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Ann Thorac Surg 2000;70:2087-2090
© 2000 The Society of Thoracic Surgeons

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Original article: cardiovascular

Cardiac troponin I release after open heart surgery: a marker of myocardial protection?

^a Service de Chirurgie Thoracique et Cardiovasculaire, Service de Biochimie, CNRS UPRES A 7054, Association Claude Bernard, Hôpital Henri Mondor, Créteil, France

Accepted for publication May 8, 2000.

Address reprint requests to Dr Vermès, Service de Chirurgie Thoracique et Cardiovasculaire, Hôpital Henri Mondor, 51, avenue du Maréchal De Lattre de Tassigny, 94010 Créteil, France
e-mail: loisance{at}univ-paris12.fr

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. Unlike creatine kinase MB isoenzyme, cardiac troponin I (cTnI) is a highly specific marker of myocardial injury. Its release has recently been studied after coronary artery bypass grafting operation. However, its significance after open heart surgery (OHS) remains to be determined. This protein release could be a marker of myocardial protection. We sought to study cTnI release after OHS in patients with normal coronary arteries and to compare it with cTnI release in patients after coronary artery bypass graft (CABG) surgery.

Methods. Eighty-five patients undergoing OHS and 86 patients undergoing CABG were enrolled in the study. CTnI concentrations were measured in serial venous blood samples drawn before surgery and immediately, 12 hours, 24 hours, 48 hours, and 5 days after aortic unclamping.

Results. In the OHS group and in the CABG group without acute myocardial infarction (AMI), cTnI peaked at 12 hours postoperatively (6.35 ± 6.5 and 5.38 ± 8.55 ng/mL, respectively) and normalized on day 5 postoperatively (0.57 ± 2 and 0.72 ± 1.62 ng/mL, respectively). CTnI concentration did not differ significantly between the OHS group and the CABG group in the absence of AMI for any samples considered. In the CABG group, 2 patients had AMI. In the OHS group, cTnI levels at 12 hours postoperatively were found to correlate closely with CPB and aortic cross-clamping (ACC) times, contrary to the CABG group, which correlated only with occurrence of AMI. CTnI release was independent of age and ejection fraction in either group.

Conclusions. cTnI release in patients after OHS with normal coronary arteries has the same profile as cTnI release in patients after CABG in the absence of AMI. However, its peak at 12 hours postoperatively is only correlated to ACC and CPB times, which is contrary to cTnI release after CABG surgery. This observation suggests that cTnI could be a marker of myocardial ischemia after OHS.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Cardiac troponin is a reliable specific marker of myocardial injury [1–3], more specific and sensitive than total creatine kinase (CK) activity and CK mass [4]. It has been suggested that cardiac troponin I (cTnI) specificity to detect myocardial injury may be greater than that of cardiac troponin T [5]. Moreover, cTnI is an independent predictive factor of cardiac events in patients with unstable angina [6].

After abdominal aortic surgery, specificity of cTnI as a marker to exclude postoperative myocardial infarction has been demonstrated by Ben Ayed and associates [7]. However, in the postoperative period after cardiac surgery, diagnosis of acute myocardial infarction (AMI) remains difficult to establish. Aortic cross-clamping induces myocardial ischemia, which results in increased serum levels of the usual biochemical markers and interferes with the diagnosis of AMI.

Previous studies have suggested that cTnI concentration may represent a valuable marker to confirm the diagnosis of postoperative myocardial infarction in coronary artery bypass graft (CABG) patients [8, 9]. However, limited reports are available to assess the use of cTnI as a marker of myocardial ischemia after open heart surgery (OHS) [10]. The use of these markers could be of some interest to assess the quality of myocardial protection during procedures.

The purpose of this study was to measure cTnI release after OHS in patients with normal coronary arteries compared with cTnI release after CABG and to assess cTnI as a marker of myocardial injury after OHS.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Patients
One hundred eighty-seven patients, indicated for OHS or CABG, were enrolled prospectively from November 1997 to November 1998 in this study. Exclusion criteria were: patients with poor image quality to allow echocardiographic evaluation of segmental wall motion abnormalities (12 patients); patients with left bundle branch block or paced rhythm on 12-lead electrocardiogram (ECG) (4 patients); and patients with significant lesion on coronarography in the OHS group. A significant lesion was considered for greater than 50% stenosis on left anterior descending artery, right coronary artery, or circumflex or for greater than 40% stenosis on left main artery. No emergencies were included.

Procedure
Out of 171 patients, 85 underwent OHS (OHS group) (aortic replacement, n = 66; mitral replacement, n = 1; mitral repair, n = 8; Bentall, n = 10) and 86 underwent CABG (CABG group) with two- or three-vessel disease. An average of three grafts per patient were performed with 75% of arterial grafts.

All patients underwent moderate hypothermic cardiopulmonary bypass (28°C to 32°C). Myocardial protection was achieved using a cold antegrade crystalloid cardioplegia solution (Fabiani solution).

Preoperative measures for each patient included cTnI plasma level, ECG, and baseline echocardiography. Troponin I assays were performed immediately after procedure, and repeated at 12 hours, 24 hours, 48 hours, and 5 days after surgery. ECG was obtained daily.

Echocardiography analysis
Echocardiographic assessment was performed preoperatively and 5 to 7 days after surgery. We used a commercially available ultrasound imaging system without second harmonic imaging capabilities (Vingmed 800) with a 2- to 5-Mhz transducer. Complete ultrasonic examination was performed by a single experienced echocardiographer without knowledge of clinical and biochemical informations. The American Society of Echocardiography 16-segment model [11] was used, except for septal wall motion analysis because of the postoperative septal shift.

Myocardial infarction criteria
Perioperative myocardial infarction was defined as new persistent regional wall motion abnormalities on echocardiographic studies associated with electrocardiographic alterations after surgery (new Q wave > 0.04 ms in, at least, two contiguous leads).

Plasma level troponin I determination
A blood sample was obtained on lithium heparinate and a measurement was performed without delay on plasma after centrifugation (3,000 g for 15 minutes). CTnI was measured on a Stratus II analyzer (Dade Behring, Maurepas, France), which uses two monoclonal antibodies specific for cardiac troponin that recognize different epitopes.

In this procedure, the sample is pipetted onto the center portion of a square piece of glass fiber paper, which contains the monoclonal antibody responsible for capture of the analyte. After a short incubation, a conjugate reagent containing a monoclonal antibody labeled with an alkaline phosphatase is pipetted onto the reaction zone. During the second incubation period, the labeled antibody reacts with the cTnI, which has been bound by the capture antibody. Any unbound labeled antibody is subsequently eluted from the reaction zone by applying a substrate wash solution. The enzymatic rate generated by the bound antibody fraction, which is directly proportional to the cTnI concentration in the sample, is measured by front surface fluorescence. The normal range is less than 0.4 ng/mL and the cutoff for acute myocardial infarction is 1.5 ng/mL.

Statistical analysis
Statistical analysis was performed using SPSS statistical software (SPSS Inc, Chicago, IL). Continuous variables were expressed as mean ± standard deviation and compared with an unpaired two-tailed t test. Categorical variables, expressed as percentages, were analyzed with Pearson’s ² test or with Fisher’s exact test when expected values were less than 5. CTnI concentrations in the CABG group versus the OHS group were compared using repeated-measures analysis of variance. Risks factors responsible for increasing CTnI concentrations in the two different groups were studied with a linear regression test for continuous variables (age, ejection fraction [EF], cardiopulmonary bypass [CPB] time, aortic cross-clamping [ACC] time), with Krushall-Wallis nonparametric test for grafts per patients variable, and with Mann-Whitney nonparametric test for AMI variable. A multivariate linear regression analysis was performed including variables with p less than 0.2. A two-tailed p less than 0.05 was taken for statistical significance.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
Table 1 shows preoperative, operative, and postoperative characteristics of the 171 patients enrolled in the study. Age, gender, and ACC time did not differ significantly between the two groups. EF was significantly lower in the CABG group, but remained within normal range. No AMI occurred in the OHS group.

View larger version (14K): [in this window] [in a new window]   Fig 1. cTnI concentration time courses in OHS group and CABG group without AMI. Results are expressed as mean ± confidential interval. (AMI = acute myocardial information; CABG = coronary artery bypass graft; OHS = open heart surgery.)

	Comment

Top Abstract Introduction Patients and methods Results Comment References

In our study, we demonstrated that, in the OHS group, cTnI peak values were reached at 12 hours after aortic unclamping, followed by a mono-exponential decline leading to disappearance after day 5 postoperatively in the absence of complication. Compared with the CABG group in the absence of postoperative AMI, there were no significant differences in cTnI levels after 12, 24, and 48 hours, and after day 5 postoperatively. These findings are not in agreement with Etievent and associates’ observation [10]. In a population of 20 aortic valvular replacements with normal coronary arteries and 20 CABG, they showed a significantly higher cTnI concentration at 6 and 12 hours postoperatively in the CABG group. However, this discrepancy could be explained by a smaller total number of patients (1 patient in the CABG group had postoperative AMI) and different sensibility in postoperative AMI detection in the absence of echocardiography.

In our study, 2 CABG patients had ECG and echocardiographic evidence of perioperative myocardial infarction with very high cTnI levels. Simple and multiple linear regression analysis revealed a close correlation between measurements of cTnI at 12 hours postoperatively and AMI in the CABG group (p < 0.02 and p < 0.001, respectively), thereby suggesting that this protein is a highly specific marker of perioperative AMI.

In the OHS group, multivariate linear regression analysis revealed that cTnI release at 12 hours postoperatively correlated to CPB and ACC times. We could not observe the same correlation in the CABG group. These findings suggest that the postoperative increase in cTnI levels, in the CABG group, results from several factors, including most certainly cross-clamping time, but also from quality of revascularization, quality of myocardial protection, route of delivery of cristalloid cardioplegia [15], and type of cardioplegia [16].

Indeed, Chocron and associates [15] observed in patients with left main coronary artery stenosis a different cTnI release pattern depending on the route of cardioplegia delivery. In contrast, we observed a positive correlation in the OHS group with normal coronary arteries between cTnI release at 12 hours postoperatively and CPB and ACC times. This suggests that cTnI is a reliable marker of myocardial ischemia as described by Etievent and associates [10] and could depict the quality of myocardial protection used for this procedure in the absence of any coronary artery disease. Moreover, cTnI release at 12 hours postoperatively was not correlated with age or EF in both groups.

The results of our study suggest that release of cTnI in the OHS group with normal coronary arteries is only related to the length of CPB time and ACC time, as opposed to the CABG group. In this latter group, cTnI release could depend on other parameters that remain to be elucidate (quality of revascularisation, route of delivery of cardioplegia, etc). After OHS, cTnI release could be a marker of myocardial injury. Further studies are required to assess the prognostic value of cTnI release after cardiac surgery.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

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