Prospective, Comprehensive Assessment of Cardiac Troponin T Testing After Coronary Artery Bypass Graft Surgery
Background— The significance and clinical role of cardiac troponin testing after coronary artery bypass grafting remain unclear.
Methods and Results— Cardiac troponin T (cTnT) was measured during the first 24 hours after coronary artery bypass graft surgery in 847 consecutive patients. Only 17 patients (2.0%) had new Q waves or left bundle-branch block after surgery; however, cTnT elevation was observed in nearly all subjects, with a median cTnT concentration of 1.08 ng/mL overall. Direct predictors of postoperative cTnT values included preoperative myocardial infarction (P<0.001), preoperative intraaortic balloon pump (P<0.001), intraoperative/postoperative intraaortic balloon pump (P<0.001), number of distal anastomoses (P=0.005), bypass time (P<0.001), and number of intraoperative defibrillations (P=0.009), whereas glomerular filtration rate (P<0.001), off-pump coronary artery bypass grafting (P=0.003), and use of warm cardioplegia (P=0.02) were inversely associated with cTnT values. A linear association was seen between cTnT levels and length of stay and ventilator hours, and in an analysis adjusted for the Society for Thoracic Surgery Risk Model, cTnT remained independently prognostic for death (odds ratio, 3.20; P=0.003), death or heart failure (odds ratio, 2.04; P=0.008), death or need for vasopressors (odds ratio, 2.70; P<0.001), and the composite of all 3 (odds ratio, 2.57; P<0.001). In contrast to consensus-endorsed cTnT cut points for postoperative evaluation, a cTnT <1.60 ng/mL had a negative predictive value of 93% to 99% for excluding various post-coronary artery bypass graft surgery complications.
Conclusions— cTnT concentrations after coronary artery bypass graft surgery are nearly universally elevated, are determined by numerous factors, and are independently prognostic for impending postoperative complications when used at appropriate cut points.
Received November 23, 2008; accepted June 26, 2009.
Although coronary artery bypass grafting (CABG) is of considerable benefit for those in need for revascularization, it may nonetheless be associated with significant perioperative and postoperative myocardial damage and necrosis, which may occur in varying degrees.1 Multiple mechanisms have been proposed to explain the finding of myocardial injury after CABG: Intraoperative injury may result from cardiac manipulation, inadequate myocardial protection, and intraoperative defibrillation; in addition, postoperative myocardial injury may be associated with acute loss of bypass grafts.2 Regardless of the multiple modes of injury that may occur around the time of CABG, cardiomyocyte necrosis may be detected through measurement of cardiac enzymes such as creatine kinase or of more specific markers such as cardiac-specific troponin (cTn). Depending on the assay used, these markers may be detectable in essentially all patients undergoing CABG.3,4 The prognostic value of cTn measurement after cardiac surgery has been studied,3,5–8 but many of these analyses included a mixture of cardiac procedures, including valve replacement/repair and aortic grafting. Furthermore, no analyses examined patients within the context of recent consensus guidelines for the detection of postoperative myocardial infarction (MI). These guidelines state: “Biomarker values more than five times the 99th percentile of the normal reference range during the first 72 hour following CABG, when associated with the appearance of new pathological Q-waves or new left bundle-branch block (LBBB), or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium, should be considered as diagnostic of a CABG-related myocardial infarction (type 5 MI)”.9 Although consensus guidelines appropriately emphasize the importance of clinical evidence together with biomarker testing, noting that MI cannot be diagnosed solely with results from cTn testing, inadequate sensitivity and specificity of ECG in the post-CABG setting and limited availability of routine imaging on every patient could theoretically lead to a heavier emphasis on biomarker testing after CABG. This therefore increases the relevance of a good understanding of cTn release in this context.
Clinical Perspective on p 850
In a small pilot study of patients undergoing cardiac surgery, we previously reported the diagnostic and prognostic roles of cardiac troponin T (cTnT), demonstrating that a cTnT >1.60 ng/mL predicted morbidity and mortality out to 1 year after surgery.3,6,8 In this prior analysis, however, we included patients undergoing all forms of cardiac surgery, not specifically CABG; furthermore, we did not consider patients as a function of consensus guidelines for cTn measurement after CABG. Therefore, in a new cohort of patients, we wished to reexamine the utility of cTnT for the postoperative evaluation of patients undergoing CABG, with specific efforts to identify predictors of post-CABG cTnT values, and to examine the value of post-CABG cTnT for predicting complications.
All study procedures were approved by the hospital Institutional Review Board. A total of 847 consecutive patients who underwent isolated CABG during a 1-year period at the Massachusetts General Hospital were enrolled. Patients were identified on admission to the surgical intensive care unit (ICU), and a study coordinator collected clinical variables prospectively via chart review. Comprehensive clinical details were collected for each patient.
Variables such as demographics, past medical history, prior medication use, cardiac catheterization results, presenting cardiac syndrome, preoperative glomerular filtration rates using the Modification of Diet in Renal Disease formula,10 type of surgery, number of bypass grafts, bypass/ischemic times, intraoperative complications, and postoperative data, including ICU length of stay, number of hours of postoperative mechanical ventilation, results of postoperative ECG, and other postoperative outcomes, were collected on the Society of Thoracic Surgeons (STS) Adult Cardiac Surgery Database Data Collection Form (complete form may be viewed at http://www.sts.org/documents/pdf/AdultCV2.61DCF.pdf). Patients were followed up for outcomes to 30 days by the cardiac surgery research nurse per STS protocol.
The occurrence of new Q waves/LBBB was assessed. In addition, other complications were prospectively defined as need for vasopressor agents for >24 hours postoperatively (the mean for the group as a whole; vasopressors in this analysis were defined as epinephrine, norepinephrine, dobutamine, and milrinone); postoperative heart failure diagnosed by managing physician and identified via chart abstraction; and all-cause mortality by 30 days.
In an exploratory manner, patients were separated on the basis of MI within a week of surgery. The value of cTnT for risk assessment in these patients was examined.
Biochemical Analysis for Myocardial Necrosis
Serial blood samples were drawn on arrival to the surgical ICU and at 6 to 8 and 18 to 24 hours after surgery. Levels of serum cTnT were measured with the third-generation cTnT assay (Roche Diagnostics, Indianapolis, Ind) on an Elecsys 2010 platform (Roche Diagnostics). The highest cTn value during the first 24 hours was taken as peak cTnT; unless specifically ordered by the managing clinician outside of this analysis, cTnT levels were not used for clinical decision making.
Univariable followed by multivariable linear regression analyses were done to identify predictors of postoperative cTn values. Clinical characteristics such as age, presenting syndrome, and medical history, as well as surgical variables such as type of cardioplegia, ischemic time, bypass time, number of grafts placed, intraoperative defibrillations, and need for preoperative, intraoperative, or postoperative intraaortic balloon pump placement, were entered into the model. Variables with a value of P<0.05 in univariable screen were retained for evaluation in the multivariable model; for both univariable and multivariable analyses, variables were expressed with β coefficients, and only those variables with a value of P<0.05 were retained in the final multivariable model. Associations between cTnT levels and ICU length of stay, total ventilator hours, and total hospital length of stay were examined using bivariate correlations with Spearman analyses.
Receiver-operating characteristic testing evaluated the utility of the peak cTnT value during the first 24 hours postoperatively for identifying patients with impending complications such as death, the composite of death and heart failure and of death and vasopressor requirements, and the triple composite of death, heart failure, and vasopressors use. Postoperative heart failure was identified via chart abstraction of managing physician judgment; vasopressor requirement was defined as the need for use of more than the median vasopressor medications for the group as a whole (1 drug) for >24 hours; in an exploratory manner, a 48-hour time horizon also was explored, as was the need for >1 simultaneous vasopressor. cTnT concentrations among those with complications were compared with those without complications through the Wilcoxon rank-sum test.
cTnT values were considered as a function of several cut points for all patients and then separately for on-pump CABG (ONCAB) and off-pump CABG (OPCAB) subgroups with corresponding positive predictive value and negative predictive value (NPV) for various complications generated. Several cTnT cut points were considered, including 0.01 ng/mL (corresponding to the 99th percentile for a healthy population11), 0.03 ng/mL (the cut point yielding 10% coefficient of variation), 0.10 ng/mL (the current cut point endorsed by the STS for detection of post-CABG MI), and 0.15 ng/mL (the consensus definition of MI detection after cardiac surgery9). Finally, we examined a cTnT ≥1.60 ng/mL, corresponding to the cut point we reported earlier as a predictor of impending adverse outcome.
Multivariable logistic regression models incorporating age plus log-transformed cTnT in 1 model and then all variables in the STS risk score plus log-transformed cTnT were done for all subjects and for those undergoing OPCAB. Statistical analyses were performed with SPSS software (Chicago, Ill). All P values were 2 sided, with a value of P=0.05 used to indicate significance.
Patient Demographics and Clinical Factors
Baseline demographics of study patients (including past medical history, extent of coronary artery disease, presenting cardiac syndrome, and preoperative medication use) are detailed in Table 1. Patients underwent CABG for treatment of multivessel coronary artery disease in the context of the following index diagnoses: stable angina (54%), non-ST-segment elevation MI (28%), unstable angina pectoris (5%), and ST-segment elevation MI (8%). One hundred twenty-nine subjects (15%) had acute heart failure during the week before surgery, often in association with other syndromes; heart failure was the primary presenting syndrome in 4%.
Perioperative variables are detailed in Table 1. For those undergoing ONCAB, the median bypass time for the study patients was 107 minutes (interquartile range [IQR], 83 to 130 minutes). Myocardial protection strategies used included anterograde cold cardioplegia in 324 (38%), anterograde warm cardioplegia in 291 (34%), and retrograde cardioplegia in 309 (36%), most often warm. Cold fibrillatory arrest without cardioplegia was used in 149 patients (18%); 84 patients (10%) underwent OPCAB. The mean number of CABG grafts implanted was 3.55 (SD, 1.16).
Postoperative cTnT Values
The peak median cTnT was 1.08 ng/mL (IQR, 0.60 to 1.73 ng/mL). Among all patients undergoing CABG, 99.4% had a cTnT ≥0.01 ng/mL, 98.9% had a cTnT ≥0.03 ng/mL, 97.5% had a cTnT ≥0.10 ng/mL, 96.6% had a cTnT ≥0.15 ng/mL, and 36.7% had a cTnT ≥1.60 ng/mL.
New Q Wave/LBBB After CABG
Seventeen patients (2%) had either new Q waves (8, 0.9%) or new LBBB (9, 1.1%) on the day after CABG. The median cTnT in these patients was 1.48 ng/mL (IQR, 1.02 to 2.11 ng/mL). None died or had postoperative heart failure, but 10 (58.8% of the group or 1.2% of the overall cohort) had a prolonged need for vasopressors.
Predictors of cTnT Concentrations
Univariable and multivariable direct and inverse predictors of cTnT concentrations are depicted in Table 2 and include numerous variables from the preoperative, intraoperative, and postoperative settings. Notably, in the final model, new Q waves or LBBB on the postoperative ECG was not independently associated with postoperative cTnT values. Among those with available preoperative cTn values (m=122), we found no association with postoperative cTnT values.
Resource Use and Postoperative Complications
A significant correlation was present between postoperative cTnT levels and ICU length of stay (r=0.14, P<0.001), total postoperative ventilator hours (r=0.21, P<0.001), and total hospital length of stay (r=0.14, P<0.001). Nine patients died; 11 patients had postoperative heart failure; and 80 patients required significant vasopressor support. Considering outcomes in terms of composite events, there were 18 patients with death or heart failure, 81 patients with death or significant vasopressor requirement during ICU stay, and 85 patients with the triple composite of death, heart failure, or significant vasopressor requirement.
In receiver-operating characteristic analyses, the peak postoperative cTnT level had an area under the curve of 0.74 (95% confidence interval [CI], 0.57 to 0.92; P=0.004) for death, 0.67 (95% CI, 0.58 to 0.78; P=0.001) for death and heart failure, 0.72 (95% CI, 0.66 to 0.78; P<0.001) for death and significant vasopressor requirement, and 0.70 (95% CI, 0.64 to 0.76; P<0.001) for the triple composite of death, heart failure, or significant pressor requirement. Among those with available preoperative cTnT results, a generally similar area under the curve was observed for postoperative complications (results not shown).
A dichotomous relationship was seen between cTnT level and postoperative complications (Figure 1). Compared with survivors, patients who died (n=9) had higher cTnT concentrations during the first 24 hours after CABG (3.41 ng/mL [IQR, 1.06 to 7.41 ng/mL] versus 1.07 ng/mL [IQR, 0.60 to 1.71 ng/mL]; P=0.02).
In a similar fashion, those 18 patients developing postoperative heart failure and death had significantly higher median cTnT compared with those who did not (1.38 ng/mL [IQR, 1.16 to 3.49 ng/mL] versus 1.07 ng/mL [IQR, 0.60 to 1.72 ng/mL]; P<0.001), and 81 patients with significant postoperative pressor requirement and death showed a similar cTnT pattern (1.78 ng/mL [IQR, 1.14 to 4.11 ng/mL] versus 1.01 ng/mL [IQR, 0.58 to 1.61 ng/mL]; P<0.001).
In addition, we examined whether an even longer time horizon for pressor need (48 hours) was associated with higher cTnT values and found that patients requiring vasopressors greater than this time point had higher cTnT concentrations (1.85 ng/mL; IQR, 1.22 to 5.20) compared with those who did not (1.00 ng/mL; IQR, 0.60 to 1.25 ng/mL; P<0.001). In addition, those patients requiring >1 vasopressor at any time during their ICU stay showed a similar pattern of cTnT release during the first 24 hours, with significantly higher values compared with those who did not require multiple vasopressors (1.72 versus 1.02 ng/mL; P<0.001).
Eighty-five patients had at least 1 of the 3 prespecified complications; among these patients, the median cTnT was 1.60 ng/mL (IQR, 1.14 to 3.93 ng/mL), significantly higher than in those who had an uncomplicated postoperative course (median cTnT, 1.01 ng/mL; IQR, 0.58 to 1.61; P<0.001). This frequency of complications was directly proportional to the level of cTnT within the first 24 hours (Figure 2). A comparison of patients with an MI within a week before surgery and those without showed no difference in the area under the curve for cTnT across all outcome measures (Table I of the online-only Data Supplement).
In a multivariable logistic regression model adjusted for the STS risk score, cTnT values significantly predicted early postoperative complications of death (odds ratio [OR], 3.20; 95% CI, 1.5 to 6.9; P=0.003), death or heart failure (OR, 2.04; 95% CI, 1.2 to 3.5; P=0.008), death or vasopressor need (OR, 2.70; 95% CI, 2.0 to 3.6; P=<.001), and the triple composite of death, heart failure, or vasopressor need (OR, 2.57; 95% CI, 1.9 to 3.4; P<0.001; Table 3). In an effort to better understand the relationship between intraoperative predictors of postoperative cTnT values and outcomes and how such relationships would be modified with the results of cTnT, we examined the individual prognostic ramification of intraoperative predictors of cTnT for each outcome measure. We found in the context of cTnT results that only an intraoperatively placed intraaortic balloon pump remained a significant predictor of death (OR, 132.5; 95% CI, 19.7 to 890.4; P<0.001), death or heart failure (OR, 9.72; 95% CI, 3.24 to 29.1; P<0.001), death or vasopressor need (OR, 23.8; 95% CI, 6.44 to 87.6; P<0.001), or the composite of all 3 (OR, 9.24; 95% CI, 3.10 to 27.6; P<0.001).
cTnT Cut Points
At the current cut point endorsed by the STS (0.10 ng/mL), cTnT had unacceptable performance for prediction of post-CABG events, with nearly 98% having an “elevated” cTnT. In a similar manner, consensus-recommended cut points for post-CABG MI detection9 had similarly poor performance; nearly 97% of subjects had an elevated cTnT, obscuring any diagnostic or prognostic meaning with unacceptable value for predicting any complication that might accompany “MI.”
For example, at 0.15 ng/mL, as a predictor of death, cTnT had a sensitivity and NPV of 100% but had an extremely poor specificity of 3.1%, with a corresponding positive predictive value of only 1.1% and a misclassification rate of 96%. Among those with new Q waves or new LBBB, using consensus-endorsed cut points, we observed a 100% sensitivity, but it was associated with a specificity of 4.2% and a similarly high misclassification rate.
In an effort to better understand the associations between cTnT values and clinical events, on the basis of prior findings,3,6,8 we examined a cTnT cut point of 1.60 ng/mL and found that for prediction of death after CABG, this cut point had a sensitivity of 56% (95% CI, 21 to 86), a specificity of 73% (95% CI, 69 to 76), an NPV of 99.3%, and most important, a much lower misclassification rate of 28%. In a similar manner, a cTnT <1.60 ng/mL had an NPV of 98.1% for death or heart failure, 94% for death or vasopressor need, and 93% for death, heart failure, or vasopressor need.
ONCAB Versus OPCAB Surgery
A detailed comparison of ONCAB versus OPCAB can be found in the Results section of the online-only Data Supplement. Briefly, the OPCAB patients generally had lower postoperative cTnT values compared with ONCAB patients (0.33 versus 1.08 ng/mL; P<0.001). Nonetheless, among patients undergoing OPCAB, 72.6% of patients had a cTnT above the consensus-recommended cut point; only 13.1% had a cTnT ≥1.60 ng/mL. Despite generally lower postoperative cTnT values in those undergoing OPCAB, concentrations of cTnT remained prognostically meaningful, and a cTnT cut point of ≥1.60 ng/mL had an NPV of 91% to 97% for a variety of complications, with essentially identical performance in ONCAB and OPCAB cases.
Measurement of serum cTn is the gold standard for the biochemical evaluation of myocardial injury in several clinical situations,9 including the diagnosis and risk stratification of patients with acute coronary syndromes12,13 and those undergoing noncardiac surgery.14 However, the situation is less clear for the use of cTn measurement after cardiac surgery because it is widely accepted that cTn release may occur after cardiac surgery in a manner that may be difficult to interpret.15 Indeed, given that cTn release is extraordinarily common—if not universal—after heart surgery, the conceptual application of its measurement for “MI” detection is challenging; nonetheless, cTn measurement may offer value for the prediction of risk after cardiac surgery.3,6,8,16 Complicating the issue, recent guidelines defined the optimal cTn cut point for post-CABG MI surveillance as 5 times the upper reference limit (eg, cTnT ≥.15 ng/mL). The ramifications of this are considerable because the choice of cut point is crucial to avoid risk for an incorrect diagnosis of post-CABG MI. Therefore, given our prior work in the area,3,6,8 we undertook a large prospective study of CABG patients to comprehensively evaluate and validate the use of cTnT testing in this setting.
We found that cTnT levels are detectable in nearly all patients after CABG and almost always in the absence of clinically obvious regional MI. Although cTnT elevation in this setting is common, it should not necessarily be considered insignificant because cTnT concentrations relate to several relevant preoperative, intraoperative, and postoperative risk factors, and when cTnT is significantly elevated, the risk for an adverse outcome is heightened. We found a continuous association between cTnT values and risk for adverse outcomes: A higher likelihood for adverse events was noted with greater release of cTnT.
Certain considerations in the interpretation of cTnT results after surgery are necessary. For example, although cTnT concentrations partition well with outcome after CABG, factors that predict their elevation may not necessarily be considered in the receiver-operating characteristic analyses that we performed. For example, a cTnT in a patient with a 3-hour bypass time is very different from a similar cTnT in someone with a much shorter bypass time. Nonetheless, across a wide range of patients, cTnT had excellent NPV for excluding complications.
Although studies of cTn testing after CABG have shown some degree of heterogeneity of optimal cut points for cTn measurement to predict risk,5,16–18 our data are consistent with our prior reports,3,6,8 pointing toward the need for a cTn cut point considerably higher than that used for the detection of spontaneous coronary events. The challenge is considering the very reason for measurement of cTn after CABG. Although useful for the detection of spontaneous MI in patients with acute coronary syndrome, use of cTn measurement after CABG is considerably more complex. Our data would suggest that myocardial injury in the context of CABG is essentially universal; thus, the use of cTnT to identify post-CABG “MI” may be somewhat challenging. Nonetheless, cTnT values in our study were predicted by a number of easily ascertainable factors, and cTnT elevation—especially when significant—was clearly and conclusively associated with adverse outcomes after surgery. In this regard, cTnT was additive to the STS risk score for risk prediction, and when used at a cut point considerably higher than consensus-recommended levels, cTnT delivered excellent NPV for excluding impending major postoperative complications. Thus, rather than using cTnT to diagnose “MI” after surgery (which occurred in only 2% of our cohort), clinicians could theoretically apply postoperative cTnT testing to better understand delayed recovery after CABG—a far more common scenario—while simultaneously using the prognostic value of the marker to exclude the likelihood for other major postoperative complications such as heart failure or death.
At present, we argue that a better mechanistic understanding of cTnT release after CABG is now necessary. Van Lente et al19 showed poor correlation between changes in cardiac biomarker activity and ultimate evidence of post-CABG MI at autopsy. Magnetic resonance imaging analyses of patients with elevated cTn after CABG have similarly shown more diffuse, nonregional injury patterns rather than regional MI.20 Other studies have, in contrast, associated elevated cTn values after surgery with a higher likelihood for postoperative CABG graft loss.21 Thus, the mechanism of cTn elevation in this context is likely multifactorial, which is supported by results of our and other data.22,23 It is interesting and notable that in a multivariable model, new postoperative Q waves or LBBB was not associated with cTnT values; this may represent confounding by association with other factors that remained in the model such as use of intraaortic balloon counterpulsation or preoperative MI.
We found that an MI within a week of CABG was independently associated with cTnT concentrations postoperatively, a finding comparable to that in patients undergoing percutaneous revascularization.24 However, although it has been shown that among patients undergoing percutaneous revascularization, prognostic associations between cTn release and outcomes are more likely due to preprocedural release than related to procedural myocardial injury, separating those patients with pre-CABG MI demonstrated no difference in the value of cTnT for predicting outcomes. This likely speaks to the magnitude of release of cTnT in the context of CABG, which is typically considerably higher than most cTn releases seen in the context of percutaneous revascularization procedures. In short, relatively minor preoperative elevations in cTn are not likely to obscure the considerable release seen in those patients with a complication.
It is worthwhile to briefly address the similarities and differences between cTnT and cTnI assays. Although different biologically and analytically, both assays have been shown to be sensitive and specific for identifying MI and predicting mortality in this setting, and both have been endorsed for such use (and for post-CABG evaluation) by consensus guidelines.9 However, multiple assays exist for cTn measurement, with considerable heterogeneity with respect to analytical sensitivity, precision, and reference ranges. This partially explains the different optimal cTn cut points in various studies in post-CABG testing.3,17,25,26 The results of studies similar to ours have clearly shown the utility of both cTnI and cTnT for prognostication purposes in the postcardiac surgery setting; however, no large-scale comparative data between cTnI and cTnT are available in this population. Such studies are needed to better understand the similarities and differences of the various cTn methods in this setting.
Although our study is one of the largest systematic assessments of serum cTnT for the evaluation of post-CABG patients to date, it has limitations. First, although the optimal cTnT cut point in this study of 1.60 ng/mL appeared to be of value, our study was a retrospective analysis; thus, validation of this cut point in a prospective fashion is now needed. Furthermore, the optimal cTnT cut point that we identified should be evaluated further across a wider range of surgeons and institutions because a healthier patient population might require a lower threshold to obtain the same associations with outcome.
In addition, the relatively small number of outcomes, consistent with the contemporary nature of our study population, limits our power to estimate the prognostic role for cTnT; nonetheless, our results are robust and the overall message is clear: Excessive cTnT release after CABG is associated with a deleterious outcome. Another major limitation of our study is the nonavailability of preoperative cTnT values for a significant proportion of patients in the study. However, in a relatively small proportion of patients for whom these data were available, the value of post-CABG cTnT appeared preserved for predicting complications, with an area under the curve that was slightly higher than among those without a preoperative measurement. An explanation for the higher area under the curve may be that those with a high likelihood for preoperative myocardial necrosis—and hence a higher-risk subgroup—would have preoperative measures of cTnT available. Such patients would therefore be at higher risk for complications, and cTnT would likely be more useful in this group. Another issue is that relatively few subjects had a glomerular filtration rate <30 mL · min−1 · 1.73m−2; because cTnT is significantly affected by reduced renal function, it is possible that the value of cTnT for post-CABG surveillance of such patients with severe renal insufficiency would be reduced. Finally, we do not have data on the use of volatile anesthetic agents in our subjects, which have been suggested to affect post-CABG cTn levels.27
In a cohort of patients undergoing CABG, we found that detectable postoperative levels of cTnT are seen almost universally. Such elevations typically occur in the absence of regional MI and reflect preoperative, intraoperative, and postoperative factors. Importantly, we have shown marked cTnT elevations after CABG surgery to be prognostically meaningful. Ultimately, strategies to limit cTn release after surgery should be explored to reduce the risk for the complications that are strongly predicted by this biomarker.
Sources of Funding
Dr Mohammed is supported by the Dennis and Marilyn Barry Fund for Cardiac Research. Dr van Kimmenade is sponsored by a research fellowship grant from the Interuniversity Cardiology Institute of the Netherlands. Dr Januzzi is supported in part by the Balson Scholar Fund.
Dr Januzzi has received grant funding, speaker’s fees, and honoraria from Roche Diagnostics (maker of cTnT). The other authors report no conflicts.
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The role of serum troponin measurement is well defined in the diagnosis and risk stratification of acute coronary syndromes. However, the situation is less clear for the use of troponin measurement after cardiac surgery because troponin is released in essentially all such patients. Therefore, we undertook a prospective study of 847 patients to comprehensively evaluate and validate the use of troponin T testing for risk assessment in this setting. In addition, we studied patients within the context of recent consensus guidelines for the detection of post-coronary artery bypass grafting (CABG) myocardial infarction. Only 2% of subjects had a post-CABG myocardial infarction; however, we found that troponin T concentrations were elevated in essentially all patients and were determined by several relevant preoperative, intraoperative, and postoperative factors. Importantly, very elevated troponin T concentrations were correlated with more resource use and poorer outcomes and were additive to the Society for Thoracic Surgery risk score for prognostication after CABG. Whereas the consensus-endorsed cut point for troponin T (0.15 ng/mL) was overly sensitive and less clinically useful for either post-CABG diagnosis of myocardial infarction or risk assessment, a higher troponin T of <1.60 ng/mL provided excellent negative predictive value for excluding relevant complications in post-CABG setting. Troponin testing after CABG is therefore valuable for postoperative risk assessment, particularly when applied at the correct cut points.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.108.837278/DC1.