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J Thorac Cardiovasc Surg 2003;126:1222-1223
© 2003 The American Association for Thoracic Surgery
Brief communication |
a Departments of Anesthesia and Pharmacology and Therapeutics, Centre for Anesthesia and Analgesia, University of British Columbia, Vancouver, British Columbia, Canada
Received for publication October 3, 2002; accepted for publication March 25, 2003.
* Address for reprints: Dr David M. Ansley, University of British Columbia, Department of Anesthesiology, Room 3200, 3rd Floor JPP, 910 West 10th Ave, Vancouver, BC, Canada V5Z 4E3
daansley{at}interchange.ubc.ca
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Low cardiac output syndrome (LCOS) adversely affects 6% to 25% of patients following cardiac surgery.1,2 Identifying factors associated with the risk of LCOS is integral to the development of new strategies to address this clinical problem. 15-F2t–isoprostane is a novel biologically active marker of lipid peroxidation and a potent vasoconstrictor3 known to induce ventricular dysfunction following experimental ischemia-reperfusion.4 Description of 15-F2t–isoprostane generation during cardiac surgery is limited, and the clinical relevance of its release and metabolism is unknown. We wanted to determine if a relationship exists between 15-F2t–isoprostane generation and early myocardial function following warm heart surgery.
Methods
Following ethics board approval and informed consent, 30 patients scheduled for coronary artery bypass grafting (CABG; n = 24) or combined valve replacement/CABG (n = 6) procedures utilizing normothermic (34°-37°C) cardiopulmonary bypass (CPB) and warm antegrade intermittent blood/crystalloid (8:1) cardioplegia were enrolled. Cardiac index (CI) was determined intraoperatively and the first 6 postoperative hours using a pulmonary artery catheter in 26 of 30 patients.
Central venous blood was sampled at baseline, at 30 minutes of global myocardial ischemia, and at 10 (Rep-10), 30 (Rep-30), and 120 minutes after aortic declamping (reperfusion) for measurement of plasma free 15-F2t–isoprostane by enzyme immunoassay (EIA) using a highly specific rabbit 15-F2t–isoprostane antibody. The linearity and accuracy of the assay was assessed in triplicatewith EIA buffer spiked with 15-F2t–isoprostane standard over therange of 3.9 of 250 pg/mL. The best assay linearity relationship exists between 7.8 to 125 pg/mL (R2 = 0.9998). The intra-assay and interassay coefficient of variation was less than 9% or less than 14.7% when plasma free 15-F2t–isoprostane was in the range of 14 to 58 pg/mL.
Student t test was used to compare preanesthesia and during CPB patient data. Isoprostane data were compared by 2-way analysis of variance with Bonferroni's correction (GraphPad Prism). Correlations were evaluated by the Pearson test and 95% confidence intervals derived. The differences were considered significant at P < .05.
Results
The demographic and perioperative data for the 30 patients are presented in Table 1. No perioperative myocardial ischemia was detected in any patient.
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Postoperative cardiac index was 
2.2 L · min · m2 in 6 of 26 patients in whom the 15-F2t–isoprostane concentration did not change or increased during 10 to 30 minutes of reperfusion. These patients required 
2 inotropes (n = 6) for postoperative hemodynamic stabilization. In contrast, 15-F2t–isoprostane decreased exponentially during reperfusion in patients who did not need inotropic support (n = 7). There was no significant difference in duration of ACC and CPB, mean systemic oxygenation during surgery, hemoglobin content of cardioplegia, volume and frequency of cardioplegia, or systemic oxygen tension during CPB between these subgroups.
A significant negative correlation was observed between postoperative CI and percentage change in plasma 15-F2t–isoprostane concentration from Rep-10 to Rep-30 for 26 patients (Figure 1; r = 0.7278; 95% CI: -0.8699 to -0.4740, P < .0001). Postoperative cardiac index did not correlate with baseline 15-F2t–isoprostane nor with the 15-F2t–isoprostane concentration during ischemia (P > .1).
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Evidence documenting the clinical relevance of oxidant stress in cardiac surgery is lacking. 15-F2t–isoprostane formation has been implicated in PTCA-associated complications such as coronary vasospasm,5 but investigation of a role in myocardial stunning is required. The relationship between 15-F2t–isoprostane formation and postoperative cardiac function, if one exists, is unknown.
The mechanism of cardiac depression seen in our patients has yet to be determined. Postoperative myocardial ischemia was not evident. To the best of our knowledge, we provide first evidence that 15-F2t–isoprostane formation and metabolism may be a factor in postoperative recovery of cardiac function. We describe an association between the level of plasma free 15-F2t–isoprostane and postoperative CI. Although elevated primarily during ischemia, the pattern of 15-F2t–isoprostane degradation during reperfusion appears clinically relevant. In this series of patients, persistent intraoperative elevation of 15-F2t–isoprostane during reperfusion was associated with increased need for hemodynamic stabilization following CABG surgery. This occurs independent of the timing and hemoglobin content of cardioplegic protection, 2 factors in low cardiac output syndrome. Alterations in its formation, metabolism, and elimination during surgery may explain these effects.
Determination of the mechanism(s) will be important in the development of new therapies that prevent or treat postoperative cardiac depression. A role for 15-F2t–isoprostane in the pathogenesis of myocardial IRI is suggested. However, this hypothesis requires further testing with agents designed to antagonize its effects to confirm if a cause-and-effect relationship indeed exists.
Acknowledgments
We acknowledge Mr L. G. Franciosi for statistical advice.
References
and E2) in isolated guinea pig hearts. J Cardiovasc Pharmacol. 1997;29:789–794[Medline]This article has been cited by other articles:
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  Z. Xia, K.-H. Kuo, P. R. Nagareddy, F. Wang, Z. Guo, T. Guo, J. Jiang, and J. H. McNeill N-acetylcysteine attenuates PKC{beta}2 overexpression and myocardial hypertrophy in streptozotocin-induced diabetic rats Cardiovasc Res, March 1, 2007; 73(4): 770 - 782. [Abstract] [Full Text] [PDF]
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 Z. Xia, Z. Huang, and D. M. Ansley Large-Dose Propofol During Cardiopulmonary Bypass Decreases Biochemical Markers of Myocardial Injury in Coronary Surgery Patients: A Comparison with Isoflurane. Anesth. Analg., September 1, 2006; 103(3): 527 - 532. [Abstract] [Full Text] [PDF]
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 Z. Xia, K.-H. Kuo, D. V. Godin, M. J. Walker, M. C. Y. Tao, and D. M. Ansley 15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1366 - H1372. [Abstract] [Full Text] [PDF]
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