CLINICAL RESEARCH
Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery
Giora Landesberg, MD, DSc* ,*,
Vadim Shatz, MD*,
Inna Akopnik, MD ,
Yehuda G. Wolf, MD,
Michael Mayer, DSc ,
Yacov Berlatzky, MD,
Charles Weissman, MD* and
Morris Mosseri, MD||
* Department of Anesthesiology, Jerusalem, Israel
Department of Critical Care Medicine, Jerusalem, Israel
Vascular Surgery, Jerusalem, Israel
Clinical Biochemistry, Jerusalem, Israel
|| Cardiology at Hadassah Medical Center, Jerusalem, Israel
Manuscript received April 15, 2003;
revised manuscript received May 13, 2003,
accepted May 20, 2003.
* Reprint requests and correspondence: Dr. Giora Landesberg, Department of Anesthesiology and Critical Care Medicine, Hadassah University Hospital, Jerusalem, Israel 91120.
gio{at}cc.huji.ac.il
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Abstract
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OBJECTIVES: The aim of this study was to determine the long-term prognosis with postoperative markers of myocardial ischemia and infarction.
BACKGROUND: Cardiac troponins (cTn) are superior to creatine kinase-MB fraction (CK-MB) in detecting perioperative myocardial infarction (PMI). However, their threshold levels signifying PMI and their long-term prognostic value are not yet determined.
METHODS: A cohort of 447 consecutive patients who underwent 501 major vascular procedures was prospectively studied. Perioperative continuous 12-lead electrocardiogram monitoring, cardiac troponin-I (cTn-I) and/or cardiac troponin-T (cTn-T), and CK-MB levels on the first three postoperative days, and long-term survival were determined. The association of different cutoff levels of CK-MB, troponin, and ischemia duration with long-term survival was investigated.
RESULTS: Between 14 (2.9%) and 107 (23.9%) of the patients sustained PMI, depending on the biochemical criteria used. Elevated postoperative CK-MB, cTn, and prolonged (>30 min) ischemia, at all cutoff levels examined, predicted long-term mortality independent of the preoperative predictors: patient's age, type of vascular surgery, previous myocardial infarction, and renal failure (Cox multivariate analysis). Both CK-MB >10% and cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml independently predicted a 3.75-fold and 2.06-fold increase in long-term mortality (p = 0.006 and 0.012, respectively). Similarly, both CK-MB >5% and cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml independently predicted a 2.15-fold and 1.89-fold increase in mortality (p = 0.018 and 0.01, respectively). Patients with both these markers elevated had a 4.19-fold increase in mortality (p < 0.001).
CONCLUSIONS: Postoperative CK-MB and troponin, even at low cutoff levels, are independent and complementary predictors of long-term mortality after major vascular surgery.
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Abbreviations and Acronyms
| | ACS | = acute coronary syndrome(s) | | CAD | = coronary artery disease | | CK-MB | = creatine kinase-MB fraction | | cTn | = cardiac troponin | | ECG | = electrocardiogram/electrocardiograph/ electrocardiographic | | MI | = myocardial infarction | | PMI | = perioperative myocardial infarction |
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Postoperative myocardial infarction (MI) and major cardiac complications occur in more than 4% of the patients with either established diagnosis of coronary artery disease (CAD) or risk factors for CAD, who undergo major non-cardiac surgery (1,2). In the U.S., 1.5 to 2 million patients are at such risk for postoperative infarction each year (3). There is marked variability in the reported short- term mortality (<10% to 70%) (4–6), and there are very few data on the long-term prognosis after postoperative infarction (2,7,8). Unlike non-surgical MI, the clinical diagnosis of perioperative MI (PMI) is often difficult or even impossible, when based on the presence of two of the classical triad: cardiac symptoms, typical electrocardiographic (ECG) findings, and biochemical markers. The silent nature of perioperative infarction, the subtle and transient ST-depression ECG changes resulting in non–Q-wave infarction (4), and the claimed low specificity of creatine kinase-MB fraction (CK-MB) isoenzyme (9) all lead to inconsistencies in the diagnosis of PMI and to uncertainty as to the long-term significance of perioperative markers of MI.
Cardiac troponins (cTn) are highly sensitive and specific biochemical markers for myocardial necrosis and predict increased risk of mortality and reinfarction in patients presenting with acute coronary syndrome (ACS) (10,11). In surgical patients too, cTn have been shown to identify postoperative MI better than CK-MB isoenzyme (4,9,12,13). However, in the absence of typical signs and symptoms of MI, the diagnosis of postoperative MI has to rely heavily on the rise and fall of biochemical markers, especially on cTn (14). It is yet unclear, however, whether postoperative infarction detected predominantly on the basis of these markers bears the same clinical and prognostic implications as non-surgical infarction and, therefore, requires similar surveillance and treatment. Moreover, whereas in non-surgical patients with unstable coronary syndromes even the smallest increase in cardiac troponin-I (cTn-I) or cardiac troponin-T (cTn-T) is associated with worse outcome (15), there is as of yet no consensus concerning the threshold levels of cTn signifying postoperative MI, leading researchers to use different concentrations for its diagnosis.
The present study aims to determine whether elevated postoperative troponin levels have significant prognostic implications and to define the plasma concentrations of cTn-I and cTn-T and CK-MB that correlate with postoperative myocardial ischemia based on continuous 12-lead ECG monitoring and with long-term survival. This was prospectively examined in a large cohort of vascular surgery patients.
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Methods
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After approval by the Institutional Review Board and informed consent, 447 consecutive patients who underwent 501 major vascular surgical procedures (231 carotid endarterectomies, 77 abdominal aortic operations, and 193 lower-extremity bypass procedures) at the Hadassah University Hospital from July 1997 to June 2001 were studied. The 49 patients who had more than one operation were included only once in the study. Those with no perioperative cardiac event or increase in cardiac markers were included on their first operation. If, however, one of the operations was complicated by a cardiac event or an increase in a cardiac marker, only that operation was included. None of the patients had unstable coronary syndrome in the three months preceding surgery. All preoperative chronic cardiovascular medications, including ß-blockers and aspirin, were continued until the day of surgery and resumed as soon as possible postoperatively. After completion of surgery, patients were maintained in the recovery room or intensive care unit until at least the morning after surgery and were monitored with continuous intra-arterial blood pressure. The preoperative clinical findings and the perioperative cardiac complications were recorded prospectively.
Continuous 12-lead ECG recording.
Continuous 12-lead ECG recording has been described previously (4). In brief, before induction of anesthesia, patients were connected to a continuous 12-lead ECG monitor (Solar 7000, Marquette Electronics, Milwaukee, Wisconsin), wired to a Cardiac Review Station (ST-Guard, Marquette Electronics), which automatically stored all 12-lead ECG complexes every minute and measured the absolute and relative ST-segment deviation at 60 milliseconds after the J point in all leads compared with their preoperative baseline. Episodes of ST-segment deviation, defined as ST depression or elevation of  0.2 mV in one lead or 0.1 mV in two contiguous leads that lasted more than 10 min, were automatically detected and marked by the ST-Guard. ST deviations lasting <10 min were ignored. Monitoring was continued for at least 48 h and up to 72 h. All 12-lead ST-segment trends were reviewed and periods marked by the ST-Guard, as ST-segment deviations were inspected visually and ST deviations caused by artifacts or pure up-sloping ST-segment depression were not considered as ischemia. Each patient's longest and cumulative ischemia duration, as well as the number of ischemic events was recorded.
Biochemical markers of MI.
The cTn-I and/or cTn-T levels and CK-MB were measured in all patients immediately after surgery and every morning in the first three postoperative days. If either one of these markers was elevated, its measurement was continued for the next days until its return to normal values. Until January 1999 only troponin-I was available in our institution. From January 1999, cTn-T served as the primary indicator for MI, whereas cTn-I was used mainly for confirmation in patients with impaired renal function exhibiting high levels of troponin-T. Troponin-I was measured using a Stratus II analyzer (Dade-Behring, Inc., Marburg, Germany) by mass immunoassay with two monoclonal specific antibodies. Troponin-T was measured by an electrochemiluminescence immunoassay on the Elecsys 2010 system (Boehringer Ingelheim GmbH, Germany).
Biochemical cutoff levels.
Three different cutoff levels of cTn were examined: 1) cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml. These were the receiver operator characteristic curve medical decision cutoffs for MI defined by the manufacturers of these assays. 2) cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml, which correspond to the lowest levels with <10% imprecision or coefficient of variation for these assays (16). 3) cTn-I >3.1 ng/ml and/or cTn-T >0.2 ng/ml, which, based on previous studies including ours (4,5,9,17), showed a better correlation with postoperative ischemia and infarction.
The CK was measured by a Vitros dry chemistry analyzer (Ortho Clinical Diagnostics, Johnson & Johnson) using dry slide technology. The upper limit of normal for CK total was 170 IU. The upper limit of normal for CK-MB/total CK in our laboratory was 10%; however, the cutoff level of 5% that is more often used for defining MI (18) was also investigated.
Clinical cardiac complications.
Clinical MI was diagnosed by the treating physicians independent of this study, if cTn-I >1.5 ng/ml and/or cTn-T >0.1 were associated with at least one of the following: typical ischemic symptoms, ECG changes indicative of ischemia, or new pathologic Q-waves (12). Prolonged chest pain, signs and symptoms of congestive heart failure, and new persistent arrhythmia were considered attributable to PMI if they were temporally associated with elevated cardiac markers. Cardiac death was defined as death secondary to MI, arrhythmia, or congestive heart failure.
Long-term survival.
Long-term survival was recorded from the hospital's information system, which is constantly updated by the Israeli Ministry of the Interior with all newly deceased individuals along with the date of their death.
Statistical analyses.
Chi-square analyses were used to compare dichotomous variables between groups of patients. Kaplan-Meier log-rank test and univariate and multivariate Cox regression models were used to compare survival among groups and to define predictors of long-term survival. All potential preoperative predictors with p < 0.1 on univariate survival analysis were included in the Cox multivariate regression analysis, and a backward conditional selection method was used for variable selection by the model. A value of p  0.05 was considered statistically significant. All the analyses were performed using SPSS version 10.0 (SPSS Inc., Chicago, Illinois).
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Results
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The demographic and preoperative clinical data on the 447 patients are summarized in Table 1.
Myocardial ischemia.
During 25,622 patient-hours of continuous 12-lead ECG monitoring (51.4 ± 15.7 h/patient), 66 patients had 104 ischemic episodes; all but one were denoted only by ST-segment depression alone. One patient had episodes of ST depression in the chest leads associated with ST elevation in the inferior leads. The duration of the longest ischemic episode in each patient was 16 ± 62 min (range, 11 to 625 min), and the cumulative ischemia duration of each patient was 23 ± 101 min (range, 11 to 1,150 min). The longest ischemic episode lasted over 30 min in 44 (9.8%) of the patients and over 60 min in 23 (5.1%) of the patients.
MI.
Between 14 (2.9%) and 107 (23.9%) of the patients sustained postoperative MI, depending on the biochemical criteria used (Table 2). Only 17.7% to 61.9% of them had signs or symptoms attributable to infarction. None of the patients had new Q-waves.
Each of the biochemical criteria for MI was associated with prolonged postoperative ischemia. The higher levels of troponin and CK-MB were associated with a higher incidence of prolonged postoperative ischemia (Table 2).
Sixteen (3.6%) patients were diagnosed by the treating physicians as having postoperative MI, based on the combination of elevated cTn with ECG findings and/or prolonged chest pain. Twelve (2.8%) of these patients had symptoms attributable to MI: five experienced chest pain, eight had congestive heart failure (one suffered from both). All 12 patients had both elevated cTn levels and prolonged (>60 min) postoperative ischemia. Two other patients died shortly after postoperative infarction (8 and 32 days postoperatively); none of them had typical symptoms of MI, and the diagnosis was made on the basis of the biochemical markers and the 12-lead ECG findings. Three additional patients died postoperatively from non-cardiac causes. All other patients left the hospital in stable condition.
Long-term survival.
During the one- to five-year follow-up period (mean: 32.3 ± 13.8 months), 82 patients (18.3%) died. Table 3 summarizes the univariate and multivariate Cox survival analysis of the preoperative and postoperative predictors of survival. By multivariate Cox regression analysis, age, type of vascular surgery (lower-extremity bypass surgery), previous MI, and renal insufficiency were the only preoperative predictors of long-term survival.
All cutoff levels of CK-MB, cTn, and ischemia duration examined predicted long-term survival by univariate analysis (Figs. 1 to 3). Similarly, when the multivariate model included the preoperative predictors in addition to the markers of infarction (each time a single marker was included in the model), the following markers independently predicted mortality, in the order of severity: 1) prolonged ischemia 60 min; 2) CK-MB >10%; 3) cTn-I >3.1 ng/ml and/or cTn-T >0.2 ng/ml; 4) CK-MB >5%; 5) prolonged ischemia 30 min; 6) cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml; and 7) cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml (Table 3).
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Figure 3 Kaplan-Meier survival curves of all patients divided according to their longest postoperative ischemia duration: Group I—ischemia duration <15 min; Group II—15 min < ischemia duration > 30 min; Group III—ischemia duration >30 min. Group III had worse long-term survival than Group I (p = 0.008, by log-rank test).
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When all postoperative markers of ischemia and infarction were included with the preoperative predictors in the multivariate analysis, only the following markers independently predicted mortality: 1) CK-MB >10%; 2) postoperative ischemia >60 min; and 3) cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml (odds ratio = 2.77, 2.20, and 1.64, p = 0.043, 0.033, and 0.054, respectively). If only the biochemical markers were included with the preoperative predictors in the multivariate analysis, both CK-MB >10% and cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml independently predicted mortality (odds ratio = 4.21 and 1.96, p = 0.002 and 0.005, respectively). If only the lowest cutoff levels of CK-MB and cTn were included, both CK-MB >5% and cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml independently predicted mortality (odds ratio = 2.14 and 1.89, p = 0.018 and 0.01, respectively). Finally, if the lowest cutoff levels of CK-MB and cTn were excluded from the multivariate analysis, both CK-MB >10% and cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml independently predicted mortality (odds ratio = 3.75 and 2.06, p = 0.006 and 0.012, respectively).
In additional analysis, patients who had both CK-MB >5% and cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml had a 4.19-fold increase in mortality (p = 0.001). Similarly, patients with both CK-MB >10% and cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml had a 4.04-fold increase in mortality (p = 0.007).
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Discussion
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The main finding of the present study is that even minor elevations in cTn or CK-MB during the first three postoperative days predict increased risk of long-term mortality after major vascular surgery. Between 14 (2.9%) and 107 (23.9%) of the patients sustained postoperative MI or minor myocardial damage, depending on the cutoff levels of the biochemical marker. Higher levels of biochemical markers, corresponding to a larger volume of myocardial injury or infarction, predicted worse survival: CK-MB >10% and cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml predicted 3.75-fold and 2.06-fold increase in long-term mortality, independent of the preoperative predictors: patient's age, type of vascular surgery, previous MI, and renal failure; CK-MB >5% and cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml independently predicted a 2.15-fold and 1.89-fold increase in mortality. We have previously shown that prolonged, silent ST-depression-type postoperative ischemia leads to an elevation in troponin and to overt postoperative MI (4). In the present study too, prolonged postoperative ischemia and elevated troponin levels were strongly correlated (Table 2). Prolonged >30 min and >60 min postoperative ischemia was associated, respectively, with a 2.6-fold and 3.7-fold increase in adjusted long-term mortality (Table 3).
Two previous studies investigated the effect of postoperative cTn measurements on outcome after non-cardiac surgery, and both studies followed their patients for only six months after surgery. Lopez-Jimenez et al. (19) evaluated the prognostic significance of postoperative cTn-T on cardiac complications after non-cardiac surgery. In their study, troponin-T >0.1 ng/ml correlated with overall cardiac complications, which included cardiac death, nonfatal MI, or admission for unstable angina during the six months of follow-up. Abnormal CK-MB values were not associated with subsequent complications in that study. Recently, Kim et al. (20) showed that routine troponin-I measurement on the first three postoperative days predicted all-cause mortality in the first six months after vascular surgery. Yet, no comparison was made with the parallel measurements of CK-MB or ischemia duration. More importantly, 12 (67%) of the 18 patients who died during follow-up died within the first eight weeks after surgery, thus limiting the ability of that study to infer the effect of troponin on long-term survival. The present study corroborates and expands on those observations by its in-depth analysis of the biochemical markers as well as perioperative ischemia and by its longer duration of follow-up after surgery.
Troponin levels and MI.
There is still an unresolved debate as to which cutoff levels of troponin should be used to define a clinically important MI. The conventional cutoff values, those obtained by titration of troponin to a population of patients with medical diagnosis of MI using receiver operator characteristic curve analyses, were troponin-I >1.5 and troponin-T >0.1 ng/ml for the assays used in our study. On the other hand, the American College of Cardiology/European Society of Cardiology task force stated in their consensus document for the redefinition of MI (14) that, because cTn are so specific to myocardial necrosis, even minor increases in troponin levels to greater than the 99th percentile of normal population, in the setting of documented myocardial ischemia, should be considered as MI. However, the level of precision of most troponin assays at this low range is still inadequate. Therefore, somewhat higher cutoff levels are suggested based on <10% imprecision or coefficient of variation. These levels of cTn-I >0.6 and cTn-T >0.03 ng/ml for our assays were used in the present study. Both the conventional cutoff levels, cTn-I >1.5 and/or cTn-T >0.1 ng/ml, by which 8.9% of the patients were identified as having postoperative MI, and the lower cutoff levels, cTn-I >0.6 and/or cTn-T >0.03 ng/ml, by which 23.9% of the patients had postoperative MI or minor myocardial damage, predicted long-term survival in accordance with recent findings in different kinds of patients with unstable coronary syndromes (21,22).
Troponin versus CK-MB.
The CK-MB levels predicted long-term mortality independent of cTn. Fifteen (3.4%) patients had CK-MB >5% but troponin-I <0.6 ng/ml and troponin-T <0.03 ng/ml; 3 (20%) of these 15 patients died during follow-up. In comparison, 88 (19.6%) patients with elevated troponin (cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml) had normal postoperative CK-MB (<5%); 26 (29.5%) of them died during follow-up. Thus, troponin alone detected more patients with infarction and increased risk of mortality than CK-MB alone. It is important to note, however, that CK-MB >10% was associated with worse adjusted long-term survival than troponin-I >1.5 ng/ml and/or troponin-T >0.1 (odds ratio = 5.31 vs. 2.37, respectively), and similarly, CK-MB >5% predicted worse prognosis than the lower cutoff levels of troponin (Table 3). This observation may be explained by the higher sensitivity of troponin than CK-MB to even small MI or minimal necrosis, such that have less impact on prognosis than CK-MB. Whether CK-MB was more sensitive than troponin in detecting myocardial necrosis in a minority (3.4%) of the patients without increase in troponin, or reflected skeletal muscle injury due to more extensive surgery or lower-extremity ischemia and therefore worse survival (skeletal muscle may contain up to 10% CK-MB [23]), could not be determined by this study. However, patients with both elevated CK-MB and troponin had a 4.19-fold increase in mortality, whereas patients with only one of these markers had a 2.0- to 2.2-fold increase in mortality.
Clinically evident infarction.
Only 25 (5.6%) of the patients satisfied the conventional clinical definition of MI according to the World Health Organization, i.e., the existence of at least two of the three criteria: prolonged chest pain, elevated CK-MB or cTn, and ischemic ECG changes (24). However, even in these patients the diagnosis of MI was not possible unless there was routine postoperative measurement of biochemical markers and continuous ECG monitoring, because only 16 (3.6%) of the patients had prolonged chest pain or congestive heart failure suspicious of overt MI. Our data corroborate those published by Kim et al. (20) wherein 12% of the patients had elevated troponin-I on routine postoperative surveillance, yet only 3% had clinical infarction according to the World Health Organization definition. Therefore, routine monitoring of cTn, CK-MB, and silent ischemia in the first postoperative days may provide important information on both the short-term and long-term risk of major vascular surgery patients.
The present study is also significant from the aspect of the pathophysiology of PMI. Recent studies have emphasized the prognostic importance of even minor elevations of cTn in patients with unstable coronary syndromes. Patients undergoing elective major vascular surgery constitute a different type of cardiac patients than those with unstable coronary syndromes. The former often have long-standing, yet stable CAD, and their postoperative cardiac events are typically caused by stress-induced, ST-depression-type ischemia leading to infarction (4). It has been long debated whether this type of silent postoperative ischemia and infarction is as prognostically meaningful as an ACS. In contrast to the older literature that cited 36% to 70% in-hospital mortality after PMI (25), current data show that early mortality after perioperative infarction is less than 10%, similar to that of non-ST-elevation-type infarction in non-surgical patients (4,19). This study further shows that long-term survival after even minor perioperative infarction is significantly impaired, in line with what occurs after ACS in non-surgical patients.
Study limitations.
Routine biochemical markers were measured only on the first three postoperative days. Therefore, MI evolving later than the third postoperative day may have been missed by our study protocol. However, previous studies have shown that the majority (>80%) of postoperative MI occur on the first two days after surgery (3,4,5,19). Therefore, although extending the biochemical marker measurements to the rest of the convalescence period could possibly identify more patients at increased risk for long-term mortality, it was not likely to affect the main findings of our study significantly.
We did not investigate the causes of the long-term deaths. Although the availability of such data could strengthen the study, numerous previous studies showed that the majority of deaths in vascular surgery patients are cardiac in nature and that close to half of the other non-cardiac causes of death are cardiovascular (26–29). Because not all our patients were prospectively followed for the entire follow-up period, we felt that retrospective collection of the causes of death might introduce significant inaccuracy to our data.
Although in the vast majority of postoperative patients the elevation of cardiac-specific markers is due to ischemic heart disease, there may be other clinical conditions such as pulmonary embolism, sepsis and renal failure, that may cause elevations of these markers and lead to an adverse prognosis.
Conclusions.
Cardiac troponin, CK-MB, and prolonged postoperative ischemia predict long-term mortality after major vascular surgery. Troponin and CK-MB have an independent effect on long-term survival, and the combination of both is associated with even worse survival. Further studies are needed to test whether routine measurement of postoperative cardiac markers is cost-effective and whether more aggressive diagnostic and treatment strategies for patients with postoperative MI improve survival.
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Acknowledgments
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We thank Prof. Bradly Efron from the Statistics Department at Stanford University for reviewing the statistical analyses and for his important suggestions concerning the statistical design of this study. Additionally, we wish to thank Prof. Richard L. Popp, MD, from the Cardiovascular Division at Stanford University for his editorial assistance in preparing the manuscript.
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References
|
|---|
1. Ashton CM, Petersen NJ, Wray NP, et al. The incidence of peri-operative myocardial infarction in men undergoing noncardiac surgery. Ann Intern Med. 1993;118:504–510[Abstract/Free Full Text]
2. Mangano DT, Browner WS, Hollenberg M, Li J, Tateo IM. Long-term cardiac prognosis following noncardiac surgery: The Study of Perioperative Ischemia Research Group. JAMA. 1992;268:233–239[Abstract/Free Full Text]
3. ACC/AHA guideline update on perioperative cardiovascular evaluation for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). 2002. Available at: American College of Cardiology, www.acc.org; American Heart Association, www.americanheart.org
4. Landesberg G, Mosseri M, Zahger D, et al. Myocardial infarction following vascular surgery: the role of prolonged, stress-induced, ST-depression-type ischemia. J Am Coll Cardiol. 2001;37:1858–1863[Abstract/Free Full Text]
5. Badner NH, Knill RL, Brown JE, et al. Myocardial infarction after noncardiac surgery. Anesthesiology. 1998;88:572–578[CrossRef][Medline]
6. Mangano DT. Perioperative cardiac morbidity. Anesthesiology. 1990;72:153–184[Medline]
7. McFalls EO, Ward HB, Santilli S, Scheftel M, Chesler E, Doliszny KM. The influence of perioperative myocardial infarction on long-term prognosis following elective vascular surgery. Chest. 1998;113:681–686[Abstract/Free Full Text]
8. Yeager RA, Moneta GL, Edwards JM, Taylor LM Jr, McConnell DB, Porter JM. Late survival after perioperative myocardial infarction complicating vascular surgery. J Vasc Surg. 1994;20:598–604[Medline]
9. Adams JE, Sicard GA, Allen BT, et al. Diagnosis of perioperative myocardial infarction with measurement of cardiac troponin I. N Engl J Med. 1994;330:670–674[Abstract/Free Full Text]
10. Ham CW, Ravkilde J, Gerhardt W, et al. The prognostic value of serum troponin T in unstable angina. N Engl J Med. 1992;327:146–150[Abstract]
11. 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]
12. Lee TH, Thomas EJ, Ludwig LE, et al. Troponin T as a marker for myocardial ischemia in patients undergoing major noncardiac surgery. Am J Cardiol. 1996;77:1031–1036[CrossRef][Medline]
13. Metzler H, Gries M, Rehak P, Lang T, Fruhwald S, Toller W. Perioperative myocardial cell injury: the role of troponins. Br J Anaesth. 1997;78:386–390[Abstract/Free Full Text]
14. Myocardial infarction redefined—a consensus document of the Joint ESC/ACC committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36:959–69
15. Morrow DA, Cannon CP, Rifai N, et al. TACTICS-TIMI 18 Investigators. Ability of minor elevations of troponins I and T to predict benefit from an early invasive strategy in patients with unstable angina and non-ST elevation myocardial infarction: results from a randomized trial. JAMA. 2001;286:2405–2412[Abstract/Free Full Text]
16. Apple FS, Wu AHB. Myocardial infarction redefined: role of cardiac troponin testing. Clin Chem. 2001;47:337–339
17. Bodor GS, Porter S, Ladt Y, Ladenson JH. Development of monoclonal antibodies for an assay of cardiac troponin-I and preliminary results in suspected cases of myocardial infarction. Clin Chem. 1992;38:2203–2214[Abstract/Free Full Text]
18. Ravel R. Clinical Laboratory Medicine: Clinical Application of Laboratory Data. Chicago, IL: Year Book Medical Publishers; 1995. p. 335
19. Lopez-Jimenez F, Goldman L, Sacks DB, et al. Prognostic value of cardiac troponin T after noncardiac surgery: 6-month follow-up study. J Am Coll Cardiol. 1997;29:1241–1245[Abstract]
20. 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]
21. Lindahl B, Toss H, Siegbahn A, Venge P, Wallentin L. Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease. N Engl J Med. 2000;343:1139–1147[Abstract/Free Full Text]
22. Kaul P, Newby LK, Fu Y, et al. Troponin T and quantitative ST-segment depression offer complementary prognostic information in the risk stratification of acute coronary syndrome patients. J Am Coll Cardiol. 2003;41:371–380[Abstract/Free Full Text]
23. Apple FS. Tissue specificity of cardiac troponin I, cardiac troponin T and creatine kinase-MB. Clin Chim Acta. 1999;284:151–159[CrossRef][Medline]
24. WHO MONICA Project Investigators. World Health Organization MONICA Project (monitoring trends and determinants of cardiovascular disease): a major international collaboration. J Clin Epidemiol. 1988;41:105–114[CrossRef][Medline]
25. London MJ, Mangano DT. Assessment of perioperative risk. Stoelting RK. Advances in Anesthesia. Chicago, IL: Year Book Medical Publishers; 1988. p. 53–87
26. Jamieson WR, Janusz MT, Miyagishima RT, Gerein AN. Influence of ischemic heart disease on early and late mortality after surgery for peripheral occlusive vascular disease. Circulation. 1982;66(Suppl):I92–I97
27. Hertzer NR, Young JR, Beven EG, et al. Late results of coronary bypass in patients presenting with lower extremity ischemia: the Cleveland Clinic Study. Ann Vasc Surg. 1987;1:411–419[Medline]
28. L'Italian GJ, Cambria RP, Cutler BS, et al. Comparative early and late cardiac morbidity among patients requiring different vascular surgery procedures. J Vasc Surg. 1995;21:935–944[CrossRef][Medline]
29. Norman PE, Semmens JB, Lawrence-Brown MM. Long-term relative survival following surgery for abdominal aortic aneurysm: a review. Cardiovasc Surg. 2001;9:219–224[CrossRef][Medline]
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Authors/Task Force Members, D. Poldermans, J. J. Bax, E. Boersma, S. De Hert, E. Eeckhout, G. Fowkes, B. Gorenek, M. G. Hennerici, B. Iung, et al.
Guidelines for pre-operative cardiac risk assessment and perioperative cardiac management in non-cardiac surgery: The Task Force for Preoperative Cardiac Risk Assessment and Perioperative Cardiac Management in Non-cardiac Surgery of the European Society of Cardiology (ESC) and endorsed by the European Society of Anaesthesiology (ESA)
Eur. Heart J.,
November 2, 2009;
30(22):
2769 - 2812.
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O. Schouten, E. Boersma, S. E. Hoeks, R. Benner, H. van Urk, M. R.H.M. van Sambeek, H. J.M. Verhagen, N. A. Khan, M. Dunkelgrun, J. J. Bax, et al.
Fluvastatin and Perioperative Events in Patients Undergoing Vascular Surgery
N. Engl. J. Med.,
September 3, 2009;
361(10):
980 - 989.
[Abstract]
[Full Text]
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S. Ausset, V. Minville, C. Marquis, O. Fourcade, N. Rosencher, D. Benhamou, and Y. Auroy
Postoperative myocardial damages after hip fracture repair are frequent and associated with a poor cardiac outcome: a three-hospital study
Age Ageing,
July 1, 2009;
38(4):
473 - 476.
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G. Landesberg, W. S. Beattie, M. Mosseri, A. S. Jaffe, and J. S. Alpert
Perioperative Myocardial Infarction
Circulation,
June 9, 2009;
119(22):
2936 - 2944.
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S. Bevilacqua, S. Romagnoli, F. Ciappi, C. Lazzeri, S. Gelsomino, C. Pratesi, and G. F. Gensini
Anesthesia for Carotid Endarterectomy: The Third Option. Patient Cooperation During General Anesthesia
Anesth. Analg.,
June 1, 2009;
108(6):
1929 - 1936.
[Abstract]
[Full Text]
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D. Bolliger, M. D. Seeberger, G. A. L. Lurati Buse, P. Christen, B. Rupinski, L. Gurke, and M. Filipovic
A Preliminary Report on the Prognostic Significance of Preoperative Brain Natriuretic Peptide and Postoperative Cardiac Troponin in Patients Undergoing Major Vascular Surgery
Anesth. Analg.,
April 1, 2009;
108(4):
1069 - 1075.
[Abstract]
[Full Text]
[PDF]
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C. P. Chong, Q. T. Lam, J. E. Ryan, R. N. Sinnappu, and W. K. Lim
Incidence of post-operative troponin I rises and 1-year mortality after emergency orthopaedic surgery in older patients
Age Ageing,
March 1, 2009;
38(2):
168 - 174.
[Abstract]
[Full Text]
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A. K. Saenger and A. S. Jaffe
Requiem for a Heavyweight: The Demise of Creatine Kinase-MB
Circulation,
November 18, 2008;
118(21):
2200 - 2206.
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B. HARTE and A. K. JAFFER
Perioperative beta-blockers in noncardiac surgery: Evolution of the evidence
Cleveland Clinic Journal of Medicine,
July 1, 2008;
75(7):
513 - 519.
[Abstract]
[Full Text]
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G. Gregoratos
Current Guideline-Based Preoperative Evaluation Provides the Best Management of Patients Undergoing Noncardiac Surgery
Circulation,
June 17, 2008;
117(24):
3134 - 3144.
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K. Thygesen, J. S. Alpert, A. S. Jaffe, H. D. White, and on behalf of the Joint ESC/ACCF/AHA/WHF Task Force
Reply
J. Am. Coll. Cardiol.,
May 6, 2008;
51(18):
1826 - 1827.
[Full Text]
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J. A. Wolfe Barry, J. H. Barth, and S. J. Howell
Cardiac troponins: their use and relevance in anaesthesia and critical care medicine
CEACCP,
April 1, 2008;
8(2):
62 - 66.
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[PDF]
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G. Landesberg and M. Mosseri
PRO: Preoperative Coronary Revascularization in High-Risk Patients Undergoing Vascular Surgery
Anesth. Analg.,
March 1, 2008;
106(3):
759 - 763.
[Full Text]
[PDF]
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K. Thygesen, J. S. Alpert, A. S. Jaffe, H. D. White, and On behalf of the Joint ESC/ACCF/AHA/WHF Task Force
Intraoperative myocardial infarction in non-cardiac surgery: is a universal definition feasible? reply
Eur. Heart J.,
February 2, 2008;
29(4):
567 - 568.
[Full Text]
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O. Schouten, J. J. Bax, and D. Poldermans
Preoperative cardiac risk assessment in vascular surgery patients: seeing beyond the perioperative period
Eur. Heart J.,
February 1, 2008;
29(3):
283 - 284.
[Full Text]
[PDF]
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E. O. McFalls, H. B. Ward, T. E. Moritz, F. S. Apple, S. Goldman, G. Pierpont, G. C. Larsen, B. Hattler, K. Shunk, F. Littooy, et al.
Predictors and outcomes of a perioperative myocardial infarction following elective vascular surgery in patients with documented coronary artery disease: results of the CARP trial
Eur. Heart J.,
February 1, 2008;
29(3):
394 - 401.
[Abstract]
[Full Text]
[PDF]
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R. Wiessner, K. Hannemann-Pohl, R. Ziebig, H. Grubitzsch, B. Hocher, O. Vargas-Hein, A. Lun, I. Schimke, and L. Liefeldt
Impact of kidney function on plasma troponin concentrations after coronary artery bypass grafting
Nephrol. Dial. Transplant.,
January 1, 2008;
23(1):
231 - 238.
[Abstract]
[Full Text]
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NACB WRITING GROUP MEMBERS, A. H.B. Wu, A. S. Jaffe, F. S. Apple, R. L. Jesse, G. L. Francis, D. A. Morrow, L. K. Newby, J. Ravkilde, W.H. W. Tang, et al.
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Use of Cardiac Troponin and B-Type Natriuretic Peptide or N-Terminal proB-Type Natriuretic Peptide for Etiologies Other than Acute Coronary Syndromes and Heart Failure
Clin. Chem.,
December 1, 2007;
53(12):
2086 - 2096.
[Abstract]
[Full Text]
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S. Mantha, J. Foss, J. E. Ellis, and M. F. Roizen
Intense Cardiac Troponin Surveillance for Long-Term Benefits Is Cost-Effective in Patients Undergoing Open Abdominal Aortic Surgery: A Decision Analysis Model
Anesth. Analg.,
November 1, 2007;
105(5):
1346 - 1356.
[Abstract]
[Full Text]
[PDF]
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L. A. Fleisher, J. A. Beckman, K. A. Brown, H. Calkins, E. L. Chaikof, K. E. Fleischmann, W. K. Freeman, J. B. Froehlich, E. K. Kasper, J. R. Kersten, et al.
ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery) Developed in Collaboration With the American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, and Society for Vascular Surgery
J. Am. Coll. Cardiol.,
October 23, 2007;
50(17):
e159 - e242.
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L. A. Fleisher, J. A. Beckman, K. A. Brown, H. Calkins, E. L. Chaikof, K. E. Fleischmann, W. K. Freeman, J. B. Froehlich, E. K. Kasper, J. R. Kersten, et al.
ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery)
Circulation,
October 23, 2007;
116(17):
e418 - e500.
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F. W. LoGerfo
Carotid Stents: Unleashed, Unproven
Circulation,
October 2, 2007;
116(14):
1596 - 1601.
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Z. A. Ali, C. J. Callaghan, E. Lim, A. A. Ali, S.A. Reza Nouraei, A. M. Akthar, J. R. Boyle, K. Varty, R. K. Kharbanda, D. P. Dutka, et al.
Remote Ischemic Preconditioning Reduces Myocardial and Renal Injury After Elective Abdominal Aortic Aneurysm Repair: A Randomized Controlled Trial
Circulation,
September 11, 2007;
116(11_suppl):
I-98 - I-105.
[Abstract]
[Full Text]
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P.-G. Chassot, A. Delabays, and D. R. Spahn
Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction
Br. J. Anaesth.,
September 1, 2007;
99(3):
316 - 328.
[Abstract]
[Full Text]
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E. R. Mohler III, S. Mantha, A. B. Miller, D. Poldermans, A. B. Cropp, L. B. St. Aubin, C. B. Billing JR, and L. A. Fleisher
Should troponin and creatinine kinase be routinely measured after vascular surgery?
Vascular Medicine,
August 1, 2007;
12(3):
175 - 181.
[Abstract]
[PDF]
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T. S. Perlstein and J. A. Beckman
Peri-operative cardiac biomarker surveillance: a strategy in need of a goal
Vascular Medicine,
August 1, 2007;
12(3):
211 - 213.
[PDF]
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Y. Le Manach, G. Godet, P. Coriat, C. Martinon, M. Bertrand, M.-H. Fleron, and B. Riou
The Impact of Postoperative Discontinuation or Continuation of Chronic Statin Therapy on Cardiac Outcome After Major Vascular Surgery
Anesth. Analg.,
June 1, 2007;
104(6):
1326 - 1333.
[Abstract]
[Full Text]
[PDF]
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M. Raux, G. Godet, R. Isnard, P. Mergoni, J.-P. Goarin, M. Bertrand, M. Fleron, P. Coriat, and B. Riou
Low negative predictive value of dobutamine stress echocardiography before abdominal aortic surgery
Br. J. Anaesth.,
December 1, 2006;
97(6):
770 - 776.
[Abstract]
[Full Text]
[PDF]
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A. O. Adesanya, J. A. de Lemos, N. B. Greilich, and C. W. Whitten
Management of perioperative myocardial infarction in noncardiac surgical patients.
Chest,
August 1, 2006;
130(2):
584 - 596.
[Abstract]
[Full Text]
[PDF]
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E. W. Moretti, M. F. Newman, L. H. Muhlbaier, D. Whellan, R. P. Petersen, D. Rossignol, C. B. McCants Jr, B. Phillips-Bute, and E. Bennett-Guerrero
Effects of Decreased Preoperative Endotoxin Core Antibody Levels on Long-term Mortality After Coronary Artery Bypass Graft Surgery
Arch Surg,
July 1, 2006;
141(7):
637 - 641.
[Abstract]
[Full Text]
[PDF]
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M. N. Vicenzi, T. Meislitzer, B. Heitzinger, M. Halaj, L. A. Fleisher, and H. Metzler
Coronary artery stenting and non-cardiac surgery--a prospective outcome study
Br. J. Anaesth.,
June 1, 2006;
96(6):
686 - 693.
[Abstract]
[Full Text]
[PDF]
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L. F. Souza
Anesthesia research needs definitions.
Anesth. Analg.,
April 1, 2006;
102(4):
1287 - 1287.
[Full Text]
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S. J. Howell, J. P. Thompson, A. F. Nimmo, C. Snowden, N. D. Edwards, J. Carlisle, M.-S. Suleiman, and A. Baumbach
Relationship between perioperative troponin elevation and other indicators of myocardial injury in vascular surgery patients
Br. J. Anaesth.,
March 1, 2006;
96(3):
303 - 309.
[Abstract]
[Full Text]
[PDF]
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C. R. Henry, D. Satran, B. Lindgren, C. Adkinson, C. I. Nicholson, and T. D. Henry
Myocardial Injury and Long-term Mortality Following Moderate to Severe Carbon Monoxide Poisoning
JAMA,
January 25, 2006;
295(4):
398 - 402.
[Abstract]
[Full Text]
[PDF]
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L. Babuin and A. S. Jaffe
Troponin: the biomarker of choice for the detection of cardiac injury
Can. Med. Assoc. J.,
November 8, 2005;
173(10):
1191 - 1202.
[Abstract]
[Full Text]
[PDF]
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F. Bursi, L. Babuin, A. Barbieri, L. Politi, M. Zennaro, T. Grimaldi, A. Rumolo, M. Gargiulo, A. Stella, M. G. Modena, et al.
Vascular surgery patients: perioperative and long-term risk according to the ACC/AHA guidelines, the additive role of post-operative troponin elevation
Eur. Heart J.,
November 2, 2005;
26(22):
2448 - 2456.
[Abstract]
[Full Text]
[PDF]
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M. Thielmann, P. Massoudy, M. Neuhauser, S. Knipp, M. Kamler, J. Piotrowski, K. Mann, and H. Jakob
Prognostic Value of Preoperative Cardiac Troponin I in Patients With Non-ST-Segment Elevation Acute Coronary Syndromes Undergoing Coronary Artery Bypass Surgery
Chest,
November 1, 2005;
128(5):
3526 - 3536.
[Abstract]
[Full Text]
[PDF]
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P.J. Devereaux, L. Goldman, S. Yusuf, K. Gilbert, K. Leslie, and G. H. Guyatt
Surveillance and prevention of major perioperative ischemic cardiac events in patients undergoing noncardiac surgery: a review
Can. Med. Assoc. J.,
September 27, 2005;
173(7):
779 - 788.
[Abstract]
[Full Text]
[PDF]
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H.-J. Priebe
Perioperative myocardial infarction--aetiology and prevention
Br. J. Anaesth.,
July 1, 2005;
95(1):
3 - 19.
[Abstract]
[Full Text]
[PDF]
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F. Bonnet and E. Marret
Influence of anaesthetic and analgesic techniques on outcome after surgery
Br. J. Anaesth.,
July 1, 2005;
95(1):
52 - 58.
[Abstract]
[Full Text]
[PDF]
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M. Thielmann, P. Massoudy, M. Neuhauser, S. Knipp, M. Kamler, G. Marggraf, J. Piotrowski, and H. Jakob
Risk stratification with cardiac troponin I in patients undergoing elective coronary artery bypass surgery
Eur. J. Cardiothorac. Surg.,
May 1, 2005;
27(5):
861 - 869.
[Abstract]
[Full Text]
[PDF]
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A. N. DeMaria, O. Ben-Yehuda, D. Berman, G. K. Feld, B. H. Greenberg, J. D. Knoke, K. U. Knowlton, W. Y.W. Lew, J. Narula, D. Sahn, et al.
Highlights of the year in JACC 2004
J. Am. Coll. Cardiol.,
January 4, 2005;
45(1):
137 - 153.
[Full Text]
[PDF]
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T. G. Monk, V. Saini, B. C. Weldon, and J. C. Sigl
Anesthetic Management and One-Year Mortality After Noncardiac Surgery
Anesth. Analg.,
January 1, 2005;
100(1):
4 - 10.
[Abstract]
[Full Text]
[PDF]
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G. Landesberg, M. Mosseri, V. Shatz, I. Akopnik, M. Bocher, M. Mayer, H. Anner, Y. Berlatzky, and C. Weissman
Cardiac troponin after major vascular surgery: The role of perioperative ischemia, preoperative thallium scanning, and coronary revascularization
J. Am. Coll. Cardiol.,
August 4, 2004;
44(3):
569 - 575.
[Abstract]
[Full Text]
[PDF]
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D. Mukherjee and K. A. Eagle
Ischemia, revascularization, and perioperative troponin elevation after vascular surgery
J. Am. Coll. Cardiol.,
August 4, 2004;
44(3):
576 - 578.
[Full Text]
[PDF]
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S. J. Howell and J. W. Sear
Perioperative myocardial injury: individual and population implications
Br. J. Anaesth.,
July 1, 2004;
93(1):
3 - 8.
[Abstract]
[Full Text]
[PDF]
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K A A Fox, J Birkhead, R Wilcox, C Knight, and J Barth
British Cardiac Society Working Group on the definition of myocardial infarction
Heart,
June 1, 2004;
90(6):
603 - 609.
[Abstract]
[Full Text]
[PDF]
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A. N. DeMaria, O. Ben-Yehuda, D. Berman, G. K. Feld, B. H. Greenberg, J. D. Knoke, K. U. Knowlton, W. Y. W. Lew, and S. Tsimikas
Highlights of the year in JACC 2003
J. Am. Coll. Cardiol.,
December 17, 2003;
42(12):
2156 - 2166.
[Full Text]
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Top
Abstract
Methods
