Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Thielmann, M.
Right arrow Articles by Jakob, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thielmann, M.
Right arrow Articles by Jakob, H.
(Chest. 2005;128:3526-3536.)
© 2005 American College of Chest Physicians

Prognostic Value of Preoperative Cardiac Troponin I in Patients With Non–ST-Segment Elevation Acute Coronary Syndromes Undergoing Coronary Artery Bypass Surgery*

Matthias Thielmann, MD; Parwis Massoudy, MD, PhD; Markus Neuhäuser, PhD; Stephan Knipp, MD; Markus Kamler, MD; Jarowit Piotrowski, MD; Klaus Mann, MD, PhD and Heinz Jakob, MD, PhD

* From the Department of Thoracic and Cardiovascular Surgery (Drs. Thielmann, Massoudy, Knipp, Kamler, Piotrowski, and Jakob), Institute for Medical Informatics, Biometry, and Epidemiology (Dr. Neuhäuser), and Department of Clinical Chemistry (Dr. Mann), West-German Heart Center Essen, University Clinic of Essen, Essen, Germany.

Correspondence to: Matthias Thielmann, MD, Department of Thoracic and Cardiovascular Surgery, West-German Heart Center, University Clinic of Essen, Hufelandstraße 55, 45122 Essen, Germany; e-mail: matthias.thielmann{at}uni-essen.de


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Study objectives: Elevated levels of cardiac troponin I (cTnI) have been associated with adverse short-term and long-term outcomes in acute coronary syndrome (ACS) patients and in patients who underwent coronary artery bypass grafting (CABG); however, the prognostic implications of preoperative cTnI determination have not been investigated so far.

Design and setting: Retrospective study in a department of cardiothoracic surgery of a university hospital.

Patients and methods: A possible correlation between preoperative cTnI levels and major adverse cardiac events (MACE) and in-hospital mortality in CABG patients with non–ST-segment elevation ACS (NSTE-ACS) was investigated. cTnI was determined in 1,978 of 3,124 consecutive CABG patients. Among these, 1,592 patients had preoperative cTnI levels < 0.1 ng/mL and therefore served as control subjects (group 1), 265 patients had NSTE-ACS with cTnI levels from 0.11 to 1.5 ng/mL (group 2), and 121 patients had NSTE-ACS with cTnI levels > 1.5 ng/mL (group 3). cTnI levels, clinical data, MACE, and in-hospital mortality were recorded prospectively. Logistic regression and receiver operating characteristic analyses were applied to determine prognostic cutoff values of cTnI.

Results: Perioperative myocardial infarction was found in 5.8% of the patients in group 1, 8.3% of the patients in group 2 (odds ratio [OR], 1.5; 95% confidence interval [CI], 0.9 to 2.5), and 18.2% patients in group 3 (OR, 3.6; 95% CI, 2.1 to 6.2; p < 0.0001, Cochran-Armitage trend test). Low cardiac output syndrome occurred in 1.5% of patients in group 1, 4.2% of patients in group 2 (OR, 2.8; 95% CI, 1.3 to 6.1), and 10.9% patients in group 3 (OR, 6.5; 95% CI, 2.9 to 14.4; p < 0.0001). In-hospital mortality was 1.5% in group 1, 3.0% in group 2 (OR, 2.0; 95% CI, 0.8 to 4.8), but 6.6% in group 3 (OR, 4.6; 95% CI, 1.9 to 11.1; p < 0.0001). Univariate and multivariate logistic regression analyses identified cTnI as the strongest preoperative predictor for MACE and in-hospital mortality, respectively.

Conclusions: Preoperative cTnI measurement before CABG appears as a powerful and independent determinant of short-term surgical risk in patients with NSTE-ACS.

Key Words: cardiac troponin I • coronary artery bypass grafting • non–ST-segment elevation acute coronary syndrome • risk stratification


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Risk stratification and outcomes research is an emerging issue in cardiovascular surgery and particularly in coronary artery bypass grafting (CABG) to predict morbidity and mortality as a measure of health-care performance.123 Although most risk scores give consistent predictions, the extent of acute preoperative myocardial injury in unstable coronary artery disease (CAD) ranging from microinfarctions due to preexisting microembolizing unstable plaques up to non-ST elevation acute coronary syndrome (NSTE-ACS) and ST-segment elevation myocardial infarction (STEMI) have not been considered adequately. Since the extent of myocardial necrosis has become an important determinant for the risk of death and adverse prognosis, it is important to develop simple noninvasive techniques to predict prognosis before cardiac surgery in order to initiate appropriate operative and perioperative treatment modalities. The advent of highly sensitive and myocardial tissue specific serologic biomarkers, such as cardiac troponins (I and T), have recently lead to a redefinition of myocardial infarction (MI) initiated by the European Society of Cardiology and the American College of Cardiology/American Heart Association Consensus document.4

However, cardiac troponins have not only fundamentally improved acute MI (AMI) detection but also enabled risk stratification in numerous clinical settings. Several clinical studies567 revealed cardiac troponins as reliable and valuable biomarkers for the prediction of short-term and long-term prognoses and the probability of death in patients with acute coronary syndromes (ACSs). Furthermore, elevated cardiac troponins in the setting of percutaneous cardiac intervention (PCI) have been demonstrated to be strongly related to an increased probability of mortality.68910 In the setting of cardiac surgery, the relationship between postoperative release of cardiac troponins and patient outcome has been well associated in previous studies.111213 Whether preoperative cardiac troponin I (cTnI) levels similarly predict surgical risk of patients with NSTE-ACS undergoing CABG is currently unknown.

An elevation of preoperative cTnI in patients undergoing CABG may be the result of bygone, ongoing, or evolving myocardial damage, which may stay unrecognized without cTnI measurement. The present study therefore focused on the clinical significance of a single preoperative cTnI serum level before cardiac surgery and its predictive value for major adverse cardiac events (MACE) and in-hospital mortality in patients with NSTE-ACS undergoing CABG.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusion
 References
 
Clinical End Points
The primary end point of the study was in-hospital mortality, defined as death from any cause within 30 days after surgery or during the same time period of hospitalization as well as postoperative MACE during the period of hospitalization including perioperative MI (PMI) and low cardiac output syndrome (LCOS). Secondary study end points were other postoperative complications such as stroke,3 new-onset ventricular arrhythmia,4 major bleeding,5 necessity for rethoracotomy,6 and postoperative renal failure requiring temporary hemodialysis.7

Selection of Patients
Patients were enrolled into the present study if they had undergone an isolated CABG procedure and a preoperative cTnI serum level had been obtained 24 h before surgery (Table 1 ). For risk analysis, patients were stratified into three groups according to preoperative cTnI levels, as previously described.14 Among these, 1,592 patients had negative preoperative cTnI serum levels < 0.1 ng/mL (group 1), 265 patients had low-level cTnI serum levels from 0.11 to 1.5 ng/mL (group 2), and 121 patients had conventional cTnI serum levels > 1.5 ng/mL (group 3).


View this table:
[in this window]
[in a new window]

  		Table 1.. Baseline Characteristics According to Preoperative cTnI Levels*

 
The remaining 1,146 of 3,124 CABG patients were not enrolled due to no preoperative cTnI measurements within 24 h before surgery or without preoperative cTnI measurement at all, but they were statistically compared with group 1 as well as the entire study cohort with preoperative cTnI measurements to ensure that the groups with and without cTnI measurements were not different. NSTE-ACS was supposed with a positive cTnI level on hospital admission and new onset of chest pain or accelerating chest pain within the previous 24 h occurring at rest or with minimal exertion, alleviated by nitroglycerin and/or rest. Patients were excluded from the study if any of the following preoperative criteria were present: (1) preoperative MI with STEMI, (2) new-onset left bundle-branch block, (3) reoperations, and (4) any concomitant heart surgery besides CABG.

Management Strategies and Medication
Standard anesthetic and monitoring techniques were used in all patients. Internal thoracic artery, radial artery, and saphenous vein grafts were used as graft conduits. Heparin was administered in order to achieve an activated coagulation time > 400s. A standard cardiopulmonary bypass (CPB) technique was used with ascending aortic and two-stage venous cannulation. During CPB, moderate hemodilution with a hematocrit level between 20% and 25% using mild systemic hypothermia (> 32°C) was maintained. Myocardial protection was achieved using antegrade and optional retrograde crystalloid (Bretschneider) cardioplegic arrest and additional topical cooling, and single aortic cross-clamping for all distal anastomosis. Proximal graft anastamoses to the aorta were performed with partial occlusion of the ascending aorta.

Postoperative management of patients was standardized. Patients were monitored with respect to arterial pressure, pulmonary pressure, and central venous pressure. A 12-lead ECG was obtained preoperatively, immediately after the arrival to the ICU and at 12 h and 24 h postoperatively and once a day thereafter. Acetylsalicylic acid, 500 mg, was administered IV within the first 6 h after surgery in the absence of significant bleeding.

Blood Sampling and Cardiac Biomarker Analysis
Venous blood samples were drawn from each patient preoperatively on hospital admission before surgery. cTnI was measured using a specific two-sided immunoassay (Dimension Flex; Dade Behring Marburg; Marburg, Germany). The detection range for cTnI was 0.04 to 40 ng/mL, requiring further dilutions if necessary. The assays reference interval was 0.00 to 0.05 ng/mL. A cTnI value > 0.1 ng/mL was considered abnormal.

Data Collection and Definitions
Detailed in-hospital and follow-up data were obtained from the patients. All preoperative, intraoperative, and postoperative data were prospectively recorded with > 1,800 variables per case and retrospectively reviewed for the present study using the institutional database according to the Heidelberger Verein zur Multizentrischen Datenanalyse e.V. 15 The study was performed with local ethics committee and institutional approval; all patients gave their informed consent.

PMI was considered to have occurred if one of the following diagnostic criteria were present: (1) a postoperative cTnI serum level > 10.5 ng/mL within the first 24 h after CABG, as previously described16 or elevated creatine kinase (CK)-MB values (more than two times the upper limit of normal).2 The appearance of ST-segment deviations at the J point in two or more contiguous leads with cutoff points ≥ 0.2 mV in leads V1, V2, or V3 and ≥ 0.1 mV in other leads or T-wave abnormalities in two or more contiguous leads or the development of new Q-waves.4 LCOS was present if high-dose inotropic support was necessary in the postoperative course during hospital stay with or without the need of an intra-aortic balloon pump (IABP).

Statistical Analysis
Data are reported as mean ± SD, and categorical variables are presented as No. (%). For all categorical variables, the odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Comparisons of categorical variables between groups were performed by a Pearson {chi}2 test or a two-sided Cochran-Armitage trend test (using equally spaced scores)17; since expected frequencies < 5 occurred, all p values were calculated exactly. Comparisons of continuous variables between groups were analyzed by Kruskal-Wallis test for one-way analysis of variance or the Jonckheere-Terpstra trend test.18 When a significant overall effect was detected, two-group comparisons were performed with the Fisher exact test for categorical variables or the Mann-Whitney U test for continuous variables. Univariate and multivariate logistic regression analyses were performed to identify preoperative independent predictors for in-hospital mortality and MACE (PMI and LCOS) and the composite study end points, respectively. All preoperative predictor variables that were identified as significant at a two-tailed nominal p value < 0.10 in univariate regression analyses were then entered into a multivariate logistic regression analysis model. Receiver operating characteristic (ROC) curve analyses were applied to determine optimal cutoff values of cTnI and to evaluate the predictive power for in-hospital mortality and MACE. A p value < 0.05 was considered to indicate statistical significance. All statistical analyses between groups were performed using statistical software (StatXact 6.0; Cytel Software Corporation; Cambridge, MA). ROC curve analyses were calculated using statistical software (SPSS version 6.0; Chicago, IL), and logistic regression analyses were also performed (SAS System, version 8; SAS Institute; Cary, NC).


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusion
 References
 
From January 2001 to September 2004, preoperative cTnI was measured in 1,978 consecutive patients scheduled for isolated CABG. Preoperative cTnI values were available in 1,978 of 3,124 patients who fulfilled the inclusion criteria and in whom primary isolated CABG had been performed. Among these patients, negative preoperative cTnI levels (≤ 0.1 ng/mL) were present in 1,592 patients (80.5%; group 1), whereas 265 patients (13.4%; group 2) had preoperative cTnI elevation (0.11 to 1.5 ng/mL), and 121 patients (6.1%; group 3) had higher preoperative cTnI elevation (> 1.5 ng/mL) [Fig 1 ].



View larger version (15K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1.. Distribution of preoperative cTnI serum levels of the groups before CABG indicated by histograms; line indicates normal curve of distribution.

 
There were no significant differences between most perioperative patient characteristics of the remaining 1,146 CABG patients, who were initially not enrolled into the study due to no preoperative cTnI measurements, except a lower incidence of smoking history, preoperative hemodialysis-dependent renal disease, and postoperative arrhythmias, compared to group 1 patients, as well as a lower incidence of preoperative hemodialysis-dependent renal disease and postoperative IABP support compared to the entire patient cohort with preoperative cTnI measurements.

Preoperative baseline characteristics and demographics of the patients were comparable with the contemporary coronary surgery patient profile. A preoperative significant difference between the groups could be observed in terms of age, smoking history, previous MI, left ventricular (LV) ejection fraction, and preoperative cTnI levels and CK activity. Regarding the preoperative medication, a highly significant difference could be observed between the groups in the preoperative oral use of angiotensin-converting enzyme inhibitors, nitrates, and aspirin (within the last week prior to surgery), as well as the preoperative continuous IV application of nitrates and heparin. As demonstrated in Table 2 the intraoperative data did not differ between groups. As shown in Table 2, a two-sided Cochran-Armitage trend test revealed a significant difference in the necessity for intraoperative and postoperative IABP between groups 2 and 3 compared to group 1 (p < 0.0001). This was accompanied by a significantly prolonged postoperative ventilation time (p = 0.04) and longer ICU (p = 0.002) and hospital stay (p = 0.04) in groups 2 and 3.


View this table:
[in this window]
[in a new window]

  		Table 2.. Intraoperative and Postoperative Characteristics According to Preoperative cTnI Levels*

 
Among the 1,978 CABG patients with preoperative cTnI measurement, 40 patients (2.0%) died in the postoperative course within 30 days or within the same time of hospital stay. No patients died intraoperatively. A one-sided Cochran-Armitage trend test revealed a significant difference of in-hospital mortality between the groups with 1.5% vs 3.3% vs 6.6%, respectively (p < 0.02). The difference of in-hospital mortality was accompanied by a significant difference in the appearance of postoperative LCOS (p < 0.0001) and the incidence of PMI (p < 0.001). Individuals with preoperatively increased cTnI levels were at increased risk for in-hospital death and major adverse events, including a twofold to threefold higher risk of death, PMI, or LCOS. Furthermore, the composite study end points of death, PMI, or LCOS (p < 0.0001) did further increase the highly significant difference between the groups (Fig 2 ). Other postoperative complications and minor adverse events such as major bleeding (> 200 mL/h in the first 6 h) and all causes of rethoracotomy were not different between the groups. The occurrence of new-onset arrhythmias (p < 0.001) and the incidence of renal failure requiring temporary hemofiltration or hemodialysis significantly differed between the groups (p < 0.0001; Table 2).



View larger version (28K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2.. Death and MACE during hospital stay stratified by preoperative cTnI serum levels; p values are overall significance between groups calculated by one-sided Cochran-Armitage trend test.

 
Patient characteristics of the entire study population categorized by in-hospital survivors vs nonsurvivors are shown in Table 3 . In terms of preoperative data, nonsurvivors were older, female, had lower body weight, had a more frequent history of stroke, peripheral vascular disease (PVD), previous PCI, Canadian Cardiovascular Society (CCS) angina class III-IV, had a lower ejection fraction, and higher cTnI serum levels than survivors. Intraoperative data showed nonsurvivors to be associated with a significantly longer aortic cross-clamp (ACC) and CPB times as well as a longer reperfusion time. All adverse events and postoperative complications occurred significantly more frequently in nonsurvivors compared to survivors (Table 3.)


View this table:
[in this window]
[in a new window]

  		Table 3.. Patient Data According to Survival Status*

 
The univariate logistic regression analysis identified some preoperative variables that were significantly associated with death, PMI, and LCOS, or with MACE as the composite study end point (Table 4 ). The final multivariate logistic regression analysis, testing the contribution of univariate risk predictors, is displayed in Table 5 . After adjustment, only age, PVD, previous PCI, and angina class III-IV, as well as preoperative cTnI levels stratified as groups 1 to 3 were significantly associated with death. Moreover, angina class III-IV and cTnI level > 1.5 ng/mL were associated with MACE (PMI and LCOS) and the composite study end points. Under the assumption that there was an exponential relation between preoperative cTnI serum levels and in-hospital death and MACE, we evaluated the effect of each increase of 1 ng/mL in cTnI on the risk ratio for mortality and MACE after adjusting for the baseline variables of Table 1, which were found in the univariate regression analysis to be statistically significant predictors of death and/or MACE. Considering the overall study population of 1,978 patients, the multivariate regression analysis showed again a significant increase in the risk ratio for death (adjusted OR, 1.1; 95% CI, 1.02 to 1.06; p < 0.001), MACE (adjusted OR, 1.1; 95% CI, 1.02 to 1.10; p < 0.001), and the composite study end point (adjusted OR, 1.1; 95% CI, 1.02 to 1.10; p < 0.001) for each increase of 1 ng/mL in cTnI (Table 6 ).


View this table:
[in this window]
[in a new window]

  		Table 4.. Univariate Factors Associated With Death, MACE, and the Composite Study End Point

 

View this table:
[in this window]
[in a new window]

  		Table 5.. Multivariate Factors Associated With Death, MACE, and the Composite Study End Point, With cTnI as a Categorical Variable

 

View this table:
[in this window]
[in a new window]

  		Table 6.. Multivariate Factors Associated With Death, MACE, and the Composite Study End Point, With cTnI as a Continuous Variable

 
ROC Curve Analysis of cTnI
The discriminative power of preoperative cTnI serum levels for in-hospital mortality and the composite study end point using ROC curve analyses yielded an area under the curve of 0.72 ± 0.08 for the study end point of death, with an optimal cTnI cutoff value of 1.5 ng/mL, a sensitivity of 75.0% and specificity of 78.5%, and an area under the curve of 67 ± 0.05 for the composite study end point with the same cutoff value of 1.5 ng/mL, a sensitivity of 63.0%, and a specificity of 71.3% (Fig 3 , Table 7 ).



View larger version (11K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 3.. ROC curve analysis of the discriminatory power of preoperative cTnI levels for (top, A) in-hospital mortality and (bottom, B) the composite adverse outcomes of death and MACE.

 

View this table:
[in this window]
[in a new window]

  		Table 7.. Cutoff Levels and Test Characteristics for Preoperative cTnI Value*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusion
 References
 
The present study demonstrates that in a surgical population of patients undergoing CABG, the existence of preoperative NSTE-ACS is associated with a significantly higher mortality within 30 days and a higher incidence of major adverse cardiac events, such as PMI or LCOS, depending on the degree of preoperative cTnI serum elevation. Furthermore, a pre-CABG cTnI level could be shown to be used as an incremental prognostic variable in this patient cohort. cTnI serum levels were either stratified into three different groups or used as a continuous variable. Patients who had undergone isolated CABG with preoperatively low level (0.11 to 1.5 ng/mL) increased cTnI values were at a twofold elevated risk, and patients with conventional (> 1.5 ng/mL) elevated cTnI values had an over fourfold increased risk of dying in hospital. A preoperatively elevated cTnI serum level could be identified as an independent predictor of risk even after adjustment for other confounding risk factors in a multivariate logistic regression model. Therefore, the present study not only confirmed the observations of prior studies in selected patients19 but also extends them in some important ways: (1) not only the risk for in-hospital mortality, but also for postoperative MACE, such as PMI or LCOS, was shown to be increased with preoperatively elevated cTnI serum levels; (2) a preoperative cTnI threshold level for increased risk was identified; and (3) these observations were made in a large, more general population of CABG patients with preoperative NSTE-ACS.

Newer markers of myocardial cell necrosis, most notably cardiac troponins (T and I), fundamentally improved the clinical diagnostic criteria for the detection of AMI, leading to a redefinition of AMI.4 Elevated cardiac troponins have been shown to be associated with adverse outcome and increased mortality rates in patients with ACS.5 More pronounced elevated serum levels of cardiac troponins on hospital admission, indicating a more extensive myocardial injury, have been unequivocally demonstrated to predict the clinical outcome and a more complicated course following primary PCI for acute STEMI.89 Patients were found to have a lower reperfusion rate, a lower success rate for primary PCI, a higher risk for in-hospital death, congestive heart failure, and a higher incidence of long-term cardiac mortality and overall cardiac events.

However, the reasons for adverse prognosis and increased mortality associated with minor elevations of cardiac troponins are not fully understood. In the setting of ACS, elevations of cardiac troponins were found to be associated with multivessel disease, complex coronary lesions with unstable and ruptured plaques, distal coronary microembolization of platelet microaggregates and plaque debris,20 as well as abnormal microvascular myocardial perfusion,9 which might be an alternative or contributory cause of minor elevations of cardiac troponins.21 In several studies,2223 it has been shown that patients with unstable CAD and elevated cardiac troponin levels had more widespread CAD than those without elevated cardiac troponin levels, and had more frequent complex coronary lesions and a visible thrombus in the culprit vessel. It has also been demonstrated that minor elevations of cardiac troponins and thus "minor myocardial damage" are present in approximately 30% of patients with resting angina and negative CK/CK-MB values.24

Cardiac troponins were studied in several noncardiac2526 and cardiac272829 surgical settings, in which most of the studies proposed a relationship between postoperative troponin elevations and short-term and/or long-term outcomes. In a clinical study,13 a single postoperative cTnI value was shown to enable the assessment of postoperative myocardial cell injury. This cTnI level was strongly correlated with long-term survival after cardiac surgery. Thus, cTnI was suggested as an additional independent variable adding to other established risk indicators.13

An earlier study19 analyzing the possible relationship between preoperative myocardial cell injury, as measured by cTnI, and postoperative patient outcome demonstrated that patients with preoperative positive (> 0.02 µg/L) serum levels of cTnI undergoing elective CABG were more likely to have postoperative complications and postoperative MI. However, in contrast to the present study, patients with preoperatively elevated cTnI levels were not at a higher risk for in-hospital mortality, although a significantly longer CPB time, more postoperative inotropic and mechanical support, and a higher incidence of postoperative IABP support were reported. The difference concerning the study results may be due to lower numbers and more selected patients in the study by Carrier et al19 and, moreover, in the present study the preoperative cTnI level was investigated as an ordinate as well as a continuous variable.

The addition of a highly sensitive biomarker, such as cTnI, indicating myocardial cellular injury that might be subclinical at the time of determination may well enrich the exciting battery of preoperative risk stratification models for patients undergoing cardiac surgery. In addition, as shown by the results of the present study, the extent of preoperative cTnI elevation indicates the degree of myocardial cellular injury and, thus, the surgical risk before CABG.

Limitations of the Study
Several points must be stressed when these findings are extrapolated. Because cTnI serum levels depend on many variables, including first of all the type of cTnI immunoassay test kit. Moreover, there might be several differences in the preoperative management and treatment of unstable patients with ACS,3031 which may result in different preoperative cTnI serum levels. The discrimination value derived in our study may not be applicable to other patient cohorts. Therefore, the derived indexes should be tested prospectively in different settings. Moreover, the prognostic ability of our multivariate regression risk model has not been tested in a validation cohort. Finally, only the short-term follow-up is reported in the present study. The influence of a pre-CABG cTnI level on the long-term follow-up is certainly unclear.

Clinical Implications
The present study suggests that a preoperative cTnI measurement in patients with NSTE-ACS due to undergo CABG can serve as an incremental variable of risk for in-hospital mortality, PMI, and LCOS. With rising serum levels of cTnI, the risk of mortality increases. Measuring cTnI is therefore useful to define individual risk profiles. Numerous suggestions and recommendations have been made to reduce the risk for CABG surgery in patients with AMI, including better selection of patients,32 optimal timing of surgery,2233 adjunctive pharmacologic therapy,34 and preoperative support with IABP.3536 Whether these recommendations should be extended for CABG in NSTE-ACS and whether the time point for surgery should be postponed or rather accelerated due to the information of a single preoperative cTnI level remains uncertain and has to be elucidated in further studies.


   Conclusion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
References
 
Preoperative cTnI measurement before emergency CABG surgery appears as a powerful and independent determinant of short-term surgical risk in patients with NSTE-ACS and, therefore, should be taken into consideration for risk stratification in those patients.


   Footnotes
 
Abbreviations: ACC = aortic cross-clamp; ACS = acute coronary syndrome; AMI = acute myocardial infarction; CABG = coronary artery bypass grafting; CAD = coronary artery disease; CCS = Canadian Cardiovascular Society; CI = confidence interval; CK = creatine kinase; CPB = cardiopulmonary bypass; cTnI = cardiac troponin I; IABP = intra-aortic balloon pump; LCOS = low cardiac output syndrome; LV = left ventricular; MACE = major adverse cardiac events; MI = myocardial infarction; NSTE-ACS = non–ST-segment elevation acute coronary syndrome; OR = odds ratio; PCI = percutaneous coronary intervention; PMI = perioperative myocardial infarction; PVD = peripheral vascular disease; ROC = receiver operating characteristic; STEMI = ST-segment elevation myocardial infarction

Presented at the 70th Anniversary Meeting of the American College of Chest Physicians, Seattle, WA, October 23 to 28, 2004, and awarded the Young Investigator Award.

Received for publication December 17, 2004. Accepted for publication June 23, 2005.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

  1. Parsonnet, V, Dean, D, Bernstein, AD (1989) A method of uniform stratification of risk for evaluating the results of surgery in acquired adult heart disease. Circulation 79(Suppl),3-12[ISI]
  2. Higgins, TL, Estafanous, FG, Loop, FD, et al Stratification of morbidity and mortality outcome by preoperative risk factors in coronary artery bypass patients: a clinical severity score. JAMA 1992;267,2344-2348[Abstract]
  3. Nashef, SAM, Roques, F, Michel, P, et al European system for cardiac operative risk evaluation (EuroSCORE). Eur J Cardiothorac Surg 1999;16,9-13[Abstract/Free Full Text]
  4. Alpert, JS, Thygesen, K, Antman, E, et al Myocardial infarction redefined: a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36,959-969[Free Full Text]
  5. Antman, EM, Tanasijevic, MJ, Thompson, B, et al Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996;335,1342-1349[Abstract/Free Full Text]
  6. Giannitsis, E, Lehrke, S, Wiegand, UKH, et al Risk stratification in patients with inferior acute myocardial infarction treated by percutaneous coronary interventions: the role of admission troponin T. Circulation 2000;102,2038-2044[Abstract/Free Full Text]
  7. Heidenreich, PA, Alloggiamento, T, Melsop, K, et al The prognostic value of troponin in patients with non-ST elevation acute coronary syndromes: a meta-analysis. J Am Coll Cardiol 2001;38,478-485[Abstract/Free Full Text]
  8. Matetzky, S, Sharir, T, Domingo, M, et al Elevated troponin I level on admission is associated with adverse outcome of primary angioplasty in acute myocardial infarction. Circulation 2000;102,1611-1616[Abstract/Free Full Text]
  9. Giannitsis, E, Muller-Bardorff, M, Lehrke, S, et al Admission troponin T level predicts clinical outcomes, TIMI flow, and myocardial tissue perfusion after primary percutaneous intervention for acute ST-segment elevation myocardial infarction. Circulation 2001;104,630-635[Abstract/Free Full Text]
  10. Herrmann, J, Haude, M, Lerman, A, et al Abnormal coronary flow velocity reserve after coronary intervention is associated with cardiac marker elevation. Circulation 2001;103,2339-2345[Abstract/Free Full Text]
  11. Fellahi, J-L, Gue, X, Richomme, X, et al Short- and long-term prognostic value of postoperative cardiac troponin I concentration in patients undergoing coronary artery bypass grafting. Anesthesiology 2003;99,270-274[CrossRef][ISI][Medline]
  12. Thielmann, M, Massoudy, P, Marggraf, G, et al Role of troponin I, myoglobin, and creatine kinase for the detection of early graft failure following coronary artery bypass grafting. Eur J Cardiothorac Surg 2004;26,102-109[Abstract/Free Full Text]
  13. Lehrke, S, Steen, H, Sievers, HH, et al Cardiac troponin T for prediction of short- and long-term morbidity and mortality after elective open heart surgery. Clin Chem 2004;50,1560-1567[Abstract/Free Full Text]
  14. Landesberg, G, Mosseri, M, Shatz, V, et al Cardiac troponin after major vascular surgery: the role of perioperative ischemia, preoperative thallium scanning, and coronary revascularization. J Am Coll Cardiol 2004;44,569-575[Abstract/Free Full Text]
  15. Vahl, CF, Tochtermann, U, Gams, E, et al Efficiency of a computer network in the administrative and medical field of cardiac surgery: concept of and experience with a departmental system. Eur J Cardiothorac Surg 1990;4,632-638[Abstract]
  16. Thielmann, M, Massoudy, P, Marggraf, G, et al Diagnostic discrimination between early graft failure and non-graft related perioperative myocardial infarction with cardiac troponin I following coronary artery bypass surgery [abstract]. Circulation 2003;108(Suppl),391-392[Abstract/Free Full Text]
  17. Neuhäuser, M, Hothorn, LA An exact Cochran-Armitage test for trend when dose-response shapes are a priori unknown. Comput Stat Data Anal 1999;30,403-412[CrossRef]
  18. Neuhäuser, M, Liu, PY, Hothorn, LA Nonparametric tests for trend: Jonckheere’s test, a modification and a maximum test. Biometr J 1998;40,899-909[CrossRef]
  19. Carrier, M, Pelletier, LC, Martineau, R, et al In elective coronary artery bypass grafting, preoperative troponin T level predicts the risk of myocardial infarction. J Thorac Cardiovasc Surg 1998;115,1328-1334[Abstract/Free Full Text]
  20. Heusch, G, Schulz, R, Haude, M, et al Coronary microembolization. J Mol Cell Cardiol 2004;37,23-31[CrossRef][ISI][Medline]
  21. Topol, EJ, Yadav, JS Recognition of the importance of embolization in atherosclerotic vascular disease. Circulation 2000;101,570-580[Free Full Text]
  22. Jurlander, B, Farhi, ER, John, J, et al Coronary angiographic findings and troponin T in patients with unstable angina pectoris. Am J Cardiol 2000;85,810-814[CrossRef][ISI][Medline]
  23. Lindahl, B, Diderholm, E, Lagerqvist, B, et al Mechanisms behind the prognostic value of troponin T in unstable coronary artery disease: a FRISC II substudy. J Am Coll Cardiol 2001;38,979-986[Abstract/Free Full Text]
  24. Katus, HA, Remppis, A, Neumann, FJ, et al Diagnostic efficiency of troponin T measurements in acute myocardial infarction. Circulation 1991;83,902-912[Abstract/Free Full Text]
  25. Kim, LJ, Martinez, EA, Faraday, N, et al Cardiac troponin I predicts short-term mortality in vascular surgery patients. Circulation 2002;106,2366-2371[Abstract/Free Full Text]
  26. Landesberg, G, Shatz, V, Akopnik, I, et al Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery. J Am Coll Cardiol 2003;42,1547-1554[Abstract/Free Full Text]
  27. Bonnefoy, E, Filley, S, Kirkorian, G, et al Troponin I, troponin T, or creatine kinase-MB to detect perioperative myocardial damage after coronary artery bypass surgery. Chest 1998;114,482-486[Abstract/Free Full Text]
  28. Fransen, EJ, Diris, JHC, Maessen, JG, et al Evaluation of "new" cardiac markers for ruling out myocardial infarction after coronary artery bypass grafting. Chest 2002;122,1316-1321[Abstract/Free Full Text]
  29. Januzzi, J, Lewandrowski, K, MacGillivray, TE, et al A comparison of cardiac troponin T and creatine kinase-MB for patient evaluation after cardiac surgery. J Am Coll Cardiol 2002;39,1518-1523[Abstract/Free Full Text]
  30. Pan, W, Pintar, T, Anton, J, et al Statins are associated with a reduced incidence of perioperative mortality after coronary artery bypass graft surgery. Circulation 2004;110(Suppl),II45-II49
  31. Fox, KAA, Mehta, SR, Peters, R, et al Benefits and risks of the combination of clopidogrel and aspirin in patients undergoing surgical revascularization for non-ST-elevation acute coronary syndrome: the Clopidogrel in Unstable Angina to Prevent Recurrent Ischemic Events (CURE) trial. Circulation 2004;110,1202-1208[Abstract/Free Full Text]
  32. Braxton, JH, Hammond, GL, Letsou, GV, et al Optimal timing of coronary artery bypass graft surgery after acute myocardial infarction. Circulation 1995;92(Suppl),II66-II68
  33. Lee, DC, Oz, MC, Weinberg, AD, et al Optimal timing of revascularization: transmural versus nontransmural acute myocardial infarction. Ann Thorac Surg 2001;71,1198-1204[Abstract/Free Full Text]
  34. Kloner, RA, Rezkalla, SH Cardiac protection during acute myocardial infarction: where do we stand in 2004? J Am Coll Cardiol 2004;44,276-286[Abstract/Free Full Text]
  35. Christenson, JT, Simonet, F, Badel, P, et al Optimal timing of preoperative intraaortic balloon pump support in high-risk coronary patients. Ann Thorac Surg 1999;68,934-939[Abstract/Free Full Text]
  36. Creswell, LL, Moulton, MJ, Cox, JL, et al Revascularization after acute myocardial infarction. Ann Thorac Surg 1995;60,19-26[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 CirculationHome page
M. Thielmann, P. Massoudy, M. Neuhauser, K. Tsagakis, G. Marggraf, M. Kamler, K. Mann, R. Erbel, and H. Jakob
Prognostic Value of Preoperative Cardiac Troponin I in Patients Undergoing Emergency Coronary Artery Bypass Surgery With Non-ST-Elevation or ST-Elevation Acute Coronary Syndromes
Circulation, July 4, 2006; 114(1_suppl): I-448 - I-453.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
P. Monteiro and on behalf of the Portuguese Registry on Acute Coro
Impact of Early Coronary Artery Bypass Graft in an Unselected Acute Coronary Syndrome Patient Population
Circulation, July 4, 2006; 114(1_suppl): I-467 - I-472.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Thielmann, M.
Right arrow Articles by Jakob, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thielmann, M.
Right arrow Articles by Jakob, H.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS