Myocardial protection with volatile anaesthetic agents during coronary artery bypass surgery: a meta-analysis [see comment]. Br J Anaesth

Department of Anaesthesia and Perioperative Medicine, Alfred Hospital, Monash University, Melbourne, Victoria, Australia.
BJA British Journal of Anaesthesia (Impact Factor: 4.85). 09/2006; 97(2):127-36. DOI: 10.1093/bja/ael149
Source: PubMed


Previous studies have investigated the role of volatile anaesthetic agents in myocardial protection during coronary artery
bypass graft (CABG) surgery, and some have identified beneficial effects. However, these studies have been too small to identify
a significant effect on myocardial infarction (MI) or mortality. We undertook a systematic overview and meta-analysis of all
randomized trials comparing volatile with non-volatile anaesthesia in CABG surgery. We identified 27 trials that included
2979 patients. There was no significant difference in myocardial ischaemia, MI, intensive care unit length of stay or hospital
mortality between the groups (all P>0.05). Post-bypass, patients randomized to receive volatile anaesthetics had 20% higher cardiac indices (P=0.006), significantly lower troponin I serum concentrations (P=0.002) and lesser requirement for inotropic support (P=0.004) compared with those randomized to receive i.v. anaesthetics. Duration of mechanical ventilation was reduced by 2.7
h (P=0.04), and there was a 1 day decrease in hospital length of stay (P<0.001). Some of these outcomes were based on a smaller number of trials because of incomplete data, largely because the individual
trials focused on one or more surrogate endpoints. We found some evidence that volatile anaesthetic agents provide myocardial
protection in CABG surgery, but larger adequately powered trials with agreed, defined outcomes need to be done to fully assess
a possible beneficial effect of volatile anaesthetic agents on the risk of MI and mortality.

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Available from: Joel Ari Symons, Aug 25, 2014
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    • "Additionally , some authors have noted similarities between endotoxin-induced immune defect and cardiac surgery (Codaccioni et al. 2009). This inflammatory response is initiated by surgical trauma, blood contact with artificial surfaces in CPB circuit and ischemia–reperfusion injury, and the degree of inflammatory response corresponds to postoperative outcome, including neuropsychological disorders (Symons and Myles 2006; Yue et al. 2008). In the present study, we observed an overall correlation between plasma KYNA concentration and NLR, a marker of inflammation (de Jager et al. 2010; Gibson et al. 2010; Zahorec 2001), in the NonSEV group. "
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    ABSTRACT: Increases in plasma kynurenic acid (KYNA) concentration relate to the severity of inflammation. The aim of this study was to analyse changes in plasma KYNA concentration and neutrophil/lymphocyte ratio (NLR) in cardiac surgery patients. Additionally, the effect of anaesthesia was analysed. Adult cardiac surgery patients under intravenous general anaesthesia were studied. Additionally, some patients received sevoflurane (SEV) prior to cardiopulmonary bypass. Plasma KYNA concentration and NLR were measured before anaesthesia, just after surgery and on postoperative days 1, 2 and 3. Patients were assigned to two groups: patients who did not receive SEV (NonSEV group) and patients who received SEV (SEV group). Forty-three patients were studied. Twenty-four of them received SEV. KYNA increased immediately after surgery and remained elevated through postoperative day 3 in the NonSEV group, whereas it was similar to the preoperative concentration in the SEV group. NLR increased immediately after surgery in both groups, and higher values were noted in the NonSEV group than in the SEV group at postoperative days 2 and 3. Plasma KYNA concentration correlated with NLR in the NonSEV group. Cardiac surgery caused an increase in NLR. Plasma KYNA increased in the NonSEV group and correlated with NLR. Administration of SEV inhibited the increase in KYNA, most likely due to its anti-inflammatory properties.
    Full-text · Article · Sep 2014 · Archivum Immunologiae et Therapiae Experimentalis
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    • "Inhaled anaesthetics are a group of agents which have shown cardioprotective effects by influencing multiple hierarchical pathways. Meta-analysis of 27 clinical trials in CABG patients described in the sevoflurane group a lower release of troponin, less inotropic support, and preserved ventricular function [100]. Sevoflurane testing is now underway in acute cardiology in STEMI patients subjected to reperfusion (SIAM trial: In terms of mechanism of action, great attention is paid to cyclosporine A, which inhibits opening of MPTP channels in the mitochondria in the post-ischaemia reperfusion stage). "
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    ABSTRACT: Cardiac surgery patients are now more risky in terms of age, comorbidities, and the need for complex procedures. It brings about reperfusion injury, which leads to dysfunction and/or loss of part of the myocardium. These groups of patients have a higher incidence of postoperative complications and mortality. One way of augmenting intraoperative myocardial protection is the phenomenon of myocardial conditioning, elicited with brief nonlethal episodes of ischaemia-reperfusion. In addition, drugs are being tested that mimic ischaemic conditioning. Such cardioprotective techniques are mainly focused on reperfusion injury, a complex response of the organism to the restoration of coronary blood flow in ischaemic tissue, which can lead to cell death. Extensive research over the last three decades has revealed the basic mechanisms of reperfusion injury and myocardial conditioning, suggesting its therapeutic potential. But despite the enormous efforts that have been expended in preclinical studies, almost all cardioprotective therapies have failed in the third phase of clinical trials. One reason is that evolutionary young cellular mechanisms of protection against oxygen handling are not very robust. Ischaemic conditioning, which is among these, is also limited by this. At present, the prevailing belief is that such options of treatment exist, but their full employment will not occur until subquestions and methodological issues with the transfer into clinical practice have been resolved.
    Full-text · Article · Aug 2014 · BioMed Research International
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    • "Different meta-analyses [18, 19] have shown that the use of anesthetic agents decreases the use of vasopressors. The statistical analysis of our study sample showed no significant quantitative differences in the use of norepinephrine, dobutamine, and nitroglycerin for the first 48 hours after admission. "
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    ABSTRACT: To compare the potential beneficial effects on markers of myocardial injury (troponin T) and renal function between sedation with sevoflurane vs propofol after cardiac surgery using extracorporeal cardiopulmonary bypass. A prospective study with sequential selection of patients undergoing coronary or coronary and valve cardiac surgery. Intraoperative anesthesia consisted in sevoflurane and remifentanil, while in the postoperative period patients were divided in two groups to receive sedation with either sevoflurane through the AnaConDa© system or propofol. The patients were sedated during a minimum of 120minutes. Markers of myocardial injury and plasmatic creatinine were measured 4, 12, 24, and 48hours after surgery. Data from 129patients, 62sedated with propofol and 67with sevoflurane, were analyzed. The analysis of the troponin T levels showed differences 12 and 48 hours after admission. Mean values at 12hours were 0.89 (standard deviation 0.55) µg.L(-1) in the propofol group and 0.69 (standard deviation 0.40) µg. L(-1)in the sevoflurane group (p = 0.026). TnT levels at 48hours were 0.60 (standard deviation 0.46) µg.L-(1)in the propofol group and 0.37 (standard deviation 0.26) µg.L(-1)in the sevoflurane group (p = 0,007). No differences were found in the groups in the creatinine levels before discharge. The post-operative sedation with sevoflurane after cardiac surgery with cardiopulmonary bypass is a valid alternative to propofol. It does not increase the number of side effects related to kidney damage in patients with no prior renal disease, leading to reduced troponin T levels 12and 48hours after admission.
    Full-text · Article · Mar 2014
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