Emergency room triage of patients with acute chest pain by means of rapid testing for cardiac troponin T or troponin I
CommentThis was a study of 773 patients evaluated in an emergency room for chest pain without ST-segment evaluation. Patients underwent troponin T and I determination; the troponin T results were immediately available and all patients with a positive test were admitted. Patients with negative troponin tests had a good prognosis -- the event rate (cardiac MI or death) within 30 days was 1.1% for patients with a negative troponin T test and 0.3% for patients with a negative troponin I test.
In addition to the limitations noted in Dr. Hlatky's editorial, there is another problem with the study that greatly limits its applicability, in my opinion. Of the 773 patients, 487 were admitted to the hospital, the vast majority with a diagnosis of unstable or stable angina. Overall, 123 patients had at least one positive troponin T test and 171 had a positive troponin I test. This means that at least 364 patients were admitted to the hospital with negative troponin T tests and at least 316 with negative troponin I tests.
Thus, a large number of patients with negative troponin tests were admitted to the hospital, mainly with the diagnoses of unstable and stable angina, and presumably received treatment for this. Their good prognosis could be in part related to in-hospital therapy (such as heparin), not only to their negative troponin tests.
Although we can conclude that patients who are appropriately treated (including hospitalization) have a good prognosis with negative troponins, we cannot conclude from this study that it is safe to discharge patients from the emergency room, even with normal EKG's and negative troponin tests, since so many patients in this study were, in fact, hospitalized. We do not know how they would have fared had they been discharged from the emergency room.
The objective of this study, according to the authors, was to demonstrate that "two negative test results on admission and four hours later (or at least six hours from the onset of chest pain) allow safe early discharge". This has not yet been persuasively accomplished, in my opinion.
December 20, 1997
ReferencesReferences related to this article from the NLM's PubMed database.
Reader CommentsDate: Sun, 21 Dec 1997
From: "Mark Leber" <firstname.lastname@example.org>
I feel that the paper contributes to improving accuracy in ruling out cardiac chest pain in the emergency room. If serial troponin I can predict greater than 99% of cardiac events within 30 days, then we could discharge patients more quickly from the emergency room, especially patients who are weak rule outs.
I agree that a prospective trial is needed to determine what combination of tests should be done (serial cpk mbs, serial troponins and serial ekgs) to best r/o cardiac events, since the troponin study was done in isolation of the other modalities ordinarily used. Also, it would be interesting to know how often troponins agreed with serial cpk mbs and ekgs.
The troponin tests are more sensitive than CPK-MB's, and more specific than the EKG. In multivariate analysis (table 4 in the article), troponins did add a significant amount of prognostic information to that derived from CPKs and from the EKG, separately and in combination. -- mj
January 11, 1998
I received the following letter from Dr. Christian Hamm, corresponding
author of this study.
Dear Dr. Jacobson,
Thank you for considering our paper on troponins for your internet journal club.
I appreciate your comments and agree that discharge of patients based on 2 biochemical tests requires further validation. However, you may have overlooked that troponins are much better parameters than CK, ECG or the clinical evaluation (see table 4). Please read our position which is clearly stated in the discussion: "bedside tests for troponin T and troponin I result in more accurate diagnoses than do previous more time-consuming methods and allow safer and more rapid decision making for most patients with acute chest pain."
I share your concerns with respect to a possible influence of hospital admissions of troponin negative patients on the prognosis. However, there is no evidence at all that any therapy today has influence on the inhospital outcome even of troponin positive patients. Moreover, if you refer to table 1 you may appreciate that most events occurred after discharge in troponin positive patients. Therefore, your point is well taken but plays very likely no major role. The answer could only be given, if you randomize patients with negative tests to hospitalization and discharge. In my view, this is, however, a very unrealistic study design. Again, I like to refer to our discussion which states: "The troponin test cannot replace the clinical evaluation of the patient with chest pain."
Thanks again for interesting comments.
With kind regards,
Christian W. Hamm, M.D. FACC
My main concern is that negative troponin tests should not be used to justify discharging patients from the ER who have a good history for unstable angina. We seem to agree on this point as well.
Date: Thu, 29 Jan 1998
I don`t understand why the patients with a myocardial infarction within 24 hours after hospitalisation were excluded from the final analysis of the results??
J.Steurer MD, Zürich
In the April 30, 1998 New England Journal of Medicine are several
to the editor about this study, two of which raise the same points
that were raised here.
Date: Wed, 10 Mar 1999
At first I was quite skeptical about the use of troponins in determining who can safely go home from the ER. However over the past several months I have routinely ordered troponin I in all of my chest pain patients and it is quite good in discriminating acute coronary syndromes from non cardiac causes. It is always elevated in my non q wave MI' s, frequently in my people with unstable angina with or without ecg changes (who subsequently have coronary disease on invasive studies) and never in those who subsequently do not have coronary disease.
I am aware that my experience is limited and anecdotal but when I combine a negative spect technetium sestamibi and a normal troponin in a patient with a normal or non diagnostic EKG I can comfortably send them home in 12-24 hrs with further followup. The insurance companies are rapidly putting pressure on us to "fast track" these patients who do not have acute ischemic syndromes and while I abhor this intrusion I dont think it will abate. However in patients where my clinical suspicion is not high, the EKG is not overtly ischemic and the troponins plus the spect technetium is non-ischemic I can usually get them home if not from the ER then in 6-12 hrs from our observation bed and feel comfortable albeit not arrogant that they will not have a life threatening event.
John D. Vance MD
This brings up a point that applies to many, if not most, studies: their frequent use for supporting an "agenda", in addition to their official purpose of furthering medical knowledge. The ability to improve our diagnostic efficiency with regard to cardiac ischemia will certainly be used (and misused) to cut costs in the ER. -- mj
Date: April 28, 1999
Dear Dr Jacobson,
As commentary on letter by Dr Vance. There is no logic in using a one off troponin test as back-up support to discharge a patient with non-diagnostic EKG if the troponin is done too early. My reading of recent literature suggests you must wait at least 6 hours from onset of pain.
I wonder if Dr Vance is drawing the troponin level at the beginning or at the end of his period of observation.
Additionally I am seeing a number of articles in the last 12 months
that seem to indicate troponin is not superior to CK-MB, especially CK-MB
sub forms. Although we have switched to troponin at my hospital I feel
the jury is still out.
Dr Paul Cunningham FACEM
Clearly, the troponin can't be used to send home a patient if drawn too soon after the onset of chest pain. It is easier to perform at the bedside and may be somewhat more sensitive than the CK, however, and thus could be used to justify admitting a patient whose story is otherwise not very convincing. -- mj
Date: June 6, 1999
From: John Vance [email@example.com]
In response to Dr. Cunninghams letter. First I perform a Troponin I at least 6 hours after the onset of chest pain. Secondly I never discharge a patient based solely on a normal troponin. They are usually in an observation unit undergoing clinical assesment, further ekgs, serum markers and usually a technetium sestamibi scan. They are then discharged usually in 12 hrs if the troponins AND the nuclear scan are BOTH normal. My comments were related to my impression that so far troponins have been an excellent predictor of cardiac events. However I am not using a normal level to justify discharging a patient from the ER. I do think that if a clinician combines a good history with the ekg, serum troponins, nuclear scans and clinical judgement he/she can safely discharge those patients with a negative workup. However if my "gut" says otherwise I will keep them in house longer regardless of the initial workup. Nonetheless for most of my chest pain patients with an "atypical" history and normal or near normal ekgs the above protocol has been very useful and so far successful.
January 24, 2000
I have recently come across this issue of using Troponin assays to screen patients at the ER. In our hospital, the Troponin T assay is available, however it takes some time before the results come out. This, along with CPKs and EKGs are all done at the ER. The parameters we use to decide whether to admit a patient for observation or not are only the ECG and the patient's clinical history. Convincing history seems to carry the greatest weight of all the available diagnostics. What I mean is, we will always admit a patient with a very clearcut history and profile even if the ECG, enzymes, and Troponins turn out to be negative at the ER. We may not even proceed to do the assays if the history was not convincing enough, and that's the time we send someone home from the ER. Moroever, we also have to consider cost as another factor that carries a lot of weight.
January 24, 2000
November 17, 2001
Date: June 14, 2001
Regarding the issue of "false positive" troponin-I results obtained from the Abbott AxSym...
There is a lot of discussion throughout the field of medical technology about the need to re-evaluate the "cut-off" point for a positive troponin I. It is pretty much common thought that the AxSym cut-off suggestion of 2.0 ng/ml is certainly calling positive some patients who are not. Although, expensive, the rapid bedside Cardiac Status test from Spectral labs seems to do a good job of matching result to patient condition. We're re-evaluating our AxSym cutoff point using the Spectral kit, along with chart and progress review.
Also, any comments that any pathologists or physicians out there might have regarding updated Troponin T testing (on the Roche Elecsys) vs Troponin I would be appreciated. Please feel free to privately email me, as well as posting to the board.
Date: August 2, 2001
Responding to Bree Ann Borof's comments from Jan. 2000, I have faced similar problems in at least three of my patients. One of them had elevated creatinine of 2.4 but the other two did not. In both of these two, CPK's were negative, history was atypical and repeat troponin was negative. So I do not know what the real significance of troponin is.
Date: August 4, 2001
A 20% false positive is high but what is the false positive in mammo?
Date: September 28, 2001
In response to the request for more info regarding falsely elevated Troponins I, have one case study that is baffling. It is a 28y female with elevated Troponin I, negative CK-MB, negative EKG, negative history other than recent history of atypical and reproducible chest pain. In addition, this patient had normal renal function. Errors in performance and technique were ruled out. I am currently searching for more information about falsely positive Troponins and would be interested in any insight you can offer.
Sincerely, P. Smith, RN
Date: November 6, 2001
We have changed our
specimen requirement to green top tubes (na heparin) to eliminate false positive
due to fibrin clots. In cases where the green top is not available an extra spin
is done before assaying for troponin.Our methodology is the Axsym. lg
December 27, 2001
Causes of raised Troponin T/I include
Severe Renal Dsease
The last two causes probably due to concomitant mild cardiac damage. Ref. JAMA, November 21, 2001-Vol 286, No 19
Olawale Ogunnuga MBChB
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