EJCTS Click here to go to Edwards website
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Milo C. Engoren
Anoar Zacharias
Thomas A. Schwann
Christopher J. Riordan
Samuel J. Durham
Aamir Shah
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Engoren, M. C.
Right arrow Articles by Shah, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Engoren, M. C.
Right arrow Articles by Shah, A.
Related Collections
Right arrow Coronary disease
Right arrow Myocardial infarction
Right arrow Myocardial protection

Eur J Cardiothorac Surg 2005;28:114-119
© 2005 Elsevier Science NL

The association of elevated creatine kinase-myocardial band on mortality after coronary artery bypass grafting surgery is time and magnitude limited

Milo C. Engoren a , * , Robert H. Habib b , c , Anoar Zacharias b , d , e , Thomas A. Schwann b , d , e , Christopher J. Riordan b , d , e , Samuel J. Durham b , d , e , Aamir Shah b , d , e

a Department of Anesthesiology, St. Vincent Mercy Medical Center, 2213 Cherry Street, Toledo, OH 43608, USA
b Department of Cardiovascular Surgery, St. Vincent Mercy Medical Center, 2213 Cherry Street, Toledo, OH 43608, USA
c Department of Medicine, Medical College of Ohio, Toledo, OH, USA
d Department of Cardiovascular Surgery, Medical College of Ohio, Toledo, OH, USA
e Department of Cardiovascular Surgery, St. Luke's Medical Center, Maumee, OH, USA

Received 21 December 2004; received in revised form 2 March 2005; accepted 4 March 2005.

* Corresponding author. Tel.: +1 419 251 4715; fax: +1 419 251 3859. (Email: engoren{at}pol.net).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Objective: The joint European Society of Cardiology and American College of Cardiology consensus statement on myocardial necrosis after revascularization stated that any amount of myocardial necrosis as detected by cardiac enzymes should be labeled a myocardial infarct. However, it also stated that more data collection is necessary to better interpret the elevation of cardiac enzymes after coronary artery bypass grafting. We sought to determine if a single postoperative value of creatine kinase-myocardial band could be used as a risk factor to help predict mortality after coronary artery bypass surgery. Methods: A retrospective analysis of prospectively collected data on 1161 patients undergoing first-time, isolated coronary artery bypass surgery utilizing normothermic cardiopulmonary bypass was conducted. Creatine kinase-myocardial band was measured the morning after surgery. Binary logistic regression, Cox proportional hazard models, and overlapping quintiles were used to illuminate the association between creatine kinase-myocardial band elevation and mortality after coronary artery bypass surgery. Results: We found a threshold value of creatine kinase-myocardial band, 40ng/mL, above which elevations were associated with increased death rates. This association held after adjustment for other factors known to contribute to postoperative mortality. However, after 1 year, there was no longer a statistically significant higher mortality associated with elevated creatinine kinase-myocardial band >40ng/mL. Conclusion: Elevation of creatine kinase-myocardial band the morning after surgery above a threshold 40ng/mL is associated with an increased risk of mortality.

Key Words: Coronary artery bypass surgery • Survival analysis • Mortality • Myocardial infarction • Myocardial injury


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
The joint European Society of Cardiology and American College of Cardiology consensus statement on myocardial necrosis after revascularization stated that any amount of myocardial necrosis as detected by cardiac enzymes should be labeled a myocardial infarct [1]. It also stated that more data collection is necessary to better interpret the elevation of cardiac enzymes after coronary artery bypass grafting (CABG). Recently, several studies have evaluated the relationship between elevated creatine kinase myocardial band (CK-MB) and short to medium (≤3 years) term outcome [2–5]. However, these studies used a variety of arbitrary definitions of what constituted elevated CK-MB, used the highest value of several measurements, and were conducted exclusively in patients who underwent hypothermic cardiopulmonary bypass.

Because CK-MB elevation generally peaks 2h after CABG surgery, but peaks 17h after a myocardial infarction [6], it should be possible to determine if a single appropriately timed CK-MB measurement could be used as a risk factor to help predict mortality in patients undergoing normothermic cardiopulmonary bypass and to (1) elucidate the length of time that this association, if any, persisted and (2) the clinically meaningful CK-MB threshold value above which long-term outcomes are adversely affected.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
Patients had general anesthesia induced with fentanyl (4–8µg/kg), diazepam (5mg), thiopental (25–250mg to achieve mean arterial pressure=70mmHg before intubation), and pancuronium (0.1mg/kg). Vecuronium (0.1mg/kg), instead of pancuronium, was used if the patient had renal failure. Anesthesia was maintained with isoflurane and small supplemental doses of fentanyl (1–2µg/kg) and diazepam (2.5–5.0mg). Typically, only isoflurane was used after separation from cardiopulmonary bypass. The goal was to have the patient extubated 4h after arrival in the ICU. During cardiopulmonary bypass the patient was actively heated to maintain urinary bladder temperature=37°C. The heart was cooled with topical ice slush and cardioplegia consisted of Plegisol (Baxter Healthcare Corp) with 1g of lidocaine hydrochloride, 50mEq KCL, and 15g of NaHCO3 (8.4%) in cold blood.

The Institutional Review Board approved this study. As it was a database review, the Board waived informed consent.

2.1. Subjects
All patients who underwent first-time, isolated CABG with cardiopulmonary bypass between January 1, 1995 and December 31, 1996 were considered for this study. Twenty-six patients were excluded for having myocardial infarction less than 24h preoperatively. Another 19 patients (1.6%) with operative mortality—defined as in-hospital death or out-of-hospital death within 30 days of surgery, as per the Society of Thoracic Surgeons definition—were analyzed only univariately due to the small number of events. The remaining 1161 patients comprised the study population to investigate 31 day to 75month mortality. All data had been prospectively entered in the database. CK-MB levels were drawn the morning after surgery in all patients. The upper limit of normal in our laboratory is 5ng/mL. Long-term patient survival data was secured from the social security death index database http://ssdi.genealogy.rootsweb.com, which was queried in September 2001 using patient name and social security number combinations for all patients. This corresponds to minimum and maximum follow-up times of 51 months (December 1996 patients) and 75 months (January 1995 patients), respectively. The cardiac surgery database was then updated for all deceased patients with the exact date of death.

2.1.1. Definitions
The Society of Thoracic Surgeons definitions were used for all entries in the database [7]. Briefly they are: Same day admit, ‘patient admitted for scheduled elective procedure on same day as procedure.’ Ever smoked, ‘a history confirming any form of tobacco use in the past.’ Diabetes mellitus, ‘a history of diabetes, regardless of duration of disease or need for anti-diabetic agents.’ Renal failure, ‘documented fasting serum creatinine level of >2.0mg/dL.’ Hypertension, ‘blood pressure exceeding 140/90mmHg or a history of high blood pressure, or the need for antihypertensive medications.’ Stroke, ‘a central neurologic deficit persisting more than 24.’ Cardiomegaly, ‘a cardiothoracic ratio >0.5 demonstrated on a preoperative chest film.’ COPD, ‘a patient who requires pharmacologic therapy for the treatment of chronic pulmonary compromise, or a patient who has a FEV1 <75% of predicted value.’ Peripheral vascular disease, ‘a history of aneurysm and/or occlusive vascular disease with or without previous extracardiac surgery.’ Cerebrovascular disease, ‘any transient ischemia attack, reversible ischemic neurologic deficit, cerebrovascular accident/stroke, or history of cerebrovascular surgery.’ Myocardial infarction, ‘the appearance of a new Q wave in two or more contiguous leads on ECG, or...having clinical, angiographic, electrocardiographic, and/or laboratory isoenzyme evidence of myocardial necrosis with an ECG showing no new Q waves.’ Congestive heart failure, the patient has ‘at least three of the following: presence of dyspnea, rales thought to represent pulmonary congestion, peripheral edema, cardiomegaly on chest X-ray, chest X-ray compatible with interstitial edema.’ Arrhythmia, ‘the presence of atrial or ventricular ectopy which may or may not require therapy...abnormal rapid ventricular rhythm causing hemodynamic collapse (tachycardia) or diffuse chaotic ventricular depolarization unable to produce and effective blood pressure (fibrillation)...intermittent failure of AV conduction manifested by electrocardiographic evidence of intermittently nonconducted P waves at physiological heart rates...multiple atrial foci that discharge without a single uniform atrial depolarization. There are no P waves and AV nodal conduction occurs in a nearly random fashion producing an irregular ventricular response.’ Preoperative diuretics, diuretics ‘taken by the patient on a chronic basis within 30 days of surgery within 24h preceeding surgery.’ Left main disease, ‘When there is >50% compromise of vessel diameter in any angiographic view.’ Perfusion time, The ‘total number of minutes on cardiopulmonary bypass.’ Transfusion, The patient received red blood cells, fresh frozen plasma, platelets, or cryoprecipitate intra- or postoperatively. Prolonged mechanical ventilation, Patient required mechanical ventilation for >24h postoperatively. Perioperative myocardial infarction, ‘new Q waves in 2 or more contiguous leads in postop 12 lead ECG.’ Predicted mortality was calculated from the Society of Thoracic Surgeons' risk assessment model [8].

2.2. Data analysis
The effect of CK-MB on survival in the 1161 operative survivors was tested in three ways: (1) Subdividing patients according to arbitrary CK-MB cutoffs may not allow a clear identification of a critical value above which outcomes are (or are not) adversely affected. We, therefore, computed Kaplan–Meier survival for CK-MB-based patient quintile groups with 67% overlapping ranging from the lowest to highest values as described by us previously [9]. In addition, we similarly analyzed the highest CK-MB decile group. From each of these curves, we extracted the survival values corresponding to 12, 24 and 48 months postCABG. This approach allows for a finer and more gradual description of the relation between the dependent (CK-MB) and independent variables (survival) and minimizes the possible effects of CK-MB heterogeneity within each analyzed subgroup. These results were then used to construct hazard functions depicting the rate of death per month for each of the groups. These functions are useful to identify the between-group variation in survival trends and the most critical period determining postoperative survival. Death hazard analysis versus time after CABG was done based on Blackstone's multiphase model via a custom made nonlinear regression routine (SigmaPlot 2000, SPSS Inc., Chicago, IL) [10]. CK-MB levels were then used to create Receiver Operator Characteristic curves. (2) Binary logistic regression for (a) all deaths and (b) deaths occurring in the first year and (3) Cox proportional hazard model for (a) all deaths and (b) all deaths occurring after the first year. In toto, 72 demographic, preoperative, intraoperative, and postoperative variables from the database were analyzed.

2.3. Statistical methods
Continuous variables were analyzed with either the unpaired t-test and presented as mean±SD or the nonparametric Mann–Whitney rank sum test and presented as median (interquartile range) depending on normality. Categorical variables were analyzed with the Chi-square test or the Fisher Exact tests depending on applicability. Binary logistic regression and Cox proportional hazard modeling was done by backwards selection and confirmed by forward selection. Because CK-MB values were not normally distributed, CK-MB values were logarithm-transformed (LN of CK-MB) and these values were used in the logistic regression and Cox proportional hazard modeling. Variables were entered if they were univariably significant at P<0.25 and were retained at P<0.05. Separate models were created to predict all deaths, those dying within their first postoperative year, and, after excluding all those who died in that year, on the remaining patients. When LN of CK-MB was not statistically significant, the multivariable models were re-calculated with LN-MB forced to remain in the models. However, the results of the other parameters are presented from the nonforced models. A P-value less than 0.05 indicated significance for all statistical tests. (SPSS 11 for Windows, SPSS, Chicago, IL).


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
Operative mortality was 1.6% and CK-MB was significantly higher in the operative mortality group 15 (9–33) vs. 39 (11–233), P=0.037. Fig. 1 shows the frequency distribution of CK-MB in the remaining 1161 patients. Their demographics are shown in Table 1 . Six patients showed EKG evidence of perioperative myocardial infarction, four were still alive at late follow-up. Nonoperative all-cause mortality at 1, 2, 3, 4, and 5 years were 3.3, 4.7, 7.1, 9.0, and 10.4%, respectively (Fig. 2 ). Cox proportional hazard modeling found that each one natural logarithm increase in CK-MB, e.g. from 10 to 27 or 40 to 109ng/mL, was associated with a 31% increase in the death rate.(Table 2 ) Because Cox proportional hazard models assume that the death rate is linearly proportional to the logarithm of the CK-MB level and that the rate is constant with time, which might not hold true, we examined the data further with overlapping quintiles. This showed an increased risk of mortality only when the CK-MB>40ng/mL. Beyond 1 year, while the hazard ratio suggested that the increased risk persisted, it did not reach statistical significance (Figs. 3 and 4 ). Two-hundred and one of the 1161 patients had CK-MB>40ng/mL. After 1 year, the overlapping quintile method suggested that the risk became independent of the CK-MB levels. The fall in death rate after 1 year and the elevated risk of death associated with CK-MB>40 was confirmed by creating Receiver Operated Characteristic curves for CK-MB levels for the first year and for the succeeding years. These showed that CK-MB levels were predictive only for the first year (Area under the curve=0.638±0.053, P=0.002, for the first year and 0.486±0.031, P=0.621, for the succeeding years). The sensitivity (=0.452) plus specificity (=0.817) of CK-MB=40 as the cutoff value to predict deaths within 1 year of surgery was within 1% of the maximum value, confirming this cutoff point as an acceptable threshold between an association between CK-MB elevation and increased death and no association. Therefore the population was divided into three groups: those who had CK-MB ≤40ng/mL and died within 1 year of surgery, those who had CK-MB>40ng/mL and died within 1 year of surgery, and those who were alive 1 year after surgery.



View larger version (18K):
[in this window]
[in a new window]
  		Fig. 1. Logarithmic distribution of CK-MB values.

 

View this table:
[in this window]
[in a new window]
  		Table 1. Patient Demographics (n=1161) of patients who survived at least 30 days
 


View larger version (18K):
[in this window]
[in a new window]
  		Fig. 2. Kaplan–Meier survival curves for different CK-MB values. (NB: The cumulative survival axis shows a cut in its value to emphasize the differences in survival).

 

View this table:
[in this window]
[in a new window]
  		Table 2. Cox Model predicting death in all patients who survived at least 30 days
 


View larger version (22K):
[in this window]
[in a new window]
  		Fig. 3. Cumulative 12, 24, and 48 months survival after CABG in CK-MB based overlapping quintile subgroups. Lines through data represent the sigmoidal regression results for better visual illustration of the trend of increased mortality for CK-MB values≥40ng/mL.

 
Binary logistic regression performed on all patients who survived 30 days but then died within 1 year of surgery found that CK-MB was associated with an increased risk of death (Table 3 -top). However, when binary logistic regression was applied separately to the two populations above and below the threshold value of CK-MB=40ng/mL, only CK-MB>40ng/mL was associated with an increased risk of dying (8.977 fold for each one logarithm increase above 40ng/mL) (Table 3-middle). Adding the other statistically significant predictors: age, left main disease, and transfusion to logarithm of CK-MB improved the area under the ROC curve to 0.855±0.026, P<0.001. CK-MB levels ≤40ng/mL were not associated with any increase risk of death (Table 3-bottom). When forced into this model, logarithm of CK-MB was not a statistically significant predictor of late mortality: P=0.839 with a wide confidence interval that included 1.0. Next, Cox proportional hazard modeling was used on all those patients who survived at least 1 year after surgery. This found that CK-MB levels were not associated with death rate in patients who survived at least 1 year (Table 4 ). Again, when logarithm of CK-MB was forced into this model, it was not statistically significant: P=0.203 with a wide confidence interval that included 1.0. Instead, it found that transfusion, longer perfusion time, and preoperative renal failure, COPD, congestive heart failure, and arrhythmia were predictive of death after 1 year.


View this table:
[in this window]
[in a new window]
  		Table 3. (top)-All patients dead at 1 year after surgery regardless of CK-MB levels
 

View this table:
[in this window]
[in a new window]
  		Table 4. Cox model—showing predictors of death in patients who survived at least 1 year after surgery Follow-up is 51–75 months after surgery
 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
We found that elevated CK-MB the morning after isolated CABG was associated with increased mortality perioperatively and within the following eleven months. Beyond 1 year, while the hazard ratio suggested that an elevated CK-MB was still associated with an increased risk of death (Fig. 4), by multivariable analyses, this was not statistically significant. The risk, although small, increased with increasing levels of CK-MB elevation above a threshold of 40ng/mL (Figs. 2 and 3). The risk persisted after adjustment for other comorbidities and intermediate outcomes. Because the standard statistical techniques of binary logistic regression and Cox proportional hazard modeling assume, respectively, a linear relationship between predictive factors and dichotomous event (death) and a risk of death that is linearly proportional to the logarithm of the CK-MB level and is constant with time, and thus may miss relationships that are nonlinear or occur above or below a threshold value, overlapping quintiles with hazard graphs were used to better define the time dependency of the relationship. This showed a threshold value for CK-MB.



View larger version (30K):
[in this window]
[in a new window]
  		Fig. 4. Top, Comparison of Kaplan–Meier survival with patients divided into those with CK-MB<40ng/mL versus≥40ng/mL (symbols) with corresponding multiphase survival model fit as described by Blackstone et al. [8] (Lines). Bottom, Relative death Hazard versus time after CABG derived as the ratio of the corresponding individual death hazard functions (CK-MB≥40/CK-MB<40) showing increased mortality for CK-MB values≥40ng/mL particularly during year 1. Hazard functions show increased mortality for CK-MB values≥40ng/mL.

 
Four previous studies evaluated the relationship between CK-MB levels and postCABG mortality [2–5]. Klatte et al. followed 2394 patients who underwent CABG as part of the GUARDIAN trial. Patients were eligible if they were ‘high-risk CABG’, but were excluded if they had ‘significant hepatic or renal impairment.’ CK-MB was determined at 8, 12, 16, and 24h after CABG and the highest value was used in their analysis. They found that elevated CK-MB predicted 6-month mortality, but follow-up was stopped at that time [2]. We included patients with hepatic and renal impairment and found that even including these patients, in whom renal impairment predicted death (Tables 1, 2 top, 3), elevated CK-MB still predicted death.

Steuer et al. studied 4911 patients with CK-MB drawn the morning after CABG [3]. They examined the relationship between CK-MB and aspartate aminotransferase (AST) and postoperative mortality using Cox proportional hazards model. Outcome was examined over four time ranges: 0–30 days and 0–3, 3–6, >6 years of follow-up. Both elevated AST and CK-MB predicted several-fold increases in death within 30 days of CABG. Beyond 30 days, they found that patients with AST>2.35µ/L had 1.5-fold (1.1–1.9, 95% confidence interval) increase in death over all years of follow-up. CK-MB was dichotomously divided into ≤ or >61µg/L. CK-MB>61µg/L was associated with a 1.5 P-fold (1.1–2.0, 95% confidence interval) increase in death over all years of follow-up. When examined over each time interval, CK-MB>61µg/L was associated with a nonsignificant increase in death: 1.3 fold (0.8–2.2) over 3 years, 1.4 fold (1.0–2.0) from 3 to 6 years, and 1.3 fold (0.8–2.2) beyond 6 years. By using 0–3 years, rather than 0–1 year as we did, without explaining why they chose that time interval, they may have missed an increased risk in the first year by averaging it with a longer time interval in which CK-MB is not a risk factor for death.

Brener et al. followed 3812 patients after first time CABG [4]. Follow-up was 1035±516 days after CABG. They found that unadjusted risk of death was constant for CK-MB≤10 times the upper limit of normal (ULN), but was nearly threefold higher when CK-MB was >10 times ULN for 3 year outcome. After correction for other predictors, CK-MB>10 times ULN was associated with a 1.3 fold (1.1–1.5) increase in mortality. They did not evaluate risk over shorter time frames. We found a similar increased risk for CK-MB>8 times ULN. But by failing to examine risk over shorter time frames they may have missed important time-dependent effects of elevated CK-MB.

Costa et al. studied 496 patients with CK-MB obtained 6, 12, and 18h after CABG or longer if these values were elevated [5]. Of 57 patients with CK-MB levels>5 times ULN, 4 died within 30 days and 2 more within the next 11 months. Of 37 patients with CK-MB levels 3–5 times ULN, 2 died within 30 days and 0 within the next 11 months. The increased one-year risk that they found from higher CK-MB values can be explained entirely on deaths within 30 days.

There are four features specific to our analysis that distinguishes it from the four prior studies. These are we: (1) objectively identify the CK-MB threshold via the overlapping ranges method [9], (2) determined the CK-MB main effect interval (1-year) via CK-MB specific death hazard functions (Fig. 4) to find if and where the mortality rates became similar between patients with high and low CK-MB levels and used that time to divide our patient into early (<1 year) and late (>1 year) deaths [10], (3) confirmed the effect with ROC curves that elevated CK-MB is associated with 1-year mortality but not later mortality and 4) conducted this study in patients undergoing normothermic cardiopulmonary bypass.

The other studies, by being only six months duration [2], by being done in 3 and 6 year intervals [3], by using only one 3 year interval [4], and by using a small population with most of the deaths occurring within the first 30 postoperative days [5] may have missed important time-dependent changes in the risk of an elevated CK-MB.

The gradually decreasing risk with time that we found after CK-MB elevation is similar to that seen after a traditional myocardial infarction. There, patients have an increased risk of dying within the immediate postMI period, but over the succeeding several weeks to months the risk gradually decreases [11–16]. The increased risk is probably related to myonecrosis. After PTCA, contrast-enhanced MRI showed discrete areas of myonecrosis only in the distribution of the target vessel and only in patients with elevated CK-MB [17]. Recently, Selvanayagam et al. showed a similar association in patients undergoing CABG [18]. Using contrast-enhanced MRI, they showed that 40% of patients undergoing CABG developed new areas of myonecrosis and that the size of myonecrosis correlated with enzyme levels.

There are several limitations to our study. First, CK-MB levels were drawn the morning after surgery rather than a constant number of hours after surgery. This would tend to blur the predictive power of CK-MB. Yet, the 10–18h time interval after surgery before CK-MB determination should provide sufficient time for CK-MB to rise after myocardial injury [6]. Second, we do not have preoperative CK-MB levels on most patients and some of the postoperative elevation may have been present preoperatively. However, we doubt that this was a significant factor. We excluded all patients who had a myocardial infarction immediately preoperatively. We did include patients who had a myocardial infarction preoperatively when the CK-MB levels had returned to normal. Third, we did not confirm the presence of myocardial necrosis by other means, such as electrocardiograms or pyrophosphate scans. Previous studies have shown that enzyme elevations predictive of myocardial damage or nonoperative all cause mortality frequently occur without electrocardiographic or even pyrophosphate scan changes [5,19–22]. Last, while we had no defined protocol for postdischarge medications, the same group of surgeons treated all patients and no major changes were made in therapy over the study duration. Specifically, all patients received aspirin and beta blockers unless clinically contraindicated. Other medicines were used as clinically appropriate.

In conclusion, a single determination of CK-MB the morning after CABG showing an elevation >40ng/mL is a risk factor for death. However after 1 year the increased risk loses its statistical significance. Patients with CK-MB>40ng/mL should be treated as if they had a myocardial infarction and should be followed closely.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

  1. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined—a consensus document of the Joint European Society of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol 2000;36:959-969.[Free Full Text]
  2. Klatte K, Chaitman BR, Theroux P, Gavard JA, Stocke K, Boyce S, Bartels C, Keller B, Jessel A. The GUARDIAN Investigators (The GUARD during Ischemia Against Necrosis). Increased mortality after coronary artery bypass graft surgery is associated with increased levels of postoperative creatine kinase-myocardial band isoenzyme release: results from the GUARDIAN trial. J Am Coll Cardiol 2001;38:1070-1077.[Abstract/Free Full Text]
  3. Steuer J, Horte LG, Lindahl B, Stahle E. Impact of perioperative myocardial injury on early and long-term outcome after coronary artery bypass grafting. Eur Heart J 2002;23:1219-1227.[Abstract/Free Full Text]
  4. Brener SJ, Lytle BW, Schneider JP, Ellis SG, Topol EJ. Association between CK-MB elevation after percutaneous or surgical revascularization and three-year mortality. J Am Coll Cardiol 2002;40:1961-1967.[Abstract/Free Full Text]
  5. Costa MA, Carere RG, Lichtenstein SV. Incidence, predictors, and significance of abnormal cardiac enzyme rise in patients treated with bypass surgery in the arterial revascularization therapies study (ARTS). Circulation 2001;104:2689-2693.[Abstract/Free Full Text]
  6. Strom S, Mogensen L, Bendz R. Serum CK-MB kinetics in acute myocardial infarction and after coronary bypass operations. Scand J Thorac Cardiovasc Surg 1979;13:61-66.[Medline]
  7. The Society for Thoracic Surgeons National Cardiac Surgery Database, Summit Medical Systems, Inc., Minneapolis, MN, USA; 1995..
  8. Edwards FH, Clark RE, Schwartz M. Coronary artery bypass grafting: the society of thoracic surgeons national database experience. Ann Thorac Surg 1994;57:12-19.[Abstract]
  9. Schwann TS, Habib RH, Zacharias A, Parenteau GL, Riordan CJ, Durham SJ, Engoren M. Effects of body size on operative, intermediate, and long-term outcomes after coronary artery bypass operation. Ann Thorac Surg 2001;71:521-531.[Abstract/Free Full Text]
  10. Blackstone EH, Naftel DC, Turner Jr ME. The decomposition of time-varying hazard into phases, each incorporating a separate stream of concomitant information. J Am Stat Assoc 1986;81:615-624.[CrossRef]
  11. Vaccarino V, Krumholz HM, Yarzebski J, Gore JM, Goldberg RJ. Sex differences in 2-year mortality after hospital discharge for myocardial infarction. Ann Intern Med 2001;134:173-181.[Abstract/Free Full Text]
  12. Galatius-Jensen S, Launbjerg J, Mortensen LS, Hansen JF. Sex related differences in short and long-term prognosis after acute myocardial infarction: 10 year follow up of 3073 patients in database of first Danish Verapamil Infarction Trial. Br Med J 1996;313:137-140.[Abstract/Free Full Text]
  13. Fiebach NH, Viscoli CM, Horwitz RI. Differences between women and men in survival after myocardial infarction. Biology or methodology?. J Am Med Assoc 1990;263:1092-1096.[Abstract/Free Full Text]
  14. He J, Klag MJ, Whelton PK, Zhoa Y, Weng X. Short- and long-term prognosis after acute myocardial infarction in Chinese men and women. Am J Epidemiol 1994;139:693-703.[Abstract/Free Full Text]
  15. Maynard C, Every NR, Martin JS, Kudenchuk PJ, Weaver WD. Association of gender and survival in patients with acute myocardial infarction. Arch Intern Med 1997;157:1379-1384.[Abstract/Free Full Text]
  16. MacIntyre K, Stewart S, Capewell S, Chalmers JW, Pell JP, Boyd J, Finlayson A, Redpath A, Gilmour H, McMurray JJ. Gender and survival: a population-based study of 201,114 men and women following a first acute myocardial infarction. J Am Coll Cardiol 2001;38:729-735.[Abstract/Free Full Text]
  17. Ricciardi MJ, Wu E, Davidson CJ, Choi KM, Klocke FJ, Bonow RO, Judd RM, Kim RJ. Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation. Circulation 2001;103:2780-2783.[Abstract/Free Full Text]
  18. Selvanayagam JB, Petersen SE, Francis JM, Robson MD, Kardos A, Neubauer S, Taggart DP. Effects of off-pump versus on-pump coronary surgery on reversible and irreversible myocardial injury. Circulation 2004;109:345-350.[Abstract/Free Full Text]
  19. Lopez-Jimenez F, Goldman L, Sacks DB, Thomas EJ, Johnson PA, Cook EF, Lee TH. Prognostic value of cardiac troponin T after noncardiac surgery: 6-month follow-up data. J Am Coll Cardiol 1997;29:1241-1245.[Abstract]
  20. Holmvang L, Jurlander B, Rasmussen C, Thiis JJ, Frande P, Clemmensen P. Use of biochemical markers of infarction for diagnosing perioperative myocardial infarction and early graft occlusion after coronary artery bypass surgery. Chest 2002;121:103-111.[Abstract/Free Full Text]
  21. Lee ME, Sethna DH, Conklin CM, Shell WE, Matloff JM, Gray RJ. CK-MB release following coronary artery bypass grafting in the absence of myocardial infarction. Ann Thorac Surg 1983;35:277-279.[Abstract]
  22. Guiteras Val P, Pelletier LC, Hernandez MG, Jais JM, Chaitman BR, Dupras G, Solymoss BC. Diagnostic criteria and prognosis of perioperative myocardial infarction following coronary bypass. J Thorac Cardiovasc Surg 1983;86:878-886.[Abstract]



This article has been cited by other articles:


Home page
 ICVTSHome page
M. Engoren, A. Zacharias, R. H. Habib, T. A. Schwann, C. J. Riordan, S. J. Durham, and A. Shah
The effect of diabetic medications on creatine kinase-myocardial band levels in patients undergoing coronary artery bypass surgery
Interactive CardioVascular and Thoracic Surgery, November 1, 2009; 9(5): 793 - 796.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
L. Petaja, M. Salmenpera, K. Pulkki, and V. Pettila
Biochemical Injury Markers and Mortality After Coronary Artery Bypass Grafting: A Systematic Review.
Ann. Thorac. Surg., June 1, 2009; 87(6): 1981 - 1992.e3.
[Abstract] [Full Text] [PDF]

Home page
 Am J Crit CareHome page
M. Engoren and C. Arslanian-Engoren
Long-term Survival in the Intensive Care Unit After Erythrocyte Blood Transfusion
Am. J. Crit. Care., March 1, 2009; 18(2): 124 - 131.
[Abstract] [Full Text] [PDF]

Home page
 Card Surg AdultHome page
S. J. Durham and J. P. Gold
Late Complications of Cardiac Surgery
Card. Surg. Adult, January 1, 2008; 3(2008): 535 - 548.
[Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Milo C. Engoren
Anoar Zacharias
Thomas A. Schwann
Christopher J. Riordan
Samuel J. Durham
Aamir Shah
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Engoren, M. C.
Right arrow Articles by Shah, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Engoren, M. C.
Right arrow Articles by Shah, A.
Related Collections
Right arrow Coronary disease
Right arrow Myocardial infarction
Right arrow Myocardial protection

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS