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Cardiac Troponin T Elevation After

Coronary Artery Bypass Grafting Is
Associated With Increased
One-Year Mortality
Sekar Kathiresan, MD, Stephen J. Servoss, MD, John B. Newell, AB, Dawn Trani, ANP,
Thomas E. MacGillivray, MD, Kent Lewandrowski, MD,
Elizabeth Lee-Lewandrowski, PhD, MPH, and James L. Januzzi, Jr., MD

The results of the present study extend the value of postoperative assessment of troponin T for the prediction
assessing troponin T for the prediction of mortality rate of in-hospital adverse outcome after coronary artery
1 year after coronary artery bypass grafting; this study bypass grafting. 䊚2004 by Excerpta Medica, Inc.
supports previous work that demonstrated the value of (Am J Cardiol 2004;94:879 – 881)

M yocardial necrosis, as demonstrated by cardiac
biomarker release, occurs almost universally
around the time of coronary artery bypass grafting
factors collected included demographics, medical his-
tory, previous medication use, cardiac catheterization
results, presenting cardiac syndrome, and, when avail-
(CABG).1,2 Multiple mechanisms may cause myocar- able, preoperative levels of troponin T. Systemic hy-
dial damage during CABG, including direct trauma pertension and hypercholesterolemia were defined as
from surgical manipulation and myocardial ischemia treatment with antihypertensive and lipid-lowering
due to inadequacies in cardioprotection, coronary ar- medications, respectively. A history of coronary artery
tery thrombosis, and acute loss of bypass grafts.3 disease was defined as previous stable angina, myo-
Because some of these causes are unavoidable, it is cardial infarction, or percutaneous coronary interven-
critical to determine the appropriate threshold of bi- tion. Information regarding surgical procedures, in-
omarker release after CABG associated with wors- cluding number of bypass grafts, bypass/ischemic
ened in-hospital and longer-term prognoses. With re- times, and intraoperative complications, was noted.
spect to in-hospital adverse events after CABG, we Blood samples were drawn on arrival to the surgi-
previously reported that an increased level of troponin cal intensive care unit (“postop”) at 6 to 8 hours and
T has greater discriminatory ability than the isoen- 18 to 24 hours after surgery and were assayed for
zyme creatine kinase-MB (CK-MB).4 However, the CK-MB mass and troponin T (Elecsys CK-MB STAT
relation between increased concentrations of troponin and Troponin T STAT Immunoassays, Roche Diag-
T after CABG and longer term adverse clinical out- nostics Corporation, Indianapolis, Indiana) on an
comes remains unknown. We determined whether in- Elecsys 1010 platform (Roche Diagnostics Corpora-
creased levels of troponin T after CABG are associ- tion).
ated with increased mortality rates after 1 year. The results of troponin T were obtained in a
blinded fashion by the study investigators; however,
METHODS the physicians caring for the patients were not blinded
All study procedures were approved by the hospital to the CK-MB results because this marker is routinely
institutional review board. One hundred thirty-six measured at our institution after cardiac surgery. Data
consecutive patients who underwent CABG without on postoperative outcomes were assessed. In-hospital
concomitant valve surgery at the Massachusetts Gen- end points are outlined in a previous report.4 Vital
eral Hospital (Boston, Massachusetts) between Octo- status at 1 year from hospital discharge was obtained
ber and November 2000 were enrolled. Patients were by a telephone interview of the referring primary care
identified on admission to the cardiac surgical inten- physician or cardiologist.
sive care unit, and a study coordinator blinded to the Cardiac marker levels were log-transformed, and
results of cardiac markers collected clinical variables comparisons of mean levels of cardiac marker be-
in a prospective manner by chart review. Clinical tween patients alive and those dead at 1 year were
made by multivariate analysis of variance with post
From the Cardiology Division, the Cardiac Surgery Division, and the hoc Bonferroni’s corrected pairwise comparisons.
Clinical Chemistry Laboratories, Massachusetts General Hospital, Bos- These tests were conducted with SYSTAT 10 (SPSS,
ton, Massachusetts. This study was supported in part by an unrestricted Inc. Chicago, Illinois). To analyze the prognostic in-
grant from Roche Diagnostics Corporation, Indianapolis, Indiana. fluence of an increased level of troponin T, marker
Manuscript received December 9, 2003; revised manuscript received
and accepted June 18, 2004.
levels were log-transformed and divided into quin-
Address for reprints: James L. Januzzi, Jr., MD, Cardiology Divi- tiles. Multivariable analysis using stepwise Cox’s pro-
sion, Massachusetts General Hospital, Bulfinch 019, 55 Fruit Street, portional hazards regression was performed to identify
Boston, Massachusetts 02114. E-mail: jjanuzzi@partners.org. independent covariates of event-free survival rate at 1

©2004 by Excerpta Medica, Inc. All rights reserved. 0002-9149/04/$–see front matter 879
The American Journal of Cardiology Vol. 94 October 1, 2004 doi:10.1016/j.amjcard.2004.06.022

45.to 12-hour.5– 8 Two alive and free of complications.9.4 ⫾ 1.3 ng/ml (0. vessels 2.05 was considered statistically sig.6–16. 2 (1.4 ng/ml (1. recent studies have established a relation between ics of the study patients are listed in Table 1 and are CK-MB after CABG and worsened medium-term out- comparable to those in previous studies on outcomes comes.07 Coronary artery disease 67% 6–12 h 7.6 (35–109) 42.6 to 1.3–10. Cox’s regression analysis DISCUSSION was conducted with BMDP 7 (BMDP Statistical Soft. variable modeling. respectively. Multivariable analysis suggested that an 18. In univariate and multi- intervals were computed. In previous 1-year follow-up. 1.7) 1. use.and 18. 2 vessels 17% 3 vessels or left main artery 73% Ejection fraction (%) 42 ⫾ 23 Presenting syndrome Congestive heart failure 13% in patients stratified by vital status are presented in Unstable angina pectoris 39% Table 2. and 0.2 (29–85) 0.42–1. The clinical significance of release of cardiac bi- RESULTS omarkers after cardiac procedures has been a subject Of 136 patients. For all significant correlation between levels of troponin T after CABG and covariates of event-free survival rate.12 Extent of coronary artery disease Data are presented as median (interquartile range) (in nanograms per 1 vessel 10% milliliter). and 7. and 18.3 to 10.6 to 16. Expressed as a Function of Mortality (n ⫽ 7) Versus Age (yrs) 67 ⫾ 12 No Mortality (n ⫽ 129) Men 77% Medical history Death No Death Diabetes 34% Marker and Timing (n ⫽ 7) (n ⫽ 129) p Value Systemic hypertension 75% Hypercholesterolemia 86% Troponin T Tobacco use 42% Postop 6.8) 1.42 to 1. of vessels grafted 3.0001).10 However. ␤ blocker 83% which were significantly higher than comparably Statins 76% timed levels of troponin T in patients who survived: Nitrates 69% Heparin 39% 1.05). confidence interval 4. Baseline demograph.3 (0. the sensitivity and specificity of after CABG.1) 0.7 18–24 h 46. Survival curves for patients with high levels (top type of cardioplegia. we describe for the first time a ware.to 24-hour specimens (each p ⬍0.5). p ⬍0.9).9 (33–97) 47. Other independent variables included dictor of a 1-year mortality rate (odds ratio 5. whereas ing syndrome.6 ⫾ 0. and was superior to CK-MB for this indication. In the present study. Stable angina pectoris 18% In the patients who died during the 1-year follow- Non–ST-segment elevation myocardial infarction 20% up.0 ng/ml (0.to 24-hour specimen) of forward stepwise regression.02 Valve disease 5% CK-MB Congestive heart failure 15% Postop 79. ejection fraction. An independent variable troponin T are displayed in Figure 1.76 (0. Inc. Seven patients (5%) died during the CK-MB in the 2 analyses were limited.5%) were lost to follow-up.8 ng/ml (3. sponding regression parameter was not significantly different from 0 at p ⬎0.58 ng/ml) was the strongest pre- erative samples. Most patients who was removed from the model only when its corre. 6. extent of CAD. year.1.76–1. cardiovascular risk factors. the 6. died were in the highest log quintile of troponin T. of controversy and has generally been defined by The 2 patients lost to follow-up were imputed to be relating marker levels to clinical outcomes. TABLE 1 Baseline Characteristics of the Subjects (n ⫽ 136) TABLE 2 Cardiac Marker Levels at Different Time Points After CABG. The differences in Repeat surgery 8% levels of troponin T between patients who were alive No. Identically timed CK-MB values did not dif- fer significantly between patients who were alive and those who were dead at 1 year. 95% the results of CK-MB testing.4 Cox’s regression analysis used (quintiles 2 through 5 in the 18. the immediate postop.3 and those who were dead at 1 year were significant for Data are presented as mean ⫾ SD or number (percentage).0 (0. 95% confidence longer term adverse outcomes. Saugus.5. the level of troponin T after CABG and a p value ⬍0. 94 OCTOBER 1.6 (13–42) 0. respectively.4 (2. repeat CABG. troponin I was found to be superior to CK-MB 880 THE AMERICAN JOURNAL OF CARDIOLOGY姞 VOL.50 Percutaneous coronary intervention 18% 6–12 h 77.5 to 232.0–9. Massachusetts).5) 0.02 Previous acute myocardial infarction 35% 18–24 h 7. demographics.26) 0.to 24-hour specimen) and low levels described previously..4 ng/ml (2.0 Aspirin 94% to 9.40 Extent of coronary artery disease.to ST-segment elevation myocardial infarction 9% Cardiac arrest 2% 24-hour median (and interquartile ranges) levels of Previous medication use troponin T were 6.0 (21–117) 21.9) 0.76 Surgical details ng/ml (0. medication CK-MB results added no independent information.8 (3. as quintile in the 18. present. All p values were 2-sided. The mean levels of cardiac markers studies.76 to 1. est log quintile (ⱖ1.2 (28–80) 0.7). The primary dependent variable was 1-year mor.26).4 (1. 2004 . and other clinical factors.to 12. 7. The primary independent variable was an 24-hour postoperative level of troponin T in the high- increased level of troponin T in any of the 3 postop.to tality rate.60–1.1). was the single best predictor of mortality rate at 1 year nificant.8).

van Ingen G. First.14 If these long-term outcome results are con.38:1070 –1077. Eur J Cardiothorac Surg 1998. Popma JJ.114:482– 486. Lincoff AM.6:E174 –E178. Goenen M. the first to assess results of troponin T and 1-year Ann Thorac Surg 2000. Sigmon KN. Jacquet L.29:1880 –1886.11.69:435– 440. and the E. Crit Care Med 2001.13:378 –384. the biochem. Fellahi JL. Cardiac troponin I as an early marker of myocardial damage after coronary low levels of troponin T (solid line) have a lower risk of mortality bypass surgery. Charac- increased risk of death within 2 years after CABG. El Khoury G. Solymoss BC. Costa MA. J Am Coll Cardiol 2001. Mahaffey KW. mize Platelet Aggregation and Coronary Thrombosis-II. Elevation of the creatine kinase myocardial isoform following other- with increased levels of troponin T after CABG may wise successful directional coronary atherectomy and stenting. Baim DS. Pelletier LC. Lincoff AM. fined—a consensus document of the Joint European Society of Cardiology/ American College of Cardiology Committee for the redefinition of myocardial infarction. Guidollet J. Moscucci M. Predictive value of perioperative cardiac ical definition of myocardial infarction after CABG troponin I for adverse outcome in coronary artery bypass surgery. Newell JB. Lichtenstein SV. Antman E. Fiemeyer A. 13. Noirhomme P. during the first year after CABG than do those with troponin T 3. Lewandrowski K. predictors. troponin T. Harrington RA. Carrier M. Piana RN. Thygesen K. or creatine kinase-MB to detect perioperative myocardial damage after coronary artery bypass surgery. pitalization and increased scrutiny for ischemic com. de Valk V. Off-pump coronary bypass grafting is associated with less addition of additional clinical events would most myocardial injury than coronary bypass surgery with cardiopulmonary bypass. Lindenboom levels after surgery. MacGillivray TE. Lewandrowski K. 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