Clinical Chemistry
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Clinical Chemistry 46: 279-281, 2000;
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(Clinical Chemistry. 2000;46:279-281.)
© 2000 American Association for Clinical Chemistry, Inc.


Technical Briefs

Plasma Troponin T and Troponin I after Minimally Invasive Coronary Bypass Surgery

Siegmund Lorenz Braun1,a, Andreas Barankay2 and Domenico Mazzitelli3

1 Institut für Laboratoriumsmedizin,
2 Institut für Anästhesiologie, and
3 Klinik für Herz- und Gefässchirurgie, Deutsches Herzzentrum München, Lazarettstrasse 36, D-80636 Munich, Germany;
a author for correspondence: fax 0049-89-1218-1013, e-mail braun{at}dhm.mhn.de

In the last decade, plasma cardiac troponin T (cTnT) and cardiac troponin I (cTnI) have been identified as specific and sensitive markers of myocardial cell injury (1)(2). During most types of cardiac surgery, some degree of myocardial injury regularly occurs that is dependent on multiple factors, such as the type and extent of the surgical procedure, the method of myocardial protection, the preoperative cardiac status of the patient, and the anesthetic procedures (3)(4). In recent years, minimally invasive direct coronary artery bypass grafting (MIDCAB) and off-pump coronary artery bypass grafting (OPCAB) have been introduced as alternative methods to coronary artery bypass grafting (CABG) (5). The potential advantages of MIDCAB and OPCAB arise from the avoidance of cardiopulmonary bypass (CPB) and cardioplegia. CPB always induces a systemic inflammatory response syndrome, and a substantial number of patients develop multiple organ dysfunction. However, there are also disadvantages of MIDCAB and OPCAB, including difficulty of performing the coronary anastomosis on the beating heart, ischemic damage during occlusion of the targeted vessel, and cardiac dislocation or compression to obtain optimal exposure of the vessels on the posterior wall. Currently, only limited data (6)(7)(8)(9) concerning the release of troponins during MIDCAB and OPCAB are available.

The aim of this investigation was to study the effect of different surgical techniques, using a latest generation assay for the determination of cTnT, and to compare cTnI results to cTnT, particularly for diagnostic sensitivity.

Twenty-six consecutive patients (8 women and 18 men; median age, 63 years; range, 40–76 years; 25th–75th percentile, 52–69 years) were entered in the prospective study after giving informed consent. Twenty-one patients had a single left internal mammary artery graft to the left anterior descending artery through a left anterior small thoracotomy (MIDCAB). Four patients with two- or three-vessel disease also underwent operations without CPB but with a median sternotomy (OPCAB) using the Octopus stabilizer (Medtronic) or the CTS stabilizer (CardioThoracic System). At the end of anastomosis, conversion to conventional CABG with use of CPB was necessary in one patient (patient 17). Perioperative myocardial infarction (PMI) was diagnosed when the following criteria were satisfied: (a) creatinine kinase MB isoenzyme activity >50 U/L [immunoinhibition assay based on optimized standard method (25 °C) of the German Society of Clinical Chemistry]; and (b) the appearance of new Q-waves or a reduction of R-waves in two or more contiguous leads.

Blood samples were collected into ammonium heparinate tubes (Sarstedt) before (sample T1) and immediately after (sample T2) revascularization. Additional samples were drawn 2 (sample T3), 3 (sample T4), and 4 (sample T5) h after revascularization and at 0600 daily thereafter (samples T6–T12, depending on length of hospital stay). After centrifugation, aliquots were stored frozen at -30 °C until assayed in batches.

The third-generation cTnT assay was performed in an Elecsys® 1010 instrument (Roche Diagnostics, Mannheim, Germany). cTnI was measured with the AxSYM®-System (Abbott Laboratories). The detection limits of the assays were 0.01 µg/L for cTnT and 0.3 µg/L for cTnI. The upper reference limit for apparently healthy individuals is 0.04 µg/L for cTnT (10) and 0.5 µg/L for cTnI (11). The general decision limits for acute myocardial infarction (suggested cutoffs, 0.2–0.5 µg/L for cTnT and 2.0 µg/L for cTnI) are not valid after cardiac surgery. Uncomplicated cases have a median cTnT at the first postoperative day of 0.29 µg/L (5th percentile, 0.11 µg/L; 95th percentile, 1.68 µg/L) after conventional CABG in our institution.

The within-run imprecision using a patient’s sample was 3.58% (mean, 0.091 µg/L; range, 0.088–0.097 µg/L; n = 10) for cTnT vs 30.6% (mean, 0.45 µg/L; range, 0.3–0.7 µg/L; n = 7) for cTnI. The between-run imprecision using "low-end" control material was 13.7% for cTnT (PCcard1 control; mean cTnT, 0.15 µg/L; n = 6) and 9.6% for the cTnI (AxSYM low control; mean, 4.2 µg/L; n = 20). A total of 241 specimen from 26 patients were analyzed. Fig. 1 shows the concentrations of cTnT (Fig. 1A ) and of cTnI (Fig. 1B ) at the different sampling points; the line represents the medians, which were <0.1 µg/L for cTnT and <1.0 µg/L for cTnI at all sampling times. The peak concentrations are listed in Table 1 . The comparison of cTnT and cTnI results showed clinically congruent results in most patients. Discrepancies in the relative increase of troponin were found in only one patient (patient 9), who had no clinical complications. The very low peak cTnT of 0.09 µg/L seems more plausible than the peak cTnI of 5.2 µg/L. The maximum cTnI concentrations in the two PMI patients (patients 11 and 20) were far above the highest cTnI values of uncomplicated cases. Currently in most institutions, patients selected for MIDCAB have mostly one-vessel disease. Therefore, comparisons of postoperative troponin concentrations in patients after MIDCAB operation with conventional CABG, where often more than three vessels are grafted, must be looked on with some reservations. After conventional CABG, a substantial postoperative increase of troponins occurs regularly (4). This is in contrast to our MIDCAB patients; we had five patients with undetectable cTnT. Only slight increases of cTnT in the range 0.01–0.1 µg/L were found in 10 patients. cTnI was below the detection limit in six patients.



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Figure 1. Kinetics of the release of cTnT (A) and cTnI (B) after MIDCAB and OPCAB.

The lines represent the median troponin values at each sampling point. For better visualization of the results at very low concentrations, a logarithmic scale was used. Sample T1 was drawn immediately before revascularization; sample T2 was drawn immediately after revascularization. Samples T3–T5 were drawn 2, 3, and 4 h after revascularization, respectively; samples T6–T12 were drawn at 0600 daily thereafter.


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Table 1. Postoperative cTnT and cTnI concentrations.

In conclusion, we found that cTnT (Elecsys) as well as cTnI (AxSYM) concentrations in plasma of patients after MIDCAB and OPCAB operations were undetectable in 20% of the cases studied and were only slightly increased in most other patients. Compared with conventional CABG, this indicates less myocardial damage and demonstrates the safety of the applied techniques. Both troponin assays generate generally comparable results.


Acknowledgments

We thank Roche Diagnostics for providing the Elecsys instrument.


References

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