Thursday, November 14, 2019

A 50-something with left shoulder pain and diffuse ST elevation

A 50-something presented with left shoulder pain.

He had an ECG recorded:
What do you think?





















There is a huge amount of ST Elevation, but to my eye it was typical of normal variant.  One might say there is terminal QRS distortion, but, although there is indeed absence of S-waves in BOTH V2 and V3, there is in fact very clear notching at the end of the QRS in both V2 and V3.

Fortunately, there was an ECG from about a year prior:



And here is one from about 10 years prior:

You can see here that the computer says "suggests pericarditis" but that I changed it to early repolarization.

Just because there is diffuse ST elevation does NOT mean it is pericarditis.
The most common etiology of diffuse ST elevation is, by far, early repolarization.



The patient had musculoskeletal shoulder pain.




===================================
MY Comment by KEN GRAUER, MD (11/14/2019):
 ===================================
A subject well worth periodic review — is the concept of Terminal QRS Distortion (T-QRS-D). Prior to working with Dr. Stephen Smith — this concept was unknown to me. When present — T-QRS-D may provide invaluable assistance for distinguishing between early repolarization vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI). To review:
  • T-QRS-— is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3. Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.
A picture is worth 1,000 words. I’ve taken the lead V3 examples in Figure-1 from previous cases posted on Dr. Smith’s ECG Blog:
  • TOP in Figure-1 — Despite marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
  •  BOTTOM in Figure-1 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).
Figure-1: Comparison between ST elevation in lead V3 due to a repolarization variant (TOPfrom 4/27/2019) — vs acute OMI (BOTTOMfrom 9/20/2015), which manifests T-QRS-D (See text).



Regarding the current case — I have put together the first 2 ECGs that were shown above (Figure-2).
  • Isn’t it tempting to say there is T-QRS-D in the initial ECG that was done in the ED ( = ECG #1 in Figure-2)? After all, there is no S wave in lead V3 ...
Figure-2: The first 2 ECGs shown in this case (See text).



COMMENT on ECG #1: The patient in this case was a 50-something man, who presented with left shoulder pain. As per Dr. Smith — there is marked ST elevation in lead V3 — with a lesser amount of ST elevation in inferior and lateral chest leads.
  • The reason the ST-T wave appearance in lead V3 of ECG #1 does not qualify as T-QRS-D — is that despite lack of an S wave in this lead, there is J-point notching (or at least J-point slurring) that is characteristic of repolarization variants.
  • Other ECG features in ECG #1 in favor of a repolarization variant instead of acute OMI include: i) A relatively short QTc interval and tall R waves in the mid-chest leads; ii) Lack of reciprocal ST depression; iii) A similar “look” to the peaked T waves that we see in at least 9 of the 12 leads in ECG #1 (compared to a more localized ST-T wave picture that is typical with acute infarction); and, iv) J-point notching or slurring that is typical for repolarization variants in no less than 7 of the 12 leads in ECG #1 (BLUE arrows in Figure-1).
BOTTOM Line: While the composite of the above features makes it more likely that ECG #1 does not reflect acute OMI — there nevertheless is a significant amount of ST elevation in multiple leads in this 50-something man who presented with new symptoms.
  • Therefore — more information was needed to attain greater certainty (ie, stat Echo looking for wall motion abnormality; additional ECGs on this patient; serial troponins).
  •  In this case — finding a prior ECG on this patient from a year earlier was revealing (ECG #2 in Figure-2). Neither the lack of S wave in lead V3, nor J-point notching or slurring were new findings (RED arrows in ECG #2). This confirmed the impression that the ST-T wave appearance in ECG #1 reflected a longterm repolarization variant in this patient.

Our THANKS to Dr. Smith for presenting this case!
  • For additional examples illustrating distinction between T-QRS-D vs repolarization variants — Review of the October 6,2015 post may prove insightful.


Tuesday, November 12, 2019

What is this Regular SVT?

===================================
MY Comment by KEN GRAUER, MD (11/12/2019):
===================================
My appreciation to Kenneth Khoo for this case. This patient was hemodynamically stable. There was debate among providers in his institution as to what the rhythm in this ECG was (Figure-1).
  • What do YOU think the rhythm is?
  • What is the differential diagnosis?
  • Why can you be virtually certain what this rhythm is even before treating and before any diagnostic maneuvers?
Figure-1: The initial ECG in this case (See text).



MApproach to this Rhythm: I reviewed the basics for rhythm interpretation in the October 16, 2019 Case from Dr. Smith’s ECG Blog. In brief — once you’ve assured that your patient is hemodynamically stable (as this patient was) — We need to assess the remaining KEY parameters. I favor this memory aid, Watch your Ps, Qs and the 3 Rs”:
  • NOTE: It does not matter in what sequence you address these 5 KEY parameters — and I often change the sequence I use depending on the tracing (ie, Which of these 5 parameters is easiest to assess in the tracing in front of you?).
  • For the tracing in Figure-1 — the rhythm is perfectly Regular. The R-R interval is almost exactly 2 large boxes — which means that the ventricular Rate is 300/2 ~150/minute. The QRS complex is narrow — so this rhythm is supraventricular! Normal atrial activity is not seen — because there are no clear sinus P waves (ie, the P wave is not clearly upright in lead II …).


QUESTION: What does the above analysis suggest to YOU thus far?



ANSWER: We’ve established that this patient is hemodynamically stable. The rhythm in Figure-1 is a regular SVT (SupraVentricular Tachycardia) at ~150/minute without clear sign of sinus P waves. The principal differential diagnosis is similar to what we derived in the October 16, 2019 Case: i) Sinus TachycardiaiiReentry SVT (either AVNRT if the reentry circuit is contained within the normal AV nodal pathway — or AVRT if an accessory pathway is involved)iii) Atrial Tachycardiaor iv) Atrial Flutter.
  • PEARL #1: The major difference between this case and the case we presented on October 16 — is that the ventricular rate is very close to 150/minute. The most commonly overlooked sustained cardiac arrhythmia (by far) is AFlutter! Over the years — I’ve seen numerous cardiologists overlook this rhythm (especially those cardiologists who do not routinely use calipers for assessment of complex arrhythmias). I fully acknowledge that I’ve overlooked AFlutter. The BEST way never to overlook the ECG diagnosis of AFlutter is to: i) Think of this diagnosis often! — andii) To assume that any regular SVT rhythm in which clear sinus P waves are not seen is AFlutter until you prove otherwise — especially IF the ventricular rate of this regular SVT rhythm is close to 150/minute (ie, ~140-160/minute range).
  • PEARL #2: The reason the ventricular rate for AFlutter is so often close to 150/minute — is that: i) The atrial rate for untreated AFlutter is almost always close to ~300/minute (ie, 250-350/minute range) — andiiUntreated AFlutter most often conducts with a 2:1 ventricular response (ie, atrial rate ~300/minute — therefore ventricular rate ~300/2 = ~150/minute).
  • PEARL #3: The expected atrial rate for flutter is likely to change IF the patient has been treated — in which case the ventricular rate in AFlutter with 2:1 AV conduction may be slower (if the patient is on antiarrhythmic medication) — or possibly even faster (if he/she has been treated by ablation).


QUESTION: We said that normal sinus P waves were not seen for the rhythm in Figure-1 — because there is no clearly upright P wave in lead II.
  • Does this mean that there is no atrial activity in Figure-1?



ANSWER: There appear to be lots of “extra deflections” in a number of leads in ECG #1 ...
  • PEARL #4: The BEST way we know to quickly determine if the “extra deflections” that we seem to be seeing in ECG #1 represent atrial activity — is to use Calipers!

We show the result of using calipers in Figure-2.

Figure-2: RED arrows indicate that the “extra deflections” are indeed regularly occurring in multiple leads (See text).



Looking for Flutter Waves: The diagnosis of AFlutter can be established in a regular SVT at ~150/minute — IF you are able to identify regular atrial activity at ~300/minuteNothing else results in a regular atrial activity at this fast of a rate (Atrial tachycardia will rarely be faster than 250/minute ... ).
  • PEARL #5: The way I look for flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the regular SVT (since IF the rhythm is AFlutter — then the atrial rate should be twice the ventricular rate if there is 2:1 AV conduction). RED arrows in Figure-1 confirm that there is indeed 2:1 atrial activity in this tracing — which tells us even before application of a vagal maneuver or administration of Adenosine (or other AV blocker) that the rhythm is virtually certain to be AFlutter.
  • PEARL #6: My GO TO leads for identifying atrial activity are: i) Lead II — which is typically the BEST lead for identifying atrial activity. In AFlutter — leads III and aVF also usually provide ready evidence of 2:1 atrial activity; ii) Lead V1 — next to lead II, lead V1 is often the 2nd-best lead in my experience for identifying atrial activity. With AFlutter — one will often see positive deflections similar to those seen in Figure-1 in this V1 lead; iii) Lead aVR is often surprisingly helpful for identifying atrial activity (RED arrows in ECG #1); andiv) IF none of the above leads suggest atrial activity — then I’ll survey the remaining 7 leads as I look for atrial activity. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.
  • PEARL #7: On occasion — atrial activity may not be readily apparent in a hemodynamically stable patient with a tachyarrhythmia. In such cases — use of an alternative lead system, such as a Lewis Lead may enhance atrial activity and facilitate rhythm determination. Figure-3 reviews how to use a Lewis Lead. The March 20, 2018 post on Dr. Smith’s ECG Blog illustrates application of a Lewis Lead in a patient in a regular SVT rhythm.

Figure-3: Use of a Lewis Lead (See text).



Our THANKS to Kenneth Khoo (from Malaysia) for sharing this case with us!



Sunday, November 10, 2019

High-Sensitivity Troponin is not a Myth, and “Myth-busting” is often another Myth to be Busted

This is published simultaneously in Emcrit

Emergency Medicine News has now published 2 “Myth-Busting” articles by Rory Spiegel which dispute the value of high-sensitivity troponin.  We call them “Fake News,” (as they cherry-pick and misrepresent several studies) and EM News would not allow rebuttal. 

The bottom line: the value of high-sensitivity troponin is NOT a myth; it helps to rule out and rule in acute MI earlier (but it is complex, and there is a lot to know).

Stephen W. Smith*
Alexander Limkakeng**
Frank Peacock***
 
Disclosures:
*Dr. Smith has researched the Abbottt Architect high-sensitivity assay with the Hennepin Healthcare Research Institute’s Biomarkers Research Lab, which has received funding from Abbottt.  He has no personal disclosures.
**Dr. Limkakeng:
Has done research into high-sensitivity troponin funded by Roche, Abbott, and Siemens.
***Dr. Peacock’s disclosures:
--Research Grants: Abbott, Boehringer Ingelheim, Braincheck, CSL Behring, Daiichi-Sankyo, Immunarray, Janssen, Ortho Clinical Diagnostics, Portola, Relypsa, Roche, Salix, Siemens. --Consultant: Abbott, Astra-Zeneca, Bayer, Beckman, Boehrhinger-Ingelheim, Ischemia Care, Dx, Immunarray, Instrument Labs, Janssen, Nabriva, Ortho Clinical Diagnostics, Relypsa, Roche, Quidel, Salix, Siemens.
--Expert Testimony: Johnson and Johnson.
--Stock/Ownership Interests: AseptiScope Inc, Brainbox Inc, Comprehensive Research Associates LLC, Emergencies in Medicine LLC, Ischemia DX LLC.

This piece is in response to an article in Emergency Medicine News, in the series "Myths in Emergency Medicine":

Myths in Emergency Medicine: Hoopla Aside, hs-cTnI is Not Catching Missed MIs.
Spiegel, Rory, MD

Dr. Spiegel was responding to this very complicated article in Lancet:

We wrote our rebuttal, and then Dr. Spiegel doubled down this month by publishing another “Myths in EM” piece in EM News: “Is hs-cTnT Worth the Downstream Testing?.

Rebuttal to the First Article

Stephen Smith, of Dr. Smith’s ECG blog, wrote this rebuttal: Smith SW.  Letter to the Editor: hs-cTnI’s True Intent.  Emergency Medicine News; 41(5):28-49; May 2019.  https://journals.lww.com/em-news/Fulltext/2019/05000/Letter_to_the_Editor__hs_cTnI_s_True_Intent.39.aspx

Alex Limkakeng and Frank Peacock also responded:

Here is the Smith response:

Note that units in contemporary assays are reported in ng/mL, and in high-sensitivity (hs) assays as ng/L (cTnI of 0.030 ng/mL is comparable to hs cTnI of 30 ng/L)

To The Editor:
I believe Rory Spiegel, MD, misinterpreted the study in his article, “Hoopla Aside, hs-cTnI is Not Catching Missed MIs.” (EMN 2019;41[2]:1; http://bit.ly/2Bv4FUd.) The high-sensitivity troponin (in this case, Abbott Architect hs troponin I) reclassified 1771 patients as acute MI (about 600 type 1) not identified by the (Abbott) contemporary assay (cTnI), and their ultimate outcome was not different from those not reclassified. (Lancet 2018;392[10151]:919; http://bit.ly/2Erob73.)

This makes it seem that the hs assay has no value, that it simply leads to more investigations without improving outcomes. The reason for this is not increased test sensitivity but the threshold used for the test's upper reference limit (URL). It also ignores the intended value of the test: earlier MI rule in or out.

The definitions of normal vs. increased for both assays are based on the 99th percentile of a normal population, which may result in varying cutpoints for normal. The upper reference limit must also be accompanied by a low coefficient of variation (CV), which statistically measures the reproducibility of the test and should not exceed 10% at the 99th percentile. Different labs have different CVs and URLs; the laboratories used in the study had a 10% CV at a relatively high URL of 40 and 50 ng/L, higher than it would be in many labs. The URL for the same (Abbott Architect) contemporary cTnI assay in the Hennepin County lab is 0.030 ng/mL, and the CV is less than 10% at this value. The higher URL would result in the cTnI assay being less sensitive in the study than it would otherwise. The hs assay uses different thresholds for women (16 ng/L) and men (34 ng/L). This is likely why women were reclassified in the study more often.

These factors may account for the differences in reclassification. Data from the UTROPIA study, in which the URL for cTnI was 0.030 ng/mL (hs-cTnI used 16 ng/L for women, 34 for men), showed fewer positive assays with the hs-cTnI than with the cTnI; that is, it resulted in fewer false-positives. (Am J Med 2017;130[12]:1431.)

It is also important to remember that “high-sensitivity” means analytical, not clinical, sensitivity. All positives and negatives are determined arbitrarily by the 99th percentile of a “normal population” without ACS symptoms; thus, as long as the 2 “normal” populations on which the 2 assays’ normal values were defined are comparable, the two assays cannot be different in the proportion of MIs identified except for the different thresholds used and the number of hours of serial troponins measured.

I like to call high-sensitivity assays “high-precision” assays because they can accurately quantify low levels of troponin, far below the 99th percentile cutpoint. This means that troponin changes at low levels can be detected in order to rule in or rule out MI earlier by using low thresholds or delta values. Small changes at low values are true changes, not just analytical noise. A single extremely low value, which can now be quantified, can all but rule out MI in patients with at least two hours of chest pain. (JAMA 2017;318[19]:1913; http://bit.ly/2MVSsMT.)

The Lancet study used values at six to 12 hours after symptom onset to diagnose myocardial injury. The contemporary (not high-sensitivity, hs) assay (cTnI) is excellent and just as sensitive as hs assays at six to 12 hours after symptom onset. The use of these late measurements negated the value of the hs assay, which is that it helps in early diagnosis of MI and early rule out. It is true that the hs assays will not catch missed MIs, but that was never the intent.

Stephen W. Smith, MD. Minneapolis, MN

Here is the response of Drs. Limkakeng and Peacock:

To the Editor:
The headline and publication reviewed in the EMN article, “Hoopla Aside, hs-cTnI is Not Catching Missed MIs” are misleading. (2019;41[2]:1; http://bit.ly/2Bv4FUd.) Rory Spiegel, MD, wrote, “Despite our hopes, it would appear that the introduction of hs-cTnI added very little to the workup of patients presenting with symptoms concerning for ACS.” On the contrary, a wide body of published research demonstrates that hs troponin can positively affect ED evaluation of ACS if properly implemented.
Our European and Asian colleagues have shown us for years that the value of a high-sensitivity troponin assay is not to identify more MIs but to identify patients who can be safely discharged home faster. Indeed, the literature is rife with examples of how this can be done. (Circulation 2017;135[16]:e923; http://bit.ly/2tzs02Q; Eur Heart J 2016;37[44]:3324; http://bit.ly/2NjMFAO.)
Our early experience at Duke University Hospital has confirmed this experience (manuscript in preparation). Thoughtful high-sensitivity troponin implementation strategies that incorporate structured risk stratification and disposition pathways significantly reduce length of ED stays, admission and stress testing rates, and costs without a concomitant increase in hard cardiovascular outcomes such as MI and death in those discharged. Note that these outcomes cannot be achieved simply by changing your troponin assay. They require an evidence-based, multidisciplinary change in the practice of ACS evaluation.
We agree that it is unfortunate that these assays have been termed high-sensitivity because their real value is high precision and reproducibility. This allows for accurate serial measurements in a short time. They also allow more precise identification of extremely low (undetectable) levels that can allow safe discharge after one lab draw in select patients who present several hours after symptom onset.
Alexander T. Limkakeng Jr., MD
Durham, NC
W. Frank Peacock, MD
Houston

Dr. Spiegel responded to all of us:
Thanks to Drs. Smith and Limkakeng and Peacock for their insightful comments. Both are well versed in their understanding of the literature surrounding the use of high-sensitivity troponins, and both argue that the results of Shah, et al., discussed in my EMN article are discordant from the remaining literature which demonstrates that high-sensitivity troponin assays can be used to safely discharge patients home from the ED without increasing the number of patients identified as positive for an acute myocardial infarction. They go on to cite a number of studies to support these claims.
While a number of studies have demonstrated that the introduction of a high-sensitivity assay allowed clinicians to send more patients home from the ED without increasing the number of patients diagnosed with AMI, an equal number have demonstrated the opposite. (Acad Emerg Med 2017;24[3]:388; http://bit.ly/2Nuefvl; Heart 2014;100[20]:1591; Emerg Med J 2012;29[10]:805; Acad Emerg Med 2014;21[7]:727; http://bit.ly/2IzUcg5.) Multiple studies have found that the use of high-sensitivity troponin is at best no better than the standard assay or at worst increases downstream testing.
In fact, all the studies that support the use of a high-sensitivity troponin are observational in nature. Their results are promising, but they are highly vulnerable to bias because of their observational design. The only other RCT I am aware of comparing the use of standard to high-sensitivity troponin assay found the high-sensitivity assay offered no clinical value over and above the standard assay. (Circ Cardiovasc Qual Outcomes 2016;9[5]:542; http://bit.ly/2U7kHuR.) The results presented by Shah, et al., are even more concerning. They suggest not only that the assay is not beneficial, but also that it may lead to more downstream care with no recognizable benefit.
Both Drs. Smith and Limkakeng offer logical reasons why the Shah results do not represent the true value of a high-sensitivity assay, and they may be correct. Shah's results may be due to how the assay was deployed rather than the assay itself. But it is just as likely that the results are a representation of what will occur when high-sensitivity assays are introduced into the clinical arena. These results should not be written off because they are discordant from a sampling of observational data supporting the use of high-sensitivity assays. Rather, it is our responsibility to empirically demonstrate the clinical value of the high-sensitivity assay before welcoming its widespread use in EDs across the country.

Drs. Smith, Limkakeng, and Peacock responded with the following, but EM News would not print it. 
So here it is:

Real Myth-Busting for high-sensitivity Troponin

Recently, in Emergency Medicine News, Rory Spiegel wrote in his "Myth Busting" column about the HighSTEACS study (1) and claimed that “the introduction of hs-cTnI added very little to the workup of patients presenting with symptoms concerning for ACS”.

This position could not be more wrong.

We countered his piece with reference to the mountains of data which contradict the idea that hs troponin adds little. He responded by stating "While a number of studies have demonstrated that the introduction of a high-sensitivity assay allowed clinicians to send more patients home from the ED without increasing the number of patients diagnosed with AMI, an equal number have demonstrated the opposite." 

In fact, the 4 articles he references do not show the opposite at all, and the 5th study, and RCT, was also mischaracterized. These are addressed point-by-point below.

His response ignores a decade of research detailing how high-sensitivity assays can beneficially impact ED patients. There are many systematic reviews, meta-analyses, and prospective randomized trials from dozens of countries and tens of thousands of patients on use of high-sensitivity troponin for safe rapid ED discharge (just for example, Zhelev Z,et al. BMJ. 2015 Jan 20;350:h15. Than MP, et al. Circ 2018; 137 (4): 354-63, Twerenbold R, et al. Eur Heart J. 2016 Nov 21;37(44):3324-3332) The literature is replete with data showing how proper implementation of high-sensitivity troponin can avoid increased workups and downstream testing, while at the same time decreasing ED length of stay and costs.

The HighSTEACS article referenced had several flaws. Most importantly, the advantage of hs troponin is its precision, which allows it to quantify very low levels of troponin, and accurately measure very small changes.  Thus, it is used for early rule-in or rule out of MI.  Measurements at 6-12 hours, as done in the HighSTEACS trial, would not be expected to result in improvements over the contemporary assay; at this time period, contrary to conventional thinking, hs troponins are neither more sensitive nor less specific.  Moreover, the finding of an increase in workups without improvement in outcomes was due to a “positive” cutoff, defined as the assay’s 99th percentile.  The 99th percentile may be used to rule out MI, but not rule it in. This common error has been recognized for years.  See the “10 Commandments of Troponins” (Jaffe, AS. Heart 2011 97: 940-946 doi: 10.1136/hrt.2009.185751). This should be considered a well-established standard for improving the clinical utility of biomarker.

It is important to remember that the most important use of hs troponin is the early rule out and rule-in of MI (early rule-in by very high levels or large deltas).  Protocols for both rule out and rule-in always have an intermediate range of values for which it is necessary to use delta troponin and other clinical data in order to make the diagnosis.

In fact, there are hundreds of articles that show the utility of hs troponins, and below we describe the 4 articles which he purports show the "opposite."
  1. (Acad Emerg Med 2017;24[3]:388; http://bit.ly/2Nuefvl; This paper actually shows that a single hs troponin (measured at time of arrival in the ED) which is below the level of detection, especially with a normal EKG, has a 99.1% sensitivity for acute MI.  It supports our argument fully; it does not show the "opposite."

Notice how all the other studies (the 3 below) cited by Dr. Spiegel are from 5 or more years prior (even 2012!), most of them gathering data from before 2010 (2007, 2008) when hs assays were not very sensitive or precise.

  1. Heart 2014;100[20]:1591; https://heart.bmj.com/content/100/20/1591   (data from 2008-2010). 
This study is downright dangerous.  The cutoff used for the contemporary assay (0.200 ng/mL) was far higher than the 99th %-ile (0.070 ng/mL).  Many patients should have been diagnosed with MI (by the contemporary assay) who were not.  In other words, the researchers used the diagnostic cutoff for the high-sensitivity assay, but a much higher cutoff (thus not sensitive) cutoff for the contemporary assay.  This would obviously lead to more "positives" for the high-sensitivity assay.  The authors set the cutoff for the contemporary assay such that many patients who actually were having an acute MI (by definition) were not diagnosed with MI.  Their conclusion might be that, because the 6 month MACE is the same in both groups, one need not diagnose every myocardial infarction.  

But with a study this small and with only a 6 month followup, and results which contradict all other studies on acute MI, it no doubt underestimates the adverse events.  All other data would show that missed MI, even with troponin values at less than 5x the upper reference limit, does lead to adverse events.  See JAMA reference below by Mills Nicholas L et al.,*** in which 39% of patients with MI whose troponin levels were between 0.05 and 0.19 ng/mL had death or MI within one year, vs. 7% of those with troponin less than 0.05 ng/mL.  Indeed, elevated troponin in the lower range from any cause is associated with worse outcomes.  Thus, this study should be ignored.  Furthermore, the high-sensitivity assay is a previous generation hs-cTnT which is not as precise as the one produced today, and so has more false positives.

  1. Emerg Med J 2012;29[10]:805; Could not get full text.  This very old study does not compare the "hs" troponin with any other strategy.  In fact, it showed fairly good sensitivity at 2 hours.  This article does not show the "opposite."

  1. Acad Emerg Med 2014;21[7]:727; http://bit.ly/2IzUcg5.)   This study had a total of 24 myocardial infarctions.  No more need be said.

***Mills study, referenced above, showing that minimally elevated contemporary troponins are associated with much worse outcomes in MI:
Mills, Nicholas L., Antonia M. D. Churchhouse, Kuan Ken Lee, Atul Anand, David Gamble, Anoop S. V. Shah, Elspeth Paterson, et al. 2011. “Implementation of a Sensitive Troponin I Assay and Risk of Recurrent Myocardial Infarction and Death in Patients with Suspected Acute Coronary Syndrome.” JAMA: The Journal of the American Medical Association 305 (12): 1210–16. https://doi.org/10.1001/jama.2011.338.


Spiegel: “The only other RCT I am aware of comparing the use of standard to high-sensitivity troponin assay found the high-sensitivity assay offered no clinical value over and above the standard assay. (Circ Cardiovasc Qual Outcomes 2016;9[5]:542; http://bit.ly/2U7kHuR.) “

  1. Circ Cardiovasc Qual Outcomes 2016;9[5]:542; used 99%ile dichotomously “normal: less than or equal to 14 ng/L and greater than 14 ng/L: myocardial injury]”
However, again, among patients classified as low or no risk by Heart Foundation Criteria, a higher rate of discharge from the ED was observed in the hs-report group (hs-report: 168 of 253 patients (66.4%) versus std-report: 148 of 263 patients (56.3%); P=0.010),

“There was no difference in angiography (hs-report: 11.9% versus std-report: 10.9%; P=0.479). . . .  However, among those with troponin levels less than 30 ng/L, a modest reduction in the primary end point was observed (hs-report: 2.6% versus std-report: 4.4%, [hazard ratio, 0.58; 95% confidence interval, 0.34–0.1.00; P=0.050).
High-sensitivity troponin reporting alone is associated with only modest changes in practice. Clinical effectiveness in the adoption of high-sensitivity troponin may require close coupling with protocols that guide interpretation and care.”

In other words, there was clinical value: 10% increase in discharges and 2% decrease in 1 year death or recurrent ACS in the subset expected to be stratified best by the hs trop, both statistically significant.

Finally, there is now a very large prospective trial that was presented at the European Society of Cardiology in August 2019.  It is the HiSTORIC trial and is by the very same HIGH-STEACS group who published the Lancet study that generated all this controversy.

_______________
Mills NL et al. high-sensitivity cardiac Troponin at presentation tO Rule out myocardial InfarCtion (HiSTORIC): a stepped-wedge cluster randomized controlled trial.

New Protocol:
Abbott Architect hs-cTnI
Exclude patients with STEMI and clearly ischemic ECG
--If presentation value less than 5 ng/L and time to presentation greater than 2 hours, then low risk.
--If less than 2 hours, or hs-cTnI greater than or equal to 5 ng/L, then obtain 3 hour troponin. If delta greater than or equal to 3, then admit for peak test.
--If presentation value greater than 99th percentile gender specific value, admit for peak test.

Compared to standard Evaluation:

--Hs Troponin less than 99th percentile at presentation if greater than 6 hours of symptoms, or
--Serial testing 6-12 hours from symptoms onset
(This protocol is no different from using contemporary troponin because at this late time period, as cTnI and hs-cTnI are not significantly different).

Outcomes:
--30-day death or MI
--Proportion discharged from ED
--Secondary safety endpoint: 1 year MI, cardiac death, unplanned revascularization, re-attendance

31,492 patients overall: standard pathway - 14,700; Early rule out 16,792

Results:
Reduced length of stay by 3.3 hours (10.1 vs. 6.8 hours)
Increased discharge from ED by 57%
One year MI and cardiac death higher in the standard group.

Conclusion: Early rule out protocol is effective and safe.

We refer interested readers to the following excellent reviews of high-sensitivity troponin implementation:
Twerenbold, R. et al. JACC 70 (8): 996–1012.https://doi.org/10.1016/j.jacc.2017.07.718.
Yader S. et al. 2016.  Am J Med 129 (4): 354–65. https://doi.org/10.1016/j.amjmed.2015.12.005.

Response to the 2nd “Myth-busting” article
Interestingly, on Nov 5, Dr. Spiegel published another “Myths in EM” piece in EM News: “Is hs-cTnT Worth the Downstream Testing?.  The piece assesses a new randomized trial of the Roche hs -cTnT (not the Abbott Troponin I, which is what was studied in the above Lancet study).  [Here is the full text of this randomized trial: A Randomized Trial of a 1-Hour Troponin T Protocol in Suspected Acute Coronary Syndromes.]   

Spiegel’s piece starts by conceding that “hs assays....will soon replace the 4th generation assays currently being used.” 

This hs-cTnT study randomized potential ACS workups to a 0/1 hour hs-cTnT protocol vs. standard care.  In the standard care arm, 0/3 hour troponins were used and the providers were blinded to any value less than 29 ng/L (the rationale for hs-cTn is to be able to precisely measure such small quantities, so this study was testing the value of knowing, vs. not knowing, the precise value of all such low troponin measurements).  The study showed that more patients are discharged (45.1% vs. 32.3%), and discharged earlier (4.6 vs. 5.6 hrs), with hs-cTnT 0/1 hour protocol. 

Somehow, Dr. Spiegel, in his zeal to bust “myths,” manages to dismiss these findings!!

As expected with hs-cTn, the overall number diagnosed with MI was not different because that is not the function of hs-cTn — it is to diagnose or rule out acute MI earlier.  Moreover, the protocol ruled out MI in 72.1% with an NPV of 99.6%; in other words, 27% of patients were not discharged even though the protocol would safely allow for it. No doubt the rate of early discharge would have been higher if providers had felt comfortable enough with the new protocol to consistently follow it, a common problem when introducing a new pathway.

By 30 days, among all 3288 patients, the hs-cTnT group (n=1646), compared to the standard group (n=1642), had less functional testing (11.0% vs. 7.5%), but the same number of angiograms, CT coronary angiograms, coronary interventions and revascularizations.  However, among the 1493 with an initial cTnT less than 29 ng/L, there were slightly more revascularizations in the group using hs-cTnT [38/1515 (2.2%) vs.15/1493 (0.9%)], partly because there were more index acute MI diagnosed (1.1% vs. 0.5%). 

The number of acute MI, unstable angina, and revascularizations following the index hospitalization were the same in both groups.  Thus, it would seem that the use of hs-cTnT diagnosed a few more patients at the index visit, without leading to any decrease in adverse 30-day outcomes after the visit.  The rate of “non-MI myocardial injury” diagnosis was also slightly higher in the hs-cTnT group (1.6% vs. 1.0%); given than acute myocardial injury is associated with high mortality, detecting it is not necessarily a bad thing. 

From the article: “The major downside of noninvasive testing are the downstream invasive testing and interventions it leads to, both of which were higher in the rapid diagnostic strategy group.” But the difference is only 1.3%, or only 23 more over 3.5 years!!

Dr. Spiegel criticizes this tiny bit of higher rate of revascularization: “What have we really accomplished if hs-cTnT leads to a decrease in noninvasive testing but increases the number of diagnostic catheterization and revascularization procedures?” 

It seems obvious to us that what we have accomplished is the diagnosis and treatment of a few more acute MI, and possibly also the diagnosis of unstable angina that would need revascularization.  Apparently, the interventionalists caring for these patients thought that their patients’ angiographic coronary disease would benefit from revascularization, probably because they opined that it was indicative of ACS.   It is also possible that some patients of the patients had stable coronary lesions, which often do not need revascularization. 

But Dr. Spiegel seems to be implying that the revascularization undertaken according to the judgment of those patients’ interventionalists was unnecessary; why would he imply that?
Similar to his criticism of the earlier article, this criticism also depends on the notion that one need not treat all acute MI nor all unstable angina, nor even diagnose them. 

 It is very likely that these patients had their lives saved by this procedure.

Spiegel’s criticism apparently assumes that because there was an absence of difference in death or acute MI at 30-days, that those interventions were unnecessary.  But studies of invasive vs. conservative management of ACS, most of which show benefit, show that benefit at 1 year, not at 30 days[1] .  A 30-day outcome is used for this trial to show that it is safe to discharge the patient if he/she can get follow up within 30 days.  If coronary disease is discovered and treated in the interim, that is not an adverse outcome.

The fact that there were more revascularizations is a benefit of hs-cTn, not a complication.  It implies that hs-cTnT helped to find signficant coronary disease.  If interventionalists saw ruptured plaque on angiogram, and this was the reason for the revascularization, then it is clear that the hs-cTnT was beneficial.  They may well have found other coronary disease that was NOT revascularized, as it was 1) not thought to be ACS or the etiology of the symptoms, or 2) was thought to be ACS but not thought to require revascularization.  Certainly not all presumed ACS with coronary disease requires revascularization (see the ICTUS trial).  But whether there is coronary intervention or not, there are other interventions for coronary disease that are very effective, mostly statins.  In fact, we know from a large CT coronary angiogram study that diagnosing non-ACS coronary disease does benefit the patient because more preventive therapies are adhered to. 

In other words, one need not do a coronary intervention in order for it to be worthwhile to make the diagnosis of acute MI or of coronary disease.

In summary, more information is better if the provider knows what to do with it.  As we all get more experience with hs-cTn, and there are more clinical trials and observational studies to guide us, the more precise information provided by high-sensitivity troponin will be beneficial to patients and to patient flow.



Myth Busting

Myth-busting is popular and fun, but it is rarely good science. It's fine and good to approach any field of knowledge or any dogma with skepticism. And it is great to really overturn untrue dogma.  But to turn skepticism into myth-busting, it is essential to comprehensively review the existing literature. If you set out intent to bust a myth, then you can easily find one or two counterexamples to a prevailing heuristic and write a "Gotcha!" piece on the topic. However, if those who advertise themselves as myth busters are not primary researchers in the area they are myth-busting, there is a risk that they will not fully understand the topic and write a misleading review based on cherry-picked studies that amounts to fake news. Many venues will be eager to publish these pieces since it will attract attention both by those interested in learning something new and by those seeking to correct the inaccurate portrayal of the literature. However, our medical publications should seek to disseminate reliable information and better vet pieces that proclaim propositions that run counter to the vast majority of existing evidence.
Good myth busting in EM:
Here are very nice examples of well substantiated myth-busting by Salim Rezaie at Rebel EM: https://rebelem.com/tag/mythbuster/.


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This is evolving literature, but there is also some who believe that stenting even stable lesions can improve patient-oriented outcome of improved symptoms and function. (I think the ORBITA study? still a little controversial).


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