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Ann Thorac Surg 2005;80:1758-1764
© 2005 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Cardiac Troponin I Release After Coronary Artery Bypass Grafting Operation: Effects on Operative and Midterm Survival

^a Division of Cardiac Surgery, Dipartimento d'Emergenza e Trapianti d'Organo, Universitá di Bari, Bari, Italy
^b Institute of Cardiology, Universitá di Bari, Bari, Italy

Accepted for publication April 18, 2005.

^_* Address correspondence to Dr Paparella, Division of Cardiac Surgery, Dipartimento di Emergenza e Trapianti d'Organo (DETO), University of Bari, Piazza Giulio Cesare 11, 70100 Bari, Italy (Email: paparella{at}tin.it).

	Abstract

Top Abstract Introduction Material and Methods Results Comment References

 
BACKGROUND: Markers of myocardial necrosis are usually elevated in patients who have undergone a coronary bypass operation with cardiac arrest. The preferred marker in detecting acute myocardial ischemia is cardiac troponin I (cTnI). However, its ability to predict short-term and, particularly, midterm outcome after coronary bypass operations is uncertain.

METHODS: Two hundred thirty unselected patients undergoing surgical revascularization had cTnI measured preoperatively and 11 times postoperatively. Receiver operating characteristic curves were constructed using cTnI postoperative peak values in order to assess the prognostic sensitivity and specificity of the test. The cut-off value of 13 ng/mL was used to assess the prognostic significance of the peak cTnI postoperative release for short-term and midterm outcomes.

RESULTS: One hundred forty-six patients (63.5%) had postoperative cTnI peak values less than 13 ng/mL (mean peak value, 6.6 ± 3.1 ng/mL) and 84 patients (36.5%) had postoperative cTnI peak values greater than 13 ng/mL (mean peak value, 45.5 ± 59.9 ng/mL). Patients with peak cTnI greater than 13 ng/mL were older and had higher preoperative cTnI values. They required both longer cross-clamp time and CPB time. Moreover, hospital death in the cTnI greater than 13 ng/mL group (9.5% versus 0.7%, p = 0.0009) was significantly higher. Multivariate analysis showed that cTnI greater than 13 ng/mL was the only independent predictor of hospital death (odds ratio 10.33, p = 0.04) and hospital death from cardiac causes. A 2-year follow-up demonstrates that cTnI postoperative release had no influence on midterm mortality and hospitalization for due to cardiac illness.

CONCLUSIONS: Cardiac troponin I is a valuable marker for immediate myocardial damage after coronary bypass operations. Its postoperative release does not predict midterm outcome.

	Introduction

Top Abstract Introduction Material and Methods Results Comment References

 
Myocardial infarction (MI), associated with coronary artery bypass grafting (CABG) operations, represents a serious and relatively frequent perioperative complication. Different reports have documented a high in-hospital and long-term mortality rate for patients with such complications [1–3].

The diagnosis of perioperative MI is often troublesome, with no standard criteria currently available to define it. The unique circumstances of the immediate postoperative course often render electrocardiograms (ECG) inaccurate in defining new ischemic events after CABG. Early postoperative pericarditis, conduction disturbances, ventricular pacing, and electrolyte and acid-base disorders may all alter the ECG's sensitivity and specificity.

Specific cardiac enzymes, creatine kinase isoenzymes MB (CK-MB), and cardiac troponins I (cTnI) and T (cTnT) are generally elevated in the serum of patients who have undergone cardiac surgery. Their postoperative values are frequently above the levels normally used to define MI. As a result, cardiac troponins are the preferred markers for the diagnosis of myocardial injury because they offer greater accuracy and a higher sensitivity compared with CK-MB [4]. The significance of cardiac enzyme plasma levels in the postoperative phase is considered uncertain as several factors (poor myocardial protection, early graft failure, intracoronary embolization, incomplete revascularization, surgical trauma) may contribute to their release. They are not routinely monitored in all cardiac surgical intensive care units because their usefulness in guiding physicians' decision-making is considered vague. To date, there have been few large prospective studies that have correlated the postoperative release of cardiac troponins with in-hospital outcome [5–8]. Thus far, only one study has reported the impact of postoperative troponin release on midterm outcome [9].

The aim of the presented study is to assess the role of postoperative cTnI in predicting in-hospital and midterm outcomes in nonselected patients undergoing CABG with cardiopulmonary bypass (CPB) and to suggest a critical use of cTn I to improve postoperative care of patients with elevated troponin release.

	Material and Methods

Top Abstract Introduction Material and Methods Results Comment References

 
Between May 2000 and June 2003, consecutive patients who underwent CABG in our institution were considered for analysis if they had serial cTn I measurements performed perioperatively at the following times: preoperatively, and at 1, 6, 12, 24, and 36 hours after the end of the operation, and from the second to the seventh postoperative day. Trained personnel prospectively recorded preoperative patient characteristics, intraoperative variables and clinical in-hospital outcome in our institutional database. Patients who had unstable angina and recent MI (less than 7 days) were included in the study as well. Patients undergoing aortic dissection surgery and those undergoing heart valve procedures with associated CABG in addition to patients transferred urgently to the operating room after complicated percutaneous coronary intervention were excluded. The approval of the local ethics committee was obtained before the study protocol was conducted.

Samples for cTn I were collected from serum and analyzed immediately after arrival at the Policlinico Hospital laboratory. Cardiac troponin I was measured according to the manufacturer recommendation by standard immunoassay techniques (Dade Behring, Newark, Delaware), and the top reference limit in a control population was 0.05 ng/mL.

Receiver operating characteristic curves were constructed using cTnI peak values for each patient for the purpose of assessing the prognostic specificity and sensitivity of the test. The receiver operating characteristics curves for hospital death (Fig 1) indicated that postoperative cTnI release is strongly associated with in-hospital death. It was decided that 13 ng/mL would be the cTnI cut-off value to assess the prognostic significance of the peak cTnI release for each in-hospital outcome variable and midterm outcome for mortality and hospitalization for cardiac causes. This cut-off value was previously used to assess short-term [8] and midterm [9] outcome based on postoperative cTnI release.

View larger version (39K): [in this window] [in a new window]   Fig 1. Receiver operating characteristics curve for cardiac troponin I relative to hospital mortality. (AUC = area under the curve.)

All patients were admitted postoperatively into the intensive care unit and extubated when hemodynamically stable, their body temperatures were back to normal, they were conscious, there was no surgical bleeding, and blood gases were at favorable levels. Postoperatively, patients received aspirin (100 mg oral or intravenous) and low molecular weight heparin (Nadroparin 2,850 U, anti-Xa, subcutaneous) 12 hours after the end of the operation in the absence of significant mediastinal bleeding. Daily 12-lead ECG was performed in all patients. They are not routinely recorded in the institutional database, however; therefore, considering the retrospective evaluation of the presented data, information regarding perioperative ECG modification will not be presented.

Operative and Midterm Outcome
To assess the relationship between cTnI postoperative release and the operative outcome, the following postoperative outcome variable have been analyzed: death and cause of death, intensive care unit length of stay, total hospital length of stay, time of mechanical ventilation, incidence of reintubations, low cardiac output syndrome, use of intra-aortic balloon pump, need of dialysis/ultrafiltration, atrial fibrillation, stroke, sepsis, surgical infections, total infections, mediastinal blood loss, blood and blood products transfusion, and reoperation for bleeding.

Definitions
Hypertension was defined as blood pressure exceeding 140/90 mm Hg, having a history of high blood pressure or needing antihypertensive medications. Patients having a history of diabetes regardless of the duration of disease or the need of antidiabetic agents were considered diabetic. Hypercholesterolemia was defined as a fasting cholesterol level greater than 200 mg/dL. Smoking history was defined as any current or past form of tobacco use. Chronic obstructive pulmonary disease (COPD) was defined as forced expiratory volume of air in One second (FEV₁) less than 75% or the need of pharmacologic therapy for the treatment of chronic pulmonary compromise. On-going refractory angina that requires the use of intravenous nitrate therapy for control was regarded as unstable angina. Left ventricular ejection fraction was obtained in all patients by planimetry of left ventriculogram. Death within the same hospital admission regardless of the cause was defined as operative mortality. Cardiac death was regarded as any death due to cardiac causes including sudden death. Low output syndrome was defined as the need for postoperative inotropic support or an intra-aortic balloon pump for more than 30 minutes in the intensive care unit to maintain systolic blood pressure greater than 90 mm Hg, mean blood pressure greater than 60 mm Hg, or the cardiac index greater than 2.2 L·min^–1 ·m^–2, despite sufficient volume substitution. Extubation criteria were hemodynamic stability, absence of surgical bleeding, fully rewarming, consciousness, optimal blood gases with FIO₂ of 0.3 or less and without the need for mechanical assistance (continued positive airway pressure/assisted spontaneous breathing less than 5 cm H₂O). Cerebrovascular disease was regarded as any transient ischemia attack, reversible ichemic neurologic deficit, or stroke. Sepsis was defined by at least two of the following clinical criteria: body temperature less than 36°C or greater than 38°C, heart rate greater than 90 beats per minute, respiratory rate greater than 20 breaths per minute, PCO₂ less than 32 mm Hg, or white blood cells greater than 12,000 or less than 4,000/µL.

Follow-Up
Patients' follow-up was analyzed in order to assess long-term outcome. In our institution, data regarding deaths and further hospitalization for cardiac reasons are prospectively recorded by trained personnel based on direct evaluation or telephone information obtained by the general practitioner, cardiologists, patients, or their relatives. Follow-up was 90% complete (199 of 221 patients) with its duration averaging 22.6 ± 10.7 months (minimum 4.6, maximum 48.4, cumulative 4,498).

Statistical Analyses
Categorical variables were presented as absolute numbers and percentages and were analyzed through ². Continuous variables were presented as the mean ± SD and analyzed through t test. Differences between study groups were considered significant if p value was 0.05 or less. Receiver operating characteristics curves were employed to evaluate the area under the curve of TnI peak for hospital mortality and to estabilish sensibility and specificity for different cut-offs of TnI peak. Stepwise logistic regression was employed to evaluate the effect of TnI peak greater than 13 mg/dL on hospital mortality. The following variables underwent univariate logistic regression for hospital mortality: sex, age, body mass index, hypertension, diabetes, hypercholesterolemia, statins therapy, smoking history, chronic obstructive pulmonary disease, unstable angina, recent MI, left ventricular ejection fraction, carotid artery stenosis greater than 60%, preoperative TnI, baseline creatinine, additive European System for Cardiac Operative Risk Evaluation (EuroSCORE), logistic EuroSCORE, grafts per patient, intramyocardial left anterior descending artery, CPB duration, cross-clamp duration, troponine I peak greater than 13 ng/mL. The variables that resulted in having p value of 0.25 or less were sex, unstable angina, smoking history, CPB duration, cross-clamp duration, troponine I peak greater than 13 ng/mL. These variables were introduced in a multivariate logistic model to evaluate the independent effect of each one on hospital mortality.

Kaplan-Meier curves were employed to evaluate survival and freedom from hospitalization for cardiac events and log-rank test was used to compare the curves. Statistical analyses were performed using the Stat-View Statistical Software Package (SAS Institute, Cary, North Carolina) and Number Cruncher Statistical System (NCSS, Kaysville, Utah).

Endpoints
The primary endpoints of the presented study are effects of cTn I greater than 13 ng/mL on postoperative and midterm mortality. Secondary endpoints are effects of cTn I greater than 13 ng/mL on postoperative morbidity and midterm hospitalization for cardiac causes.

	Results

Top Abstract Introduction Material and Methods Results Comment References

 
During the study period 230 patients were deemed eligible and therefore considered for analysis. The cTnI trend during hospitalization can be seen in Figure 2. Peak cTnI release was generally observed 24 hours after the end of the operation. One hundred forty-six patients (63.5%) had cTnI peak values less than 13 ng/mL (mean peak value, 6.6 ± 3.1 ng/mL) and 84 patients (36.5%) had cTnI peak values greater than 13 ng/mL (mean peak value, 45.5 ± 59.9 ng/mL). Table 1 lists preoperative patients' characteristics and intraoperative variables. Patients with peak cTn I greater than 13 ng/mL were older and had higher preoperative cTnI values (0.53 ± 1.67 ng/mL versus 0.18 ± 0.6 ng/mL, p < 0.001). They required a higher number of grafts (3.3 ± 0.9 versus 3.1 ± 0.9, p = 0.16) although the difference was not statistically significant. Cross-clamp time (56 ± 16 versus 52 ± 15 minutes, p = 0.002) and CPB time (119 ± 29 versus 105 ± 26 minutes, p < 0.001) were longer in this group of patients.

View larger version (11K): [in this window] [in a new window]   Fig 2. Cell plot of perioperative cardiac troponin I (cTnI) values. (d = days; h = hours.)

	Comment

Top Abstract Introduction Material and Methods Results Comment References

 
Postoperative myocardial dysfunction may be attributed to ischemia/reperfusion-induced injury, poor myocardial protection, incomplete revascularization, and graft failure. Clinically, it is manifested by low cardiac output and hypotension and may be subdivided into two subgroups: reversible injury and irreversible injury. The purpose of our study is to assess the prognostic implications of cTnI release occurring after CABG surgery on both short-term and midterm mortality. It has been previously demonstrated that in the setting of cardiac surgery, cTnI is more sensitive and specific than CK-MB in detecting perioperative MI [7, 10]. Our data demonstrate that cTnI release greater than 13 ng/mL should not be considered an innocuous event caused by heart manipulation and surgical trauma of cardiac tissues (Fig 3). Patients with peak cTnI release greater than 13 ng/mL have an extremely high risk of operative mortality (odds ratio, 10) compared with patients with cTnI less than 13 ng/mL. Peak cTnI release was generally observed 24 hours after the end of the operation. This finding agrees with previous studies that showed peak cTnI release occurring between 20 and 24 hours after the end of the operation [5, 7]. Lasocki and colleagues [8] evaluated the outcome of 502 consecutive patients (excluding patients with recent MI and high preoperative cTnI) undergoing different cardiac operations; they found that cTnI greater than 13 ng/mL 20 hours after the end of the operation was an independent predictor of in-hospital death, particularly cardiac death, and major postoperative complications.

View larger version (12K): [in this window] [in a new window]   Fig 3. Estimated risk of hospital mortality according to postoperative troponine I (TnI) peak.

Unfortunately, our data do not clearly elucidate the reasons for excessive cTnI postoperative release. Is it caused by poor myocardial protection, incomplete revascularization or early graft failure? Further studies with acute reangiographic control in patients with elevated postoperative cTnI are needed to bring light on this issue. Nevertheless, we are reluctant to believe that the extremely poor surgical outcome of cTnI greater than 13 ng/mL group may not be associated with a somehow worse myocardial revascularization. Rasmussen and colleagues [11] demonstrated graft failure in 43 of 59 patients (73%) who received acute postoperative reangiography because of a highly suspected perioperative MI.

One of the limitations of our study is that we were unable to report data regarding ECG findings. Nevertheless, the accuracy of early postoperative ECG in detecting postoperative MI has been questioned. Postoperative pericarditis, preoperative bundle branch blocks, conduction disturbances, ventricular pacing, and electrolyte and acid-base disorders may all alter ECG sensitivity and specificity. Svedjeholm and colleagues [12] and Crescenzi and associates [13] showed that the isolated appearance of new Q waves has no impact on the postoperative cardiac outcome whereas the release of myocardial necrosis biomarkers is strongly associated with postoperative cardiac events.

One of the endpoints of our study was to assess the influence of postoperative cTnI release on midterm mortality. The presented report is the largest study reporting midterm survival for CABG patients based on postoperative cTnI release. The comparison of the cTnI greater than 13 ng/mL group and the cTnI less than 13 ng/mL group patients demonstrated that there was no difference in survival during the follow-up. This is in contrast with the findings of Fellahi and colleagues [9]. In their 2-year follow-up of 169 patients with a postoperative cTnI release less than 13 ng/mL and 26 patients with postoperative cTnI greater than 13 ng/mL, they showed a significantly worse survival rate for patients with higher postoperative cTnI release. There is a significant difference in preoperative patients' characteristics and operative mortality between the studies that might explain the outcome discrepancy. Nevertheless, previous reports suggest that while cTnI is a valuable marker to detect acute myocardial necrosis, it has a poor capacity to predict long-term outcome. Instead, CK-MB release is much better able to predict long-term outcome. Three large studies showed a positive correlation between extremely high CK-MB postoperative release and worse midterm survival [14–16]. Moreover, the prognostic importance of myocardial damage after percutaneous coronary intervention stratified by CK-MB and cTnI postprocedural release has been extensively evaluated. A positive correlation between CK-MB release after percutaneous coronary intervention and worse long-term survival has always been demonstrated [17–19]. Kini and colleagues [20] evaluated 1-year survival rates of 2,873 patients who had undergone percutaneous coronary intervention. By using Cox's hazard model, they revealed that while CK-MB release more than five times normal after percutaneous coronary intervention was a strong independent predictor of mortality at follow-up, cTnI (or any troponin subgroup) elevation had no prognostic implication. Similarly, other studies demonstrated a poor correlation between post–percutaneous coronary intervention cTnI release and survival at follow-up [21, 22]. Although a study comparing the long-term survival based on cTnI or CK-MB postoperative release in patients who had undergone CABG operation is lacking, our data seem to confirm that cTnI is a poor long-term prognostic marker in patients with myocardial necrosis.

Our study confirms that cTnI release is a useful marker to predict short-term outcome after CABG operation. To decrease mortality and morbidity, future studies should address the possible benefits of acute reangiography in patients with elevated postoperative cTnI release. Our data do not support the use of cTnI as a marker for midterm prognosis after CABG operations.

	References

Top Abstract Introduction Material and Methods Results Comment References

 

1. Shaff HV, Gersh BJ, Fisher LD, et al. Detrimental effect of perioperative myocardial infarction on late survival after coronary artery bypass J Thorac Cardiovasc Surg 1984;88:972-981.[Abstract]
2. McGregor CGA, Muir AL, Smith AF, et al. Myocardial infarction related to coronary artery bypass graft surgery Br Heart J 1984;51:399-406.[Abstract/Free Full Text]
3. Chaitman BR, Alderman EL, Sheffield LT, et al. Use of survival analysis to determine the clinical significance of new Q waves after coronary bypass surgery Circulation 1983;67:302-309.[Abstract/Free Full Text]
4. Jaffe AS, Ravkilde J, Roberts R, et al. It is time for a change to a troponin standard Circulation 2000;102:1216-1220.[Free Full Text]
5. Carrier M, Pellerin M, Perrault LP, Solymoss BC, Pelletier LC. Troponin levels in patients with myocardial infarction after coronary artery bypass grafting Ann Thorac Surg 2000;69:435-440.[Abstract/Free Full Text]
6. Eigel P, van Ingen G, Wagenpfeil S. Predictive value of perioperative cardiac troponin I for adverse outcome in coronary artery bypass surgery Eur J Cardiothorac Surg 2001;20:544-549.[Abstract/Free Full Text]
7. Greenson N, Macoviak J, Krishnaswamy P, et al. Usefulness of cardiac troponin I in patients undergoing open-heart surgery Am Heart J 2001;141:447-455.[Medline]
8. Lasocki S, Provenchere S, Benessiano J, et al. Cardiac troponin I is an independent predictor of in-hospital death after adult cardiac surgery Anesthesiology 2002;97:405-411.[Medline]
9. Fellahi JL, Gue X, Richomme X, Monier E, Guillou L, Riou B. Short and long-term prognostic value of post-operative cardiac troponin I concentration in patients undergoing coronary artery bypass grafting Anesthesiology 2003;99:270-274.[Medline]
10. Benoit MO, Paris M, Silleran J, Fiemeyer A, Moatti N. Cardiac troponin Iits contribution to the diagnosis of perioperative myocardial infarction and various complication in cardiac surgery. Crit Care Med 2001;29:1880-1886.[Medline]
11. Rasmussen C, Thiis JJ, Clemmensen P, et al. Significance and management of early graft failure after coronary artery bypass grafting. Feasibility and results of acute angiography and re-revascularization Eur J Cardio-thorac Surg 1997;12:847-852.[Abstract]
12. Svedjeholm R, Dahlin LG, Lundberg C, et al. Are electrocardiographic Q-wave criteria reliable for diagnosis of perioperative myocardial infarction after coronary surgery? Eur J Cardiothorac Surg 1998;13:655-661.
13. Crescenzi G, Bove T, Pappalardo F, et al. Clinical significance of new Q wave after cardiac surgery Eur J Cardiothorac Surg 2004;25:1001-1005.[Abstract/Free Full Text]
14. Costa MA, Carere RG, Lichtenstein SV, et al. 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]
15. 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]
16. Klatte K, Chaitman BR, Theroux P, et al. Increased mortality after coronary artery bypass graft surgery is associated with increased levels of post-operative creatine kinase-myocardial band isoenzyme releaseresults from the GUARDIAN trial. J Am Coll Cardiol 2001;38:1070-1077.[Abstract/Free Full Text]
17. Kong TQ, Davidson CJ, Meyers SN, Tauke JT, Parker MA, Bonow RO. Prognostic implication of creatine kinase elevation following elective coronary artery interventions JAMA 1997;277:461-466.[Abstract/Free Full Text]
18. Saucedo JF, Mehran R, Dangas G, et al. Long-term clinical events following creatine kinase–myocardial band isoenzyme elevation after successful coronary stenting J Am Coll Cardiol 2000;35:1134-1141.[Abstract/Free Full Text]
19. Abdelmeguid AE, Topol EJ, Whitlow PL, Sapp SK, Ellis SG. Significance of mild transient release of creatine kinase-MB fraction after percutaneous interventions Circulation 1996;94:1528-1536.[Abstract/Free Full Text]
20. Kini AS, Lee P, Marmur JD, et al. Correlation of postpercutaneous coronary intervention creatine kinase-MB and troponin I elevation in predicting mid-term mortality Am J Cardiol 2004;93:18-23.[Medline]
21. Fuchs S, Kornowski R, Mehran R, et al. Prognostic value of cardiac troponin-I levels following catheter-based coronary interventions Am J Cardiol 2000;85:1077-1082.[Medline]
22. Bertinchant JP, Polge A, Ledermann B, et al. Relation of minor cardiac troponin I elevation to late cardiac events after uncomplicated elective successful percutaneous transluminal coronary angioplasty for angina pectoris Am J Cardiol 1999;84:51-57.[Medline]

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