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Asian Cardiovasc Thorac Ann 2006;14:530-535
© 2006 Asia Publishing EXchange Ltd

REVIEW PAPER

Plasma Troponin Levels After Cardiac Surgery vs After Myocardial Infarction

Dan Abramov, MD, Muhammad Abu-Tailakh, BSN, Michael Frieger, PhD, Amir Ganiel, MD, David Tuvbin, MD, Arik Wolak, MD

Department of Cardiothoracic Surgery, Soroka Medical Center, Beer Sheva, Israel

For reprint information contact: Dan Abramov, MD Tel: 972 8 640 0968 Fax: 972 8 640 0961 Email: abramov2{at}zahav.net.il, Department of Cardiothoracic Surgery, Soroka Medical Center, Beer Sheva 84101, Israel.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Raised plasma troponin, a diagnostic marker for myocardial infarction, usually occurs after cardiac surgery, leading to difficulties in diagnosing postoperative myocardial infarction. To ascertain whether the same processes influence troponin elevation in both conditions, a literature search was performed for plasma troponin elimination curves after myocardial infarction, myocardial infarction with reperfusion, and cardiac surgery. From 70 studies, 11 curves using the Stratus immunoassay kit were analyzed: 5 post-cardiac surgery (412 patients), 2 after myocardial infarction with reperfusion (169 patients), and 4 after myocardial infarction (640 patients). For each group, a new plot was formulated from the mean troponin level at each time interval. While the up-slope of the cardiac surgery curve was much steeper than that of myocardial infarction, resembling that of myocardial infarction with reperfusion, its down-slope was significantly more gentle than that of both other groups (–0.91 vs –5.31, t = 3.47, df = 8, p < 0.01). This suggests that postoperative troponin elevation involves enhanced cell permeability as seen after ischemia reperfusion rather than permanent cellular damage. The gentler down-slope may point to surgery-induced impaired troponin removal from the circulation. Due to the different mechanisms proposed, implications from post-myocardial infarction troponin levels may not be conferred on post-cardiac surgery patients.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Cardiac troponin I (cTnI) is bound to the cellular ultrastructure but has a considerable soluble pool (4%) in the myocardium.1–5 As a result of this soluble pool, its release after cell damage is almost as rapid as that of the cytosolic molecules myoglobin and creatine kinase.6 The ongoing post-ischemia release of cTnI from the contractile apparatus, which contains the other 96% of cellular cTnI, continues for days during the cellular repair process after myocardial infarction (MI). This may explain the prolonged elevation of cTnI in the circulation. Cardiac tropnin I is released as troponin I-troponin C, troponin I-troponin T, troponin I-T, and C covalent complexes.7,8 As the half-life of free cTnI in the circulation is only 5 min, the major forms of cTnI in patients are more likely to be troponin complexes that protect cTnI from degradation, thus allowing preservation of its immunoreactivity.7

During ischemia, progressive intracellular cTnI degradation takes place. Increased severity of the ischemic insult leads to more extensive degradation of cTnI and preferential release of a cTnI degradation product.9–13 Cardiac troponin I in ischemic myocardium is progressively and selectively modified through oxidation, reduction, and phosphorylation.14–25 These modified products, and not intact cTnI, are preferentially detected in the effluent from severely ischemic hearts. Nevertheless, the significance of these modified products has not been investigated despite their possible clinical importance as markers of the progression of ischemic heart disease.

Elimination of released myocardial proteins occurs in the liver, pancreas, kidneys, and reticuloendothelial system. Thus, impaired clearance from the blood (renal or hepatic failure, hypothyroidism) leads to prolonged increases.26 Reperfusion causes a true acceleration of cellular protein leakage by acute plasmalemmal disruption and not just enhanced wash-out. Thrombolytic therapy with reperfusion after MI causes a significant and rapid increase of blood cTnI levels.27–29 In patients with acute coronary syndrome, cTnI concentrations correlate strongly with morbidity and mortality.30,31 In contrast, the relationship between post-cardiac surgery levels, myocardial damage, and operative results remains unclear. In spite of this, more and more studies and clinical work are based on the postulation that post-cardiac surgery cTnI levels have the same implications as those after MI.32–41 This may not be accurate because of the complicated path of cTnI from the injured myocardial cell to the circulation, the ability of ischemia-reperfusion (common in cardiac surgery) to greatly increase plasma cTnI levels, the as yet unknown influence of surgery-induced systemic inflammation, and the impact of postoperative dysfunction of organs that eliminate cTnI. In this study, we searched the literature for serum cTnI elimination curves after MI with and without reperfusion, and compared them to post-cardiac surgery curves.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
A thorough search of the literature was performed for plasma troponin elimination curves after MI, after MI with immediate reperfusion, and after cardiac surgery. The search was performed in the Medline PubMed database using the search terms "troponin", "elimination", and "curve" in different combinations. Only articles that had information regarding changes in troponin levels over time after the above mentioned events (at least 4 post-event troponin I measurements at 4 different time points) were included. More than 70 studies were found. Due to variation in the ability of different immunoassay kits to quantify troponin I degradation products and troponin complex levels, the results from one kit cannot be compared with those from others. It was decided to concentrate on studies carried out with the kit most often used in these studies: the Stratus kit (Dade Behring, Inc., Deerfield, IL, USA).42 An advantage of the Stratus assay is that it recognizes the N-terminal portion of cTnI, so it is less susceptible to late changes in troponin structure, which usually include C-terminal degradation.42 There were 9 studies comprising 11 plasma cTnI elimination curves: 5 after cardiac surgery (412 patients), 2 after MI with reperfusion (169 patients), and 4 after MI (640 patients).43–51 Missing data were completed by direct contact with the authors of these studies.

In all these elimination curves, the data on troponin levels at each time interval were transformed from concentration units to a percentage of the peak level in the study, so that all studies received the same statistical importance, irrespective of the magnitude of the peak troponin level. Three plots were prepared from the mean of each group of studies (Figure 1Go). A linear regression equation for troponin levels over time was built, and the up- and down-slopes of the lines were compared by appropriate methods.52


Figure 1
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  		Figure 1. Mean plasma troponin-I changes after cardiac surgery and myocardial infarction (MI) with and without reperfusion.

 

   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
The up-slope of the post-cardiac surgery troponin curve was much steeper than that of the post-MI curve, and even steeper than that of post-MI with reperfusion (Figure 1Go). Statistical significance could not be calculated due to the small number of time points in the ascending graph. The down-slope of the post-cardiac surgery curve was significantly less steep than that of post-MI and post-MI with reperfusion (slope of post-MI curve, –0.91 vs post-cardiac surgery, –5.31; t = 3.47, df = 8, p < 0.01).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Greenson and colleagues53 showed that after coronary artery bypass grafting (CABG) 48% of patients had creatine kinase MB-isoenzyme elevation of more than 5 times the upper limit of normal and 21% of patients had peak troponin values more than 80 times the upper limit of normal. An important disadvantage of routine collection of cardiac enzyme data without definitive understanding of its relevance, is labeling a patient as having had postoperative MI. This has important implications for patient management, specifically, should we catheterize all patients with high cTnI levels? Should we consider longer rehabilitation periods for them? Moreover, the results of many studies in cardiac surgery have been based on the hypothesis that higher postoperative cTnI levels indicate more myocardial injury.32–41 It has been implied that because higher cTnI levels are seen after CABG with cardiopulmonary bypass, off-pump surgery inflicts less myocardial injury.54 Three mechanisms for post-cardiac surgery serum cTnI elevation have been suggested: myocardial ischemia-reperfusion injury, mechanical cardiac trauma, and re-transfusion of shed mediastinal blood rich in troponin, during or after the procedure. Several studies have tried to correlate post-CABG cTnI levels and degradation patterns to myocardial ischemic damage. It was found that cTnI degradation products after CABG are similar to those in hearts after ischemia or ischemia-reperfusion (for example cleavage of 17 cTnI C-terminal amino acids). Degradation products of cTnI are the same in all groups of patients, suggesting that the modification process is specific and selective.55

During CABG, myocardial cTnI is degraded and released in approximately two thirds of patients even before aortic crossclamping, suggesting that processes other than ischemia are involved in cTnI leakage and modification during cardiac operations.55 Such processes may include inflammation. Moreover, electron microscopy on myocardial biopsy samples taken before and after aortic crossclamping usually demonstrate normal cellular ultrastructure, implying that cTnI release can occur without cell necrosis.55 We now know that ischemic myocardial necrosis and most other types of cell death are delayed, with a substantial reversible pre-lethal phase. On moderate ischemic stress, myocardial tissue can release small amounts of macromolecules from the cytosolic compartment by mechanisms other than persistent membrane perforation.56–58 This may explain some of the post-cardiac surgery enzyme elevation. When surgical trauma is considerable, mechanical injury of myocardial cells may be a factor. For example, patients undergoing mitral valve replacement with a concomitant radiofrequency ablation procedure have an early and large release of cTnI in the absence of postoperative MI.59 Children undergoing repair of tetralogy of Fallot or ventricular septal defects have higher cTnI release than those undergoing atrial septal defect repair.60 Another source of elevated serum cardiac enzymes is re-transfusion of mediastinal shed blood that contains extremely high cTnI concentrations and creatine kinase activity.61–63 A surgery-induced systemic inflammatory response may also increase cellular permeability and cause troponin leakage.

One must be cautious when comparing studies that used different cTnI assays. Ten- to 20-fold variations in cTnI concentrations were reported when the same sample was measured by different assays.64–66 Signals generated in immunoassays with anti-cTnI monoclonal antibodies depend on the epitope region recognized by these antibodies.67 Protein regions within the cTnI molecule, which are susceptible to oxidation, reduction, phosphorylation, or degradation by proteases, are likely to exhibit variable immunoreactivity and even loss of reactivity, leading to altered signal generation in assays deploying antibodies against such regions. For example, the C-terminal portion of serum cTnI is preferentially degraded, consequently assays such as Access that recognize the C-terminal portion of the cTnI molecule tend to yield lower concentrations than those recognizing the N-terminal portion, such as Stratus and Opus.42 In this literature analysis, only elimination curves obtained with the Stratus kit were compared because it is more accurate and the most widely used among published elimination curves. We did not find enough troponin elimination curves to perform statistical analyses on other commercial kits.

Nevertheless, a similar difference between post-MI and post-cardiac surgery curves could be demonstrated: the up-slope of post-cardiac surgery cTnI elimination curves was steeper than those of post-MI with reperfusion, and both were steeper then those of post-MI curves. Therefore, we believe that the fast peak of post-cardiac surgery troponin levels expresses ischemia-reperfusion or systemic inflammation, causing enhanced cell membrane permeability rather than permanent cellular damage as seen after MI. Interestingly, the study of Noora and colleagues68 showed that while cTnI typically reaches a peak 7 hr after cardiac surgery, it peaks after 18 hr in patients with postoperative MI confirmed by electrocardiographic criteria. The down-slopes of post-cardiac surgery curves are gentler than those of post-MI and post-MI with reperfusion, suggesting that elimination of cTnI from the circulation is slower after cardiac surgery. This is probably due to surgery-induced temporary dysfunction of organs that remove troponin from the blood. Troponin I covalent complexes with troponin T and C, which appear with mild ischemia, and disappear in more severe injury.8,9 Thus, if the ischemic insult is milder after cardiac surgery than after MI, cTnI will appear mainly as a complex rather than the free form, rendering it less vulnerable to degradation, and consequently its elimination will be slower.

Our study suggests that different mechanisms may be responsible for cTnI elevation after MI and after cardiac surgery. Therefore, plasma cTnI levels in clinical practice should be different in these two situations. We believe that much more information about cellular damage, degree of ischemia, and ischemia-reperfusion after cardiac surgery could be gained from investigating the relationship between the types of troponin degradation products (oxidation, reduction, phosphorylation, degradation by proteases, and complex formation) and the clinical outcome in patients. Thus, until further investigation, we should not imply the denotation of post-MI troponin levels on post-cardiac surgery patients, nor utilize the cTnI level as a marker for perioperative MI.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
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