***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND Recent clinical and experimental data indicate that volatile anaesthetics may precondition myocardium against ischaemia and infa rct ion . The present clinical trial was design ed to verify the cardioprotective effects of desflurane in patients undergoing elective coronary artery bypass surgery . It was hypothesized that desflurane preconditioning would decrease postoperative release of troponin I and brain natriuretic peptide ( NT-proBNP ) . Besides , we have hypothesized that desflurane preconditioning would preserve the myocardium from the dysfunction following cardioplegic arrest . METHODS Twenty-eight patients were r and omly divided into two groups : Control group ( 14 patients ) and  Desflurane group ( 14 patients ) . In Desflurane group ( DS ) patients , preconditioning was elicited after the onset of cardiopulmonary bypass via a 5-min exposure to desflurane ( 2.5 minimum alveolar concentration ) , followed by a 10-min washout before aortic cross-clamping and cardioplegic arrest . The control group ( C ) patients underwent an equivalent period ( 15 min ) of pre-arrest desflurane-free bypass .  Haemodynamic measurements were obtained at six different times . The biochemistry markers of cellular damage and myocardial dysfunction ( troponin I , NT-proBNP ) were determined . Left ventricular ( LV ) function was assessed using tissue Doppler imaging ( TDI ) of mitral annulus . Two-factor repeated- measures analysis of variance was used to evaluate differences over time between groups for all parameters determined in plasma sample s and for all TDI-derived variables . RESULTS After surgery , both the troponin I values ( 2.04+/-1.09 ng/ml vs 1.44+/-0.77 ng/ml , p<0.01 after 24h and 1.62+/-0.96 ng/ml vs 1.00+/-0.24 ng/ml , p<0.01 after 72 h respectively ) and those of the NT-proBNP ( 2187+/-282.9 ng/l vs 885.4+/-117.35 ng/l , p<0.01 after 24h and 3097.9+/-226.2 vs 1393.6+/-312.07 ng/l , p<0.01 after 72 h respectively ) were less in the desflurane-treated patients . The values of TDI of mitral annulus were constantly better in desflurane-treated patients . CONCLUSIONS We can conclude that the use of desflurane in these patients provides a pharmacological preconditioning so as to reduce myocardial necrosis and improve the cardiac performance in the postoperative period Background The present study investigated the effects of propofol , desflurane , and sevoflurane on recovery of myocardial function in high-risk coronary surgery patients . High-risk patients were defined as those older than 70 yr with three-vessel disease and an ejection fraction less than 50 % with impaired length-dependent regulation of myocardial function . Methods Coronary surgery patients ( n = 45 ) were r and omly assigned to receive either target-controlled infusion of propofol or inhalational anesthesia with desflurane or sevoflurane . Cardiac function was assessed perioperatively and during 24 h postoperatively using a Swan-Ganz catheter . Perioperatively , a high-fidelity pressure catheter was positioned in the left and right atrium and ventricle . Response to increased cardiac load , obtained by leg elevation , was assessed before and after cardiopulmonary bypass ( CPB ) . Effects on contraction were evaluated by analysis of changes in dP/dtmax . Effects on relaxation were assessed by analysis of the load-dependence of myocardial relaxation . Postoperative levels of cardiac troponin I were followed for 36 h. Results After CPB , cardiac index and dP/dtmax were significantly lower in patients under propofol anesthesia . Post-CPB , leg elevation result ed in a significantly greater decrease in dP/dtmax in the propofol group , whereas the responses in the desflurane and sevoflurane groups were comparable with the responses before CPB . After CPB , load dependence of left ventricular pressure drop was significantly higher in the propofol group than in the desflurane and sevoflurane group . Troponin I levels were significantly higher in the propofol group . Conclusions Sevoflurane and desflurane but not propofol preserved left ventricular function after CPB in high-risk coronary surgery patients with less evidence of myocardial damage postoperatively Background : Two preconditioning stimuli should induce a more consistent overall cell protection . We hypothesized that remote ischemic preconditioning ( RIPC , second preconditioning stimulus ) applied during isoflurane inhalation ( first preconditioning stimulus ) would provide more protection to the myocardium of patients undergoing on-pump coronary artery bypass grafting . Methods : In this placebo-controlled r and omized controlled study , patients in the RIPC group received four 5-min cycles of 300 mmHg cuff inflation/deflation of the leg before aortic cross-clamping . Anesthesia consisted of opioids and propofol for induction and isoflurane for maintenance . The primary outcome was high-sensitivity cardiac troponin T release . Secondary endpoints were plasma levels of N-terminal pro-brain natriuretic peptide , high-sensitivity C-reactive protein , S100 protein , and short- and long-term clinical outcomes . Gene expression profiles were obtained from atrial tissue using microarrays . Results : RIPC ( n = 27 ) did not reduce high-sensitivity cardiac troponin T release when compared with placebo ( n = 28 ) . Likewise , N-terminal pro-brain natriuretic peptide , a marker of myocardial dysfunction ; high-sensitivity C-reactive protein , a marker of perioperative inflammatory response ; and S100 , a marker of cerebral injury , were not different between the groups . The incidence for the perioperative composite endpoint combining new arrhythmias and myocardial infa rct ions was higher in the RIPC group than the placebo group ( 14/27 vs. 6/28 , P = 0.036 ) . However , there was no difference in the 6-month cardiovascular outcome . N-terminal pro-brain natriuretic peptide release correlated with isoflurane-induced transcriptional changes in fatty-acid metabolism ( P = 0.001 ) and DNA-damage signaling ( P < 0.001 ) , but not with RIPC-induced changes in gene expression . Conclusions : RIPC applied during isoflurane inhalation provides no benefit to the myocardium of patients undergoing on-pump coronary artery bypass grafting OBJECTIVE The purpose of this study was to evaluate the effects of volatile anesthesia versus total intravenous anesthesia on cardiac troponin release in off-pump coronary artery bypass grafting ( OPCAB ) . DESIGN The authors performed a multicenter r and omized controlled study to compare cardiac troponin release in patients receiving either volatile anesthetics or total intravenous anesthesia for cardiac surgery on the beating heart , which is an excellent model of human myocardial ischemia . SETTING Three university hospitals . PARTICIPANTS The authors r and omly assigned 57 patients to desflurane ( volatile anesthetic )  and 55 patients to propofol ( intravenous anesthetic ) in addition to an opiate-based anesthesia for OPCAB . INTERVENTIONS The 2 groups of patients received either desflurane ( volatile anesthetic ) or propofol in addition to an opiate-based anesthesia for OPCAB .  Peak postoperative troponin I release was measured as a marker of myocardial necrosis . Prolonged hospitalization was considered as a secondary outcome . MEASUREMENTS AND MAIN RESULTS Patient mean age was 69 years , and 82 % were men . There was a significant ( p < 0.001 ) reduction in postoperative median ( 25th-75th percentiles ) peak of troponin I in patients receiving volatile anesthetics , 1.2 ( 0.9 - 1.9 ) ng/dL , compared with patients receiving total intravenous anesthesia , 2.7 ( 2.1 - 4.0 ) ng/dL. This myocardial protection result ed in a reduced ( p = 0.04 ) number ( percentage ) of patients requiring postoperative inotropes , 20 ( 35 % ) versus 31 ( 56 % ) , and a reduced number ( percentage ) of patients su bmi tted to prolonged hospitalization ( > or = 7 days ) , 7 ( 12 % ) versus 20 ( 36 % ) in the 2 groups ( p = 0.005 ) . One patient receiving total intravenous anesthesia died within 30 days of surgery . CONCLUSIONS Myocardial damage measured by cardiac troponin release could be reduced by volatile anesthetics during OPCAB . Because patients underwent cardiac surgery on the beating heart , these results could have implication s for cardiac patients undergoing noncardiac surgery Background The value of postoperative cardiac troponin I ( cTnI ) has been shown to indicate a higher risk of in-hospital death after cardiac surgery . The authors therefore assessed the long-term prognostic value of cTnI in patients undergoing elective coronary artery bypass grafting .  Methods Consecutive patients ( n = 202 ) were included and divided into two groups according to the postoperative value of cTnI ( < or ≥ 13 ng/ml ) . In-hospital mortality and nonfatal cardiac events ( delayed extubation > 24 h ; postoperative requirement of inotropic agent ; ventricular and supraventricular arrhythmia ; postoperative myocardial infa rct ion ) were recorded . Survivors were then followed up over a 2-yr period . Data are median and odds ratio ( 95 % confidence interval ) . Results Of all patients , 174 ( 86 % ) had a low cTnI ( 4.1 ng/ml ; range , 1.1–12.6 ) and 28 ( 14 % ) had a high cTnI ( 23.8 ng/ml ; range , 13.4–174.6 ) . In-hospital mortality was not significantly different ( 4 vs. 2 % ) , whereas long-term mortality ( 18 vs. 3 % , P = 0.006 ) and mortality from cardiac cause ( 18 vs. 1 % , P < 0.001 ) was greater in patients with a high cTnI. A high cTnI was a significant factor predicting death ( odds ratio , 7.3 [ 2.0–27.1 ] ) or death from cardiac causes ( odds ratio , 37.4 [ 4.2–334.4 ] ) . Nonfatal cardiac events were also more frequent in the hospital ( 64 vs. 41 % , P = 0.02 ) and within the 2-yr follow-up period ( 39%vs . 16 % , P = 0.03 ) in patients with high cTnI. Conclusion A high postoperative peak of cTnI is associated with increased risk of death , death from cardiac causes , and nonfatal cardiac events within 2 yr after coronary artery bypass grafting BACKGROUND Activation of the kinase cascade ( protein kinase C ( PKC ) , tyrosine kinase ( TK ) , and mitogen-activated protein kinase ( MAPK ) is a key feature of the transduction pathway , elicited by preconditioning signals and mediating their cardioprotective effects . We assessed whether such an activation occurred during cardiac operations and could thus represent a target for cardioprotective strategies . METHODS A total of 20 patients undergoing coronary artery bypass grafting surgery were studied . During the first 10 minutes of cardiopulmonary bypass ( CPB ) , 10 were treated with sevoflurane ( 2.5 minimum alveolar concentration ) , an inhalational anesthetic that mimics preconditioning through a similar activation of the kinase cascade . Ten case-matched patients undergoing 10 minutes of sevoflurane-free CPB served as controls . Right atrial biopsies were taken before and 10 minutes after CPB and were then processed for the measurement of PKC , TK , and p38 MAPK activities by enzyme assay techniques . Troponin I was also monitored over the first 2 postoperative days . RESULTS Compared with pre-CPB values , PKC and p38 MAPK activities ( in nanomoles per milligram of protein per minute and arbitrary units , respectively ) increased significantly and to the same extent in both groups : PKC , from 20.7+/-0.7 to 29.9+/-3.9 in controls ( p = 0.037 ) and from 18.4+/-1.1 to 23.9+/-1.8 in sevoflurane ( p = 0.016 ) ; p38 MAPK , from 88.6+/-8.5 to 312.9+/-66.2 in controls ( p = 0.005 ) and from 114.6+/-14.7 to 213.4+/-51.8 in sevoflurane ( p = 0.045 ) . Conversely , sevoflurane triggered 
    Output:
    
This is not yet the case for off-pump surgery