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Ann Thorac Surg 1998;65:1617-1620
© 1998 The Society of Thoracic Surgeons
a Cattedra di Cardiochirurgia, Università di Roma Tor Vergata, Roma, Italy
Accepted for publication January 16, 1998.
Address reprint requests to Dr De Paulis, Cattedra di Cardiochirurgia, Università di Roma, Tor Vergata, European Hospital, via Portuense 700, 00149 Rome, Italy
| Abstract |
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Methods. Thirty consecutive patients undergoing coronary artery bypass grafting who bled at least 400 mL within the first 4 hours after operation underwent reinfusion of shed blood. Thirty consecutive patients who were not autotransfused served as control. All patients underwent enzyme determination (total creatine kinase, MB fraction, lactate dehydrogenase, and troponin I) in the shed blood and in circulating blood preoperatively, at arrival in the intensive care unit, and 6, 24, and 48 hours after operation.
Results. The shed blood contained significantly higher concentration of cardiac enzymes than the circulating blood at all time intervals (p = 0.0001). The levels of creatine kinase, its MB fraction, and lactate dehydrogenase in circulating blood were significantly elevated in patients receiving autotransfusion up to 24 hours after autotransfusion. The blood levels of troponin I were not significantly different between the two group of patients at all time points. The percent fraction of MB did not increase after autotransfusion.
Conclusions. The measurement of cardiac troponin I is a useful marker for the diagnosis of perioperative myocardial infarction in patients undergoing transfusion of shed blood after coronary operation.
| Introduction |
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Recent studies have suggested that reinfusion of mediastinal and pleural drainage after coronary operation might increase cardiac enzyme levels in circulating blood, mimicking or masking a perioperative myocardial infarction [2]. As a consequence the determination of these enzyme assays in the early postoperative period might be of limited use.
The detection of postoperative myocardial infarction was recently improved by measuring the level of troponin I. This relatively new marker has been found to be as sensitive as CK-MB but more specific [3]. In this study we wanted to determine whether the use of this marker was somehow affected by autotransfusion and to compare it with the use of the other classic markers.
| Material and methods |
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Creatine kinase (normal range, 25 to 195 U/L), CK-MB (normal range, <24 U/L), and LDH (normal range, 230 to 460 U/L), were measured spectrophotometrically. Cardiac troponin I mass (normal range, 0.0 to 0.1 ng/mL) was measured with an immunoenzymatic assay ("sandwich") using two monoclonal antibodies specific for cardiac troponin I that recognize different epitopes. The immunoassays have no detectable cross-reactivity with human skeletal muscle troponin I. Comparison between the two groups and within each group were analyzed using a two-way analysis of variance for repeated measures. When significant differences were detected, pairwise comparisons were made using the Scheffé F test. Comparisons of the continuous and noncontinuous variables between the two groups were performed using an unpaired Students t test or a
2 test, respectively. Data are expressed as mean ± 1 standard deviation; probability values less than 0.05 were considered significant.
| Results |
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| Comment |
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The need for new cardiac-specific markers has recently been fulfilled by the possibility of measuring the level of troponin I in serum. Cardiac troponin I is a regulatory protein with high specificity for cardiac injury and it is not found after injury of the skeletal muscle [7]. Recent studies report that although the sensitivity of cardiac troponin I is comparable to that of CK-MB its specificity seems to be higher [8]. This aspect is of particular importance when considering the diagnosis of perioperative myocardial infarction in patients undergoing noncardiac operations or, as in our study, after coronary grafting. As a matter of fact the diagnosis of perioperative myocardial infarction can be quite difficult and often remains a diagnostic dilemma. The reason for these difficulties is because most often a perioperative myocardial infarction can occur without changes in heart rate or blood pressure and the increase of serum enzyme CK and CK-MB levels can occur as a consequence of injury to skeletal muscle. The difficulties are even more evident after coronary operation where, besides the skeletal muscle injury related to chest entry and the internal thoracic artery take down, there is also a more or less pronounced myocardial injury related to heart manipulation and myocardial protection. In this setting, classic enzyme determination has been demonstrated to be of limited use [9].
To complicate matters, Wahl and colleagues [2] recently demonstrated that autotransfusion of shed blood in the postoperative period causes elevation of cardiac enzymes, making their use less reliable in the diagnosis of perioperative myocardial infarction. Therefore, in this study we aimed to test the usefulness of troponin I in the diagnosis of postoperative myocardial infarction in patients receiving reinfusion of shed blood after coronary artery bypass grafts. The concentration of cardiac enzymes CK, CK-MB, LDH, and troponin I were all increased in postsurgical pleuropericardial shed blood. The highest values were detected in the CK concentration. Although some of these enzymes could be released from the chest wall and stroma (mostly CK and LDH) or from ventricles, atria, or aorta (CK-MB and troponin I), it is likely that some of the increase was attributable to the hemolysis that takes place in the shed blood reservoir. As a matter of fact, we previously found that the increase of cardiac enzyme concentration in the shed blood was also a function of the time that the blood was left in the reservoir [1]. However, the increase in CK, CK-MB, and LDH (but not of the percentage of the CK-MB fraction) was more evident after coronary operation than after valve operation, confirming that blood released from the chest wall mainly at the site of internal thoracic artery harvesting contains high levels of cardiac enzymes. In the study by Wahl and colleagues [2], they noted that reinfusion of pleuromediastinal drainage caused an increase of CK and LDH in the circulating blood with potential errors in the detection or exclusion of a perioperative myocardial infarction. Similarly, in this study we noted in autotransfused patients a significantly greater increase in the CK and LDH serum concentration than in patients without autotransfusion (Figs 1 and 2). These differences were significant up to 24 hours after operation and returned to normal levels (not significantly different from the control group) 48 hours after operation. Regarding the MB fraction we found significant differences only 6 hours after operation, but not significant differences thereafter. Conversely, the values of troponin I were virtually identical in autotransfused and nonautotransfused patients, indicating that this relatively new enzyme assay is not affected by autotransfusion and could be of value in the postoperative period of coronary patients undergoing autotransfusion of shed blood. Its high sensitivity associated with a probable higher specificity compared to the CK-MB fraction make the level of this enzyme particularly useful in the perioperative period where the false-positive diagnosis of myocardial infarction is more frequent. In a recent study on the evaluation of troponin I for the diagnosis of perioperative myocardial infarction after coronary operation, Mair and colleagues [3] suggested that troponin I could be superior to CK-MB mass or activity in detecting small perioperative myocardial necrosis. Nevertheless, although the sensitivity of troponin I and of CK-MB in the diagnosis of acute myocardial infarction are reported to be comparable, either in experimental or in clinical studies [10], the diagnostic window of troponin I is more prolonged. This indicates that especially in conditions where in the immediate postoperative period there are conditions (like the autotransfusion of shed blood) that can confuse enzymatic detection of perioperative myocardial infarction, the use of troponin I is helpful. Our results indicate that the autotransfusion of shed blood causes an increase in CK and LDH up to at least 24 hours after operation and therefore, during this period the diagnosis of myocardial necrosis could be missed.
Troponin I appears to have two advantages: (1) it does not appear to be influenced by autotransfusion and (2) it could detect small myocardial necrosis for a period well after 24 hours when the CK-MB levels are already decreasing toward normal values.
We did not use the more sensitive and specific enzyme immunoassays now available for measuring CK-MB mass concentrations. The use of this method could have increased the diagnostic sensitivity and specificity of CK-MB for myocardial damage. However, this method is not widely used, its cut-off values are still undefined, and other investigators [9] already demonstrated that troponin I was superior to either CK-MB mass or activity in detecting small areas of necrotic myocardial tissue.
The inclusion in the study of patients with a perioperative myocardial infarction would have better demonstrated the usefulness of troponin I in detecting myocardial damage in the presence of the confounding influence of concurrent autotransfusion of shed blood. Nevertheless, our data still indicate that in patients receiving autotransfused shed blood, continuous monitoring should not be withheld on the sole basis of the classic enzyme assays (CK, CK-MB, and LDH). Troponin I seems to be of value in avoiding a false-positive diagnosis of perioperative myocardial infarction. Furthermore, given its high sensitivity for small myocardial damage and given its persistence in plasma for up to 6 days, the troponin I marker could substitute the use of other cardiac enzymes in the perioperative period of patients undergoing coronary artery bypass grafting.
| References |
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