Best Practices for Monitoring Cardiac Troponin in Detecting Myocardial Injury

Cardiac troponin [cardiac troponin I (cTnI) and cTnT] has become globally recognized as the standard biomarker for the diagnosis of acute myocardial infarction (AMI).8 With improvements in the analytical characteristics of cardiac troponin assays, particularly imprecision at low measurable concentrations, high-sensitivity cardiac troponin (hs-cTn) assays are now being implemented worldwide; but not in the US since the Food and Drug Administration has not yet cleared them for clinical use. With the implementation of hs-cTn assays, improvements in clinical care are beginning to be observed in the peer-reviewed literature. These improvements include early rule out (early hospital discharge) and rule in (right bed for appropriate patient) for MI and improved risk stratification for patients presenting with symptoms suggestive of ischemia, with improved short- and long-term outcomes. Further hs-cTn assays have been part of solidifying the definition of myocardial injury, based on an increased cardiac troponin concentration above the 99th percentile upper reference limit. The high-sensitivity assays have improved the clinical understanding that not all cardiac troponin increases are MI and that patients with nonischemic disease also have increases in cardiac troponin that must be managed accordingly. This Q&A provides the opportunity for 3 cardiologists, 2 laboratory medicine scientists, and 1 emergency medicine physician to share their experiences with the evolving role of cardiac troponin testing in their practices. Ideally, the messages they share will assist in better harmonizing the appropriate utilization of high-sensitivity assays worldwide as we transition away from contemporary cardiac troponin assays. Should all medical centers have a uniform serial order set to assist in ruling in/out AMI? Should a single cardiac troponin order be available? What would your ideal serial order set (timing) be? Allan S. Jaffe: Medical centers would benefit from developing consistent, uniform serial orders to rule in/out AMI. These serial orders should be agreed to by emergency medicine, cardiology, internal medicine, and laboratory medicine. Given that we do not have hs-cTn assays available in the US, the best timing is still 0 (presentation), 3, and 6 h. Because many patients present late, the vast majority of rule in/out and risk stratification action is likely to occur within 3 h of the onset. Single cardiac troponin orders with the current contemporary assays are rarely of use but may have a role if one is interested in estimating infarct size. The value that correlates best with MRI-determined infarct size is the 72–96-h value. What should be discouraged, however, is the idea that one should start to rule in/out AMI and then truncate that procedure. In essence, when you start such a procedure it implies that there is at least some reasonable possibility that acute ischemic heart disease is present. Scott Sharkey: Cardiac troponin testing should be standardized throughout the US and preferably internationally, and single cardiac troponin testing should be allowed. Admission (0 h), 3, and 6 h serial orders are preferred. Timing should be from admission and not from symptom onset, as it is too hard to make a determination when symptoms began in many patients and would make timing difficult. Peter Kavsak: Having a standard serial order set would be an ideal situation. However, this is often difficult to achieve. In our hospital network, it was only through collaboration between emergency medicine, internal medicine, laboratory medicine, and cardiology that we were able to go to a standard serial order set in the emergency department and this was only possible when we transitioned to an hs-cTn assay. Presently, the laboratory does not place any restrictions on cardiac troponin testing. We have observed that a number of emergency department patients do not have a second cardiac troponin order, so clinically a single cardiac troponin result is being used. Currently, with an hs-cTn assay we have adopted a 0- and 3-h protocol, with interest from emergency medicine to shorten this time frame further. Michael C. Kontos: The optimal order pathway/order set should include 2–3 samples, with the second sample collected 2–3 h after the first (depending on assay) and the third one 6 h after the first. The third sample should be an optional one that is based on risk (i.e., low-risk patients based on standard scoring scheme would have 2 samples, while intermediate-risk 3 samples). Our current pathway allows this ability to check specific samples and a 0-, 3-, and 6-h set. Although much has been made of using a single sample for patients who present hours after symptom onset, I believe this can be confounded by an inaccurate history, in which the symptoms have been waxing/waning and the patient presents acutely due to substantially worsening symptoms. A single sample should be limited to those who have been symptom free for 2–3 h. Not asked in the question is what the optimal reporting should be. For patients having serial sampling, the absolute change between the 2 values should be reported, highlighting those values that exceed the recommended value defining a significant change for that assay. We implemented this approximately 1–2 years ago, and it has decreased the degree of confusion in trying to determine if the patient has acute coronary syndrome (ACS). Amy K. Saenger: I think that a standardized chest pain protocol with defined serial draws should be implemented within a medical center/health system. Ultimately this would provide measurable results in terms of optimizing patient care and outcomes. In my experience, streamlining the phlebotomy draws in the order set helps substantially. In the emergency department the clinician only has to order the chest pain protocol and all of the subsequent timed cardiac troponin samples are automatically queued and ordered behind the scenes. This eliminates errors related to missed orders and/or forgetting to draw the cardiac troponin sample at a specific time. A standard timed collection protocol also helps define what a clinically significant “rise and/or fall” of cardiac troponin is in a given AMI population because δ calculations require fairly stringent collection protocols. One challenge is adhering to the American Heart Association, College of American Cardiology Non-ST Elevation-ACS (AHA/ACC NSTE-ACS) guidelines, which state that clinical laboratory reports should indicate whether a clinically significant acute change in cardiac troponin has occurred, specific to the assay used. While a uniform ±20% change or ±3 SDs of the baseline cardiac troponin concentration is recommended to define a clinically significant change, in reality we do not know for certain if these are the most accurate values for each assay, nor is this information defined in the manufacturer's package insert. Ideally, a clinical study would probe and define an appropriate δ (change value) using the same set of patient samples and adjudicated based on the hs-cTn result as the gold standard. Without this information it is unrealistic to expect clinical laboratories to broadly implement reporting deltas. I would not completely limit ordering cardiac troponin as a serial order set, although one could argue that only serial order sets (not single cardiac troponin orders) should be available in the emergency department. Cardiac troponin is also used for risk stratification in other, non-ACS populations. Therefore, limiting cardiac troponin orders to only a serial order set could lead to inappropriate and/or overutilization of the test. An ideal serial order set would be 0, 3, and 6 h based on contemporary cardiac troponin assays. With hs-cTn assays I would advocate for a 0 and 2 h protocol, with the option to order additional testing at a later time point to account for late presenters. I have reservations about a baseline and 1-h sample providing relevant information regarding an acute serial change in hs-cTn unless the phlebotomy collection timing is very strict and turnaround time for results is rapid. Limits around the timing of collections should also be defined and implemented based on the efficiency and logistics of the clinical practice. Stephen Smith: Yes, there should be some flexibility in select cases. For instance, there are times when it is beneficial to get a second cardiac troponin measurement very soon after the first. In such a case, strict adherence to an every 3 or 4 h schedule could delay diagnosis. In some patients with acute coronary occlusion, the electrocardiogram (ECG) is not normal but also not diagnostic of ischemia, and the first cardiac troponin is below the limit of detection (LoD) or <99th percentile. These patients frequently have delayed diagnosis, and by the time the second cardiac troponin result returns it may be 4 h after presentation in the emergency department (e.g., the first cardiac troponin is drawn at 30 min after arrival, is resulted at 60 min and is “negative”; the second is drawn at 3.5 h after presentation and resulted at 4 h). By this time, the infarct is complete. In occasional cases in which the first cardiac troponin (0 h) is negative, it is beneficial to check a 1 h to be certain that cardiac troponin is not rising rapidly. There are studies using 0 and 1 h or 0 and 2 h hs-cTn to “rule in” MI, but they have not been promoted for contemporary cardiac troponin assays, which are the only cardiac troponin methods currently available in the US. I would not promote every 1-h contemporary cardiac troponin for rule out MI. There is only anecdotal data on such an approach for rapid rule in of MI, but I believe it may be important in select cases. A single cardiac troponin should be available in patients for whom AMI is a secondary concern. It is important for patients who need to be admitted to the hospital for 1 condition, but also need to be screened for myocardial injury. A single cardiac troponin is also very useful for low risk patients with prolonged chest pain who will be discharged. For them, any subsequent orders in a set will be automatically cancelled when the patient is no longer in the hospital and available for blood sampling. Clinical orders would be as follows. For a usual patient and when using contemporary cardiac troponin assay: 0, 3, 6, 9 h; revised when using hs-cTn to 0, 1, 3, 6 h, or 0, 2, 6 h, depending on the assay. For a high-risk patient and using contemporary cardiac troponin assay: 0, 1, 2, 3, 6, 9 h; revised when using an hs-cTn assay to 0, 1, 2, 3, 6 h. Should the ordering of cardiac troponin be limited to the diagnostic use for AMI? For what other clinical situation would you order cardiac troponin? Allan S. Jaffe: Using contemporary assays, cardiac troponin is predominantly used to diagnose AMI. However, even with contemporary assays there are data to suggest that there is useful risk stratification information in patients with congestive heart failure and that chemotherapy toxicity can be detected with approaches that might mitigate or to some extent obviate the severity of such toxicity. In addition, critically ill patients with increased concentrations are at increased risk of adverse events, predominantly mortality. It is not clear how one should use the data in this latter group; it does suggest, however, that once these patients survive the acute episode, and assuming they do not need emergent cardiovascular care, they should be evaluated to determine the reasons for the underlying increases in cardiac troponin, which likely reflect either chronic or acute cardiovascular issues. Scott Sharkey: Other reasons for ordering cardiac troponin include suspected pulmonary embolism, aortic dissection, Takotsubo cardiomyopathy, acute myopericarditis, and possibly other conditions (chemotherapy, sepsis, acute stroke, and even post-noncardiac surgery). Peter Kavsak: Cardiac troponin ordering should be limited to the investigation of myocardial injury, of which AMI is a subset. This is aptly illustrated in the Third Universal Definition of Myocardial Infarction. This is an exciting area and the possibilities are not endless, but there are many potential roles for cardiac troponin, especially for high-sensitivity assays, to improve patient care. Michael C. Kontos: Cardiac troponin can be ordered for myocarditis, pericarditis, pulmonary embolism, and chest pain. Amy K. Saenger: Although there is presently a large focus on defining the clinical performance of hs-cTn assays for the diagnosis of AMI and strategies for rapid rule out, the greatest potential for hs-cTn likely resides outside the emergency department. Cardiac troponin is equally important in the area of risk stratification, where increases clearly hold prognostic significance with contemporary cardiac troponin assays. This is magnified to an even greater extent with hs-cTn assays; applications include chronic and heart failure It would be even from an to completely limit use of cardiac troponin for only the diagnosis of AMI. Stephen Smith: Cardiac troponin helps to risk many acute and chronic conditions myocardial injury. It is useful to and/or risk myocarditis, Takotsubo cardiomyopathy, pulmonary embolism, and other acute conditions that are not as 1 or 2 AMI. Cardiac troponin is useful even to risk patients of coronary chronic conditions such as heart failure and you an to 1 cardiac troponin order set, with the that an must be for an additional Allan S. Jaffe: are very but one must be not to them with so many that the what has been It is to the what is agreed to by all those in which a cardiac troponin could be the of the is and only occur when there is that is substantially from what has been agreed to by all of the interested this would be not in that the would be that it would for what is a with the Peter Kavsak: This is an In the we have restrictions on ordering cardiac troponin that a What we were from and may be to optimal Michael C. Kontos: I would a single order set, and I think most currently do However, I would not require an for outside the I think there are too many in which cardiac troponin would be outside the standard pathway to of an that would be protocol a patient with or or in which serial at time may be It would be better to the appropriate and a care set to provide the to order cardiac troponin, such that it the for the Amy K. Saenger: I would limiting 1 cardiac troponin order set patient if there was a with overutilization of cardiac troponin order sets within my and/or cases where cardiac troponin order sets confusion and to patient care. this were not a then I would not or a of limiting orders or In my experience, for an potential in place that may result in patient care, although you could as argue order sets and and within the of the ordering is critically of the specific Stephen Smith: There is no need for cardiac troponin orders once MI is in or The only for an additional order set is a change in clinical such as a of chest pain. you of the implementation of 99th percentile upper reference for and with hs-cTn Allan S. Jaffe: For hs-cTn assays, 99th are Not only are there in reference but the majority of when there are large of patients suggest that 99th improve of risk in and in with heart failure with chronic ischemic heart and in the the use of of patients at The situation with acute ischemic heart disease is and I would argue that it is predominantly because the studies do not with It is that to have the of coronary disease as and have an increased of having a of their that are difficult to one has only a number of it would be very to this Therefore, it is likely that those studies that have a large number of patients with MI improved detection of MI in Scott Sharkey: I believe and values should be and possibly even specific to reflect the population by the A US could be and used for Peter Kavsak: This is an evolving area with much we implemented hs-cTn testing in through with emergency medicine, internal medicine, and cardiology, we to use the 99th percentile as the upper reference limit This was in a population and was also evaluated in a large clinical study with outcomes. Michael C. Kontos: This is reasonable if defined using appropriate of patients in the reference are likely to be as There would clearly need to be since there would no longer be a single value to Although many of our laboratory also use reference there are very in which a change in the result can care Having the appropriate are clearly to make it for the physician to the Amy K. Saenger: I a advocate for use of and reporting 99th for and assays. an analytical studies significant 99th For any other in the clinical laboratory where there is between reference such as there are no about reporting reference we For some cardiac troponin is argue that clinical is that 99th are those can be There and to a of use of 99th but not all have been the reference population used to the reference is defined and the study is and if a significant in the concentration between and it then we should and those which is to the 99th percentile due to or underlying is not an of Stephen Smith: It is clear that cardiac troponin values normal for are on those in and it has been that clinically significant are detected when the is for do you the role of a single cardiac troponin result at a very low concentration with a value of percentile as a for rapid of patients from the emergency Allan S. Jaffe: One must be about The that this will is particularly in low-risk A very low cardiac troponin at using an hs-cTn assay, would suggest that the patient most of the that lead to coronary heart This is because all of those result in increases in cardiac troponin, within the normal a very low value is the other the has to do with the possibility that some patients who present very early after the of AMI may not have increases at It has been that patients who within 2 h of often a that some patients with AMI can have very low values at This patient is in most of the large that at these very early rule I would advocate the use of this in the low-risk and in the intermediate-risk but would such use in high-risk patients and/or those who present early after the of symptoms. Peter Kavsak: We this of a very low and measurable cardiac troponin concentration with a high-sensitivity assay in that when we implemented the hs-cTn assay we began a sample in the low normal A low cardiac troponin concentration with other clinical and/or might be to a low cardiac troponin concentration for the rapid of emergency department Michael C. Kontos: used it could of for emergency department However, I would not be if the benefit has been There is the that a significant number of patients who have other for chest pain or possible myocardial that would require a the time to around the of a cardiac troponin will need to be In addition, the value would likely have to exceed with for emergency to I think that we have substantially increased our around how to the MI What has not been defined to my for which patients the of this is is that the vast majority of studies have been based around use of which to be to assays. Amy K. Saenger: This to in those hs-cTn assays with greater and patients for a single rapid rule out at of normal Therefore, it a to patients presenting with chest pain and an since the assay is to a majority of the assay only values in approximately of normal the assay but which allows rule out AMI with this assay. were to cardiac troponin assays with improved but not improved the time of patient clinical is with serial early after presentation having the ability to also improve clinical I do not these in the to a single low hs-cTn concentration to rule out AMI. I think there is a potential for of diagnostic use of low hs-cTn values with clinical risk A single biomarker result does not for clinical particularly given the high-risk if a result was due to sample which is to the assay. Stephen Smith: I think the use of hs-cTn at a very low concentration will be a for select especially those with chest pain of at least 2–3 h Presently, cardiac troponin concentrations is that the low values will be for clinical use. Peter Kavsak: studies on and hs-cTn concentrations in an emergency department population have made it clear that the the cardiac troponin the the risk for an adverse What is to a better patient care is the best to the of the increased cardiac troponin Stephen Smith: hs-cTn will be for risk there will be a that has 1 or hs-cTn values below a (e.g., 99th or some other low value in clinical that will depending on the baseline the of and the information available for the assay at there will be a that will be as for AMI by either a hs-cTn with a value below the 99th percentile and a clinically significant increased δ troponin, or by an hs-cTn above the 99th percentile or by 2 hs-cTn values with one or above the 99th percentile and a diagnostic and/or and the will be specific to the assay and there is data for assays to be used this The third will be nor These patients may be with still serial cardiac troponin and/or coronary or a or standard What is the clinical of hs-cTn in patients who are critically Allan S. Jaffe: This is an important These patients clearly are at increased risk because they have cardiovascular as as a It is not at all clear that can be the acute What is are studies that the of this with the idea of for A is the study with the best to an hs-cTn in patients with was and This would suggest that the cardiac that are in the cardiovascular are related to and that heart might be of It is these that could lead to Scott Sharkey: This is an that may be magnified with the use of The use of cardiac troponin in critically ill patients benefit with to and of underlying acute coronary Peter Kavsak: who are critically ill a of so using hs-cTn assays in this population may be cardiac troponin concentrations may result from of or other conditions that myocardial injury. The underlying for the in cardiac troponin concentration is especially important to determine in this Michael C. Kontos: This is one of the greatest of clinical a patient with a who has a cardiac my there are limited data on this of patients using hs-cTn assays. The use of hs-cTn assays is likely to the of values that exceed the 99th percentile. Given the severity of in these these may result in a large of patients being with studies are and should define the specific of and include and outcomes. Amy K. Saenger: This is a very area that will to There is clear that hs-cTn in provides prognostic information in critically ill There are related to measurement of cardiac troponin in critically ill patients and diagnosis of or This has on based on of or as as potential for patients who within 30 Stephen Smith: who are critically ill often have increased cardiac troponin values that they may have prognostic value. I do not that hs-cTn will have value for this critically ill patients may have 1 MI that is by the of an increased cardiac troponin, and frequently this is the only they are since the may not the I do not that hs-cTn will be substantially from contemporary cardiac troponin for this acute myocardial infarction cardiac troponin I cardiac troponin high-sensitivity cardiac troponin acute coronary syndrome electrocardiogram limit of detection upper reference limit of

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