and late release patterns of S-100beta, a marker of cerebral injury, after normothermic and moderately hypothermic CPB. Forty-eight patients undergoing coronary artery bypass grafting were randomly assigned to either the normothermia (37 degrees C) or the hypothermia (32 degrees C) group. Serum S-100beta levels were measured until 24 h after CPB. Neurological examination was performed before and after surgery. RESULTS With the exception of intraoperative blood glucose levels, there were no differences between groups. This also applied to peak S-100beta values (Gr-N: 3.5 +/- 1.9 microg/l; Gr-H: 3.5 +/- 3.4 microg/l) and values after 24 h (Gr-N: 0.32 +/- 0.16 microg/l; Gr-H: 0.35 +/- 0.28 microg/l). CONCLUSIONS The similar pattern of S-100beta release without evident neurological complications in the normothermia group does not suggest an increase in cerebral injury during normothermic CPB.

Nitric oxide (NO) supplementation may modify myocardial oxygen consumption and vascular function after ischemia. We investigated the effects of the NO donor, S-nitroso human serum albumin (S-NO-HSA), on cardiac oxygen metabolism during controlled reperfusion on normothermic cardiopulmonary bypass after severe myocardial ischemia. Pigs randomly received either S-NO-HSA or human serum albumin prior to and throughout global myocardial ischemia. Myocardial oxygen utilization is impaired at the onset of reperfusion, which is not amenable to S-NO-HSA. However, NO supplementation during ongoing supply dependency of oxygen consumption eventually leads to greater myocardial oxygen delivery and consumption. In conjunction with a better washout of lactate, this indicates an improved capillary perfusion in the S-NO-HSA group during reperfusion, which results in a better contractile function post bypass.

ObjectivesTo analyze outcome in elderly patients after surgical repair of the ascending aorta and the aortic arch as compared with their younger counterparts and to determine risk factors of mortality and permanent neurologic injury.Patients and methodsBetween January 1995 and February 2003, a total of 369 patients underwent ascending aortic and arch repair. Indications for surgical intervention were acute type A dissections in 174 (47%) patients (

A case of successful regional anticoagulation with trisodium citrate in a patient who developed heparin-induced thrombocytopenia while on continuous hemofiltration is described. Immediate citrate anticoagulation allowed for maintenance of extracorporeal circulation until effective danaparoid therapy could be established. Recommended plasma antifactor Xa levels for hemodialysis may be inadequate in some cases. Values similar to those in use during cardiopulmonary bypass could be required.

The limited availability of donor hearts means that an increasing number of transplantation candidates are temporarily or permanently supported by mechanical circulatory assist devices. We report a patient undergoing implantation of a Novacor left ventricular assist device who suffered fatal aortic dissection on postoperative day 11 after satisfactory recovery from multiple organ failure. The dissection of the aorta initially presented as an embolic peripheral ischemia. Early complete echocardiography is thus warranted to rule out dissection.

Background . The bridge to transplantation with pulsatile mechanical assist devices became a standard procedure for patients deteriorating on the waiting list. Recently, continuous flow axial impeller pumps were introduced to clinical application offering new advantages. Methods . From November 1998 till September 2000, 6 male patients (mean age 53 plus or minus 11 years) with end-stage left heart failure were implanted with a DeBakey ventricular assist device (VAD) axial-flow pump for bridge to transplantation. Results . Three patients were successfully transplanted after 74, 115, and 117 days, respectively. Two other patients died after 25 and 133 days. One patient is still on the device after 108 days. Because of modification of the implantation technique after the first 2 patients, mean pump-flow within the first 3 weeks was increased from 4.3 ± 0.6 L/min to 6.7 ± 0.3 L/min. Patients were put on regular bicycle-ergometer training and improved their exercise capacities up to a mean maximum oxygen consumption of 20.2 mL/kg/min. Conclusions . Initial implants of the DeBakey VAD demonstrated support properties comparable to pulsatile pumps but without significant restrictions for extended use.

A case of successful regional anticoagulation with trisodium citrate in a patient who developed heparin-induced thrombocytopenia while on continuous hemofiltration is described. Immediate citrate anticoagulation allowed for maintenance of extracorporeal circulation until effective danaparoid therapy could be established. Recommended plasma antifactor Xa levels for hemodialysis may be inadequate in some cases. Values similar to those in use during cardiopulmonary bypass could be required.