Tuesday, February 12, 2019

ST Depression and T-wave inversion in V2 and V3.

A middle aged male dialysis patient was found disorganized and paranoid.  He had no chest pain or dyspnea.

An ECG was recorded.  The clinician was worried about his ECG and showed it to me:
What do you think?

When I saw this ECG, I immediately recognized right ventricular hypertrophy as the cause of the ST depression and T-wave inversion in leads V2 and V3.   In other words, I was certain that this was a chronic finding on the ECG.  The worried clinician stated there are no old ECGs to compare with, and no records.  I remained certain that this was RVH as the findings are classic: Large R-wave in V1, large S-wave in lead I, and typical right precordial ST-T that mimic posterior STEMI.

If the QRS were normal, and the patient had chest pain, I would have said this was posterior MI, or possibly hypokalemia (see this post: Are These Wellens' Waves??).

Later, however, we found written records from an outside hospital:

EKG read:
Normal sinus rhythm
Right ventricular hypertrophy with repolarization abnormality
Nonspecific T wave abnormality
Prolonged QT
Abnormal ECG
No significant change since 05-17-18

Previous echo
Final Impressions:
1. Normal LV size, moderately increased wall thickness, normal global systolic function with an estimated EF of 60 - 65%.
2. Right ventricular cavity size is severely enlarged, global systolic RV function is severely reduced.
3. Severely enlarged right atrium.
4. Mildly enlarged left atrium.
5. Severe tricuspid regurgitation.
6. Severely increased estimated pulmonary pressures by tricuspid regurgitation velocity and right atrial pressure (96 mmHg plus RAP).
7. The inferior vena cava is dilated, respiratory size variation less than 50%, consistent with elevated right atrial pressure.

Learning Point:

Whenever there is abnormal repolarization (abnormal ST-T), look for abnormal depolarization (abnormal QRS).  This might include RVH, LVH, LBBB, RBBB, IVCD, WPW, paced rhythm and more.  If present, assess whether the ST-T abnormalities fit with the abnormal QRS.

2. Learn this pattern, as it is classic for RVH.  Here are some more cases of RVH, and/or large R-wave in V1, with ST-T abnormalities:

Young Woman with history of repaired Tetralogy of Fallot presents with chest pain

ST Depression and T-wave Inversions after ROSC from Resp and Cardiac Arrest after Head Trauma

A 50-something male with Dyspnea

Comment by KEN GRAUER, MD (2/12/2019):
Excellent case presented by Dr. Smith from the perspective of ECG teaching. For clarity — I’ve labeled the ECG in Figure-1.
Figure-1: ECG in this case — obtained from a middle-aged dialysis patient. No chest pain or dyspnea. (See text regarding labeling).
The interesting teaching points that impressed me about this case include the following:
  • How the History is of such critical importance! As per Dr. Smith — the fact that this middle-aged man had neither chest pain nor dyspnea dramatically reduced the likelihood of an acute cardiac or pulmonary event even before looking at the ECG. I would have interpreted this tracing very differently had the patient presented to an ED with severe new-onset chest pain or new dyspnea.
  • It is helpful that records from an outside hospital contained written interpretation of a prior ECG on this patient. This suggested that at least some of the findings present in ECG #1 (in Figure-1) were present previously. CAUTION: While clearly much better than nothing — in my experience, written report of ECG findings (even from a cardiologist) is NO substitute for finding an actual prior ECG in the old chart. Too-numerous-times-to-count I have found important ECG findings either undercalled or overcalled in a prior written report. The tracing in this case (in Figure-1) is complex. In my opinion, the only way to know if all findings are old is by lead-to-lead comparison with a prior ECG.
  • Availability of a previous Echo report can be an invaluable teaching tool — as well as proving to be tremendously helpful clinically in this case. Access to the previous Echo report in this case makes up for not having an actual copy of the prior ECG — because the previous Echo confirms high likelihood that ECG findings in this case are probably not new.
  • Regarding use as a teaching tool — the previous Echo showed severe RAE, severe RVH and markedly increased right-sided pressures — as well as mild LAE and moderate LV wall thickening. How well does the ECG in Figure-1 predict each of these findings? (See below).
The ECG in Figure-1 shows sinus rhythm at ~85/minute. Additional ECG findings (as well as non-findings) that I see include the following:
  • No sign of either LAE or RAE. Although the sinus P wave in lead II is a good size (RED arrow) — it is neither notched (as is common with LAE), nor tall enough or pointed enough in any of the inferior leads to qualify for RAE. The negative component to the P wave in lead V1 is neither deep enough nor wide enough to qualify for LAE. The positive component to the P wave in leads V1 and V2 is neither tall nor peaked, as may be seen with RAE.
  • No sign of LVH. The Echo showed moderately increased LV wall thickness. While sensitivity of the ECG is limited for picking up this type of LVH — I always find it insightful to correlate ECG findings with the far more accurate anatomic assessment possible in Echo evaluation.
  • Incomplete RBBB is presentI measure QRS width at between 0.09-0.10 second — which is within the normal range. A multiphasic (rsR’s’) complex is present in lead V1 (within the BLUE oval in V1) — in association with narrow terminal S waves in both leads I and V6 (within BLUE ovals in these leads). This qualifies as incomplete RBBB. It is common with either complete or incomplete RBBB to also see an rsR’ complex in right-sided lead III (as we do here). It is not common to see a 4-phase QRS complex (rsR’s’) in lead V1 due to simple complete or incomplete RBBB. That said, I still feel description of QRS morphology here best qualifies as incomplete RBBB. NOTE: Some anterior ST-T wave depression may be seen with incomplete RBBB. However, the amount of anterior ST-T wave depression seen here is clearly more than one should expect from simple incomplete RBBB.
  • ECG findings in favor of RVH in Figure-1 include — the relatively tall R’ wave in lead V1 — presence of numerous S waves on this tracing (ie, in leads I, II, aVL; and V2-through-V6) — the presence of incomplete RBBB — and, ST-T wave depression in leads V1-V3 consistent with RV “strain”. Clearly, the QRS complex is not wide enough to qualify as complete RBBB. Most of the time with incomplete RBBB — the R’ deflection in lead V1 is not nearly as tall as it is in Figure-1, unless there is also “something else” (ie, RVH).
  • ECG findings atypical for the dramatic degree of RAARVH and increased right-sided pressures indicated by Echo include: iLack of ECG findings suggestive of RAA; andiiLack of any hint of RV “strain” in the inferior leads. The 2 lead areas to look at when assessing for RV “strain”, are the inferior leads (II,III,aVF— and the anterior leads (V1,V2,V3). While true that RV “strain” will not always be seen in both of these lead areas — the fact that there is no sign at all of inferior ST-T wave depression (within the PURPLE rectanglesand, the somewhat less usual pattern of ST-T wave depression in the anterior leads (within RED rectangles, showing maximal ST-T wave depression in lead V2, despite only modest R wave amplitude in this lead) — to me suggested that the anterior ST-T wave depression might reflect acute cardiac or pulmonary disease. I’ll emphasize that the negative history for chest pain and dyspnea + dramatic abnormalities on the previous Echo strongly support supposition that the ECG findings in Figure-1 are not acute. My point is simply that I would not be at all certain of the chronicity of these findings had I just seen this ECG without benefit of the history and prior Echo report.
Our THANKS to Dr. Smith for presenting this highly insightful case.

  • For “My Take” on the ECG diagnosis of RVH  CLICK HERE.
  • For “My Take” on the ECG diagnosis of LAE & RAE  CLICK HERE.

Saturday, February 9, 2019

Right sided heart failure and tachycardia.

A middle-aged male presented with tachycardia, dyspnea, and 4+ bilateral leg edema.
What is the rhythm?

There had been an ice storm, and it was the busiest day in the history of our emergency department because of falls.  I reduced 12 fractures that evening and was in constant motion.   I looked at this and saw the negative component of the P-wave in V1, and immediately diagnosed sinus tachycardia.

I did a bedside echo:
There was good LV function
You can see a very large RV (closest to probe) and RA (on far right).
Lungs were clear to auscultation and there were no B-lines.

Volume overload was confirmed with this:
This shows the distended inferior vena cava (IVC), further supporting high right sided pressures and right heart failure.

So he clinically had right heart failure, subacute in onset.  If I had simply looked carefully through his chart, I would have found that this was not all new, but rather an exacerbation of a chronic problem.

Not having done that, pulmonary embolism was on the differential and we obtained a CT pulmonary angiogram:
This shows a massive right atrium and dilated right ventricle

Another slice of the CT showing the same thing:
A massively dilated right atrium

Later, I looked back at the first ECG; Here it is again:
It was suddenly clear to me from lead II across the bottom that this was atrial flutter.

Why is there a negative component to the atrial wave in V1?

Normally, one of the rapid ways to differentiate sinus from flutter is too look for a biphasic up-down atrial wave (sinus) vs. an upright atrial wave (flutter).

It turns out that there was a previous ECG to compare to:
This is clearly sinus, but with a mostly upright P-wave.
It is biphasic as usual, but the "up" component is (which is the right atrial component) is far larger than the subsequent negative deflection (representing the left atrium)

The answer has to do with the massive right atrial hypertrophy.  Normally, the P-wave in V1 is biphasic.  The initial upright part is the right atrium and the latter part, inverted, is the left atrium.  In this case, the right atrium is massively enlarged and results in almost all of the P-wave being upright.

Further complicating the problem, when the patient goes into atrial flutter, as with this presentation, the flutter wave has a large negative component due to the right atrial enlargement.

Thus, the atrial morphology is reversed in this patient, deceiving the physician (this physician) into believing it was sinus when it was really flutter.

And atrial flutter was the precipitating etiology of the patient's worsening right heart failure.

He required furosemide and ablation of the atrial flutter.

Formal Echo:

The estimated left ventricular ejection fraction is 50-55 %.
There is no left ventricular wall motion abnormality identified.
Mitral valve insufficiency mild.
The estimated pulmonary artery systolic pressure is 20 mmHg + RA pressure.
Right ventricular enlargement .
Paradoxical septal motion severe.
Decreased right ventricular systolic performance.
Tricuspid valve insufficiency severe.
Right atrial enlargement.
Based on the appearance of the IVC, the RA pressure is elevated.


RV function is probably worse than on the study of 2016. This is reflected
by more pronounced paradoxical septal motion, a lower PA pressure and
probably more TR.

Learning Point:

Atrial Flutter may have a mostly negative atrial wave on the ECG, mimicking sinus tachycardia, when there is marked right atrial enlargement.

Comment by KEN GRAUER, MD (2/9/2019):
Illustrative case by Dr. Smith — regarding acute arrhythmia interpretation. It’s so helpful to have clinical and echocardiographic correlation, with availability of a prior tracing for comparison. I focus my comments on the 2 ECGs shown in this case (Figure-1).
Figure-1: The initial ECG (= ECG #1at the time the patient presented to the ED, with comparison to a prior ECG (= ECG #2on this patient (See text).
ECG #1 (= the initial ECG in the ED)The approach to arrhythmia interpretation that I favor — is to: iFirst assess the patient hemodynamic status; and, iito use a Systematic Approach to Arrhythmia Interpretation.
  • The patient in this case presented in acute right-sided heart failure. That said, from what I surmise — immediate cardioversion was not needed — which meant there was at least “a moment” to better assess clinical parameters, including the cardiac rhythm.
  • I favor the following memory aid for recalling the 5 KEY parameters for arrhythmia interpretation: “Watch your Ps & Qand the 3 Rs”. Thus, we look for the presence of waves (or for sign of atrial activity if clear sinus rhythm is not present— QRS width — and the Rs (Rate and Regularity of the rhythm — and IF atrial activity is present, whether atrial activity is Related to neighboring QRS complexes).
  • PEARL #1: The reason I favor a systematic approach to rhythm interpretation (ie, NOT jumping to a single diagnosis — but first assessing each of the 5 KEY parameters cited above) — is that otherwise you risk premature fixation on a single rhythm diagnosis without considering other possibilities.
  • The 5 KEY Parameters: Although at first glance, it looks like sinus P waves may be present in ECG #1 — the PR interval in sinus mechanism rhythms usually shortens when heart rate increases — and, it looks like the PR interval for the upright deflection in lead II, as well as for the negative deflection in lead V1 is relatively longer-than-expected for a sinus mechanism rhythm in view of how fast the heart rate is. In addition, several leads (ie, all inferior leads, aVR, V5,V6) suggest that there may be 2:1 atrial-to-ventricular conduction. I was therefore not-at-all certain in my initial impression of ECG #1 that the rhythm was sinus.
  • It is difficult to accurately assess QRS duration for the rhythm in ECG #1. This is because of baseline artifact — and, as we’ll see in a minute — because of the underlying rhythm. So although I thought the QRS appeared to be at least of borderline duration (ie, ~0.11 second) — QRS morphology to me suggested a supraventricular rhythm.
  • The rhythm in ECG #1 is regular. I estimate the ventricular rate to be ~135/minute.
  • I’ll defer the 5th parameter (ie, Is atrial activity related to the QRS?) for a moment.
ASSESSMENT — What we have described in ECG #1, is that there is a Regular SVT at ~135/minute, without clear sign of sinus P waves. Recognition of a regular SVT with uncertain atrial activity should prompt the following Differential Diagnosis — iSinus Tachycardia (perhaps the deflections we see are sinus P waves after all …?); iia Reentry SVT (ie, AVNRT, AVRT); iiiAtrial Tachycardia; and, ivAtrial Flutter. Although other entities are possible (ie, SA nodal reentry tachycardia) — these 4 entities make up the overwhelming majority of regular SVTs that the emergency provider will see.
  • PEARL #2: By far (!!!) — the most commonly overlooked diagnosis in all of arrhythmias is atrial flutter. This is because flutter waves may be atypical in morphology, and because flutter waves may be hidden within the QRS complex and/or ST-T wave. In adults, the rate of flutter circulating within the atria in patients who have not yet been treated with an antiarrhythmic agent (that may slow the rate) is ~300/minute (usual range ~250-350/minute). By far, the most common conduction ratio in untreated AFlutter = 2:1. As a result, the ventricular rate in untreated AFlutter is almost always ~150/minute (within a range of ~135-165/minute). Therefore, the BEST way not-to-overlook the diagnosis of AFlutter is to always suspect it whenever you see a regular SVT with uncertain atrial activity at a rate of ~150/minute (ie, at a rate between ~135-165/minute). This is precisely the situation we have in ECG #1.
  • PEARL #3: Using CALIPERS facilitates diagnosis. The way I “look” for AFlutter — is to search all 12 leads for sign of atrial activity. We know lead II is the best lead for assessing sinus rhythm. The next best lead for assessing sinus rhythm is lead V1. When searching for possible 2:1 flutter activity — the best leads in my experience are leads II, IIIaVF; aVR; and V1. I generally look at these 5 leads first. After that — I then look at each of the remaining 7 leads for possible atrial activity. Set your calipers to precisely ONE HALF the R-R interval. Then see if there is any lead in which you can precisely walk out 2 deflections for each QRS complex.
  • In ECG #1  Lead aVF shows 2:1 deflections best (RED arrows). These deflections march out precisely with my calipers. There is a constant PR interval in front of each QRS complex. Since there are 2 deflections for each QRS — this means that the atrial rate = 135 X 2 = 270/minute. It would be rare indeed for ATach to go this fast (and neither sinus rhythm now reentry SVTs go this fast) — therefore the rhythm in ECG #1 is almost certainly AFlutter. And, if you step back a little bit from this tracing — there does appear to be a sawtooth pattern in each of the inferior leads.
  • In support that the RED arrows in ECG #1 truly indicate atrial activity — I’ve drawn in some vertical RED LINES that show similar 2:1 deflections in simultaneously-obtained lead aVR and lead II. Other leads that seem to show the same 2:1 activity include leads III, and possibly V5 and V6.
  • IF needed — one could confirm diagnosis of AFlutter with either a vagal maneuver or a “chemical” vagal maneuver (ie, use of Adenosine) — but using calipers has virtually already confirmed your diagnosis!
  • As per Dr. Smith — abrupt onset of the tachyarrhythmia, with resultant reduction in hemodynamically effective atrial contraction appears to be the reason for exacerbation of this patient’s condition. Management should focus on conversion to sinus rhythm.
  • P.S.: The vertical PURPLE lines in ECG #1 show that the prominent negative deflection before each QRS complex in lead V1 is not a sinus P wave. Instead it appears to be part of the flutter wave.
ECG #2 ( = the prior ECG on this patient)There are a number of interesting findings on this patient's baseline ECG:
  • Clear indication of sinus rhythm (ie, an upright P wave with fixed and normal PR interval in lead II ).
  • QRS widening in a pattern consistent with RBBB. Vertical BLUE lines in lead V1 of ECG #2 show QRS duration to be ~0.11-0.12 second, which is long enough to satisfy criteria for RBBB. Note the rSR’ pattern in lead V1 + wide terminal S waves in lateral leads I and V6 (within the BLUE circles) — which solidifies the diagnosis of RBBB.
  • There is RAE in ECG #2! Most often RAA is diagnosed by the finding of tall, peaked and pointed P waves in the inferior leads. On occasion however, you will only see a prominent pointed P wave in leads V1 or V2 — which given the clinical history here, is diagnostic of RAE in this case.
  • Note T wave inversion in leads V1 and V2 in ECG #2 (BLUE arrows). This could reflect RV “strain” — or — it could simple reflect commonly seen secondary ST-T wave changes in association with RBBB — or — it could represent both a reflection of RBBB + RV “strain”.
  • Now go back to ECG #1, and take another look at the QRS complex in lead V1. I suspect there was also RBBB in ECG #1, albeit much more difficult to see in ECG #1 due to the baseline artifact and flutter activity.
  • The Echo in this patient showed significant RAE and RVH. Note how difficult it is to diagnose RVH from the 2 ECGs in this case. This is common — as the ECG diagnosis of RVH is typically difficult, and often not apparent until late in the process. Signs consistent with RVH that we do see include relatively low voltage, lots of S waves, RBBB, T inversion on ECG #2 in leads V1 and V2 — and RAE. Keep in mind that there is only one condition in medicine that produces right atrial enlargement without also producing RVH ( = tricuspid stenosis) — so clear ECG diagnosis of RAE (as was done in ECG #2 by the prominent, peaked P waves in leads V1,V2) is an indirect clue that RVH is likely to be present (supported by the above noted ECG findings) — albeit definitive diagnosis of RVH required Echo.
  • Regarding "My Take" on a Systematic Approach to ECG Interpretation — CLICK HERE. For the part regarding systematic Rhythm Interpretation — Scroll down to Figure 4 on this web page, for the “First 2 Parameters = Rate & Rhythm).
  • For “My Take” on the ECG diagnosis of RVH  CLICK HERE.
  • For “My Take” on the ECG diagnosis of LAE & RAE  CLICK HERE.

Tuesday, February 5, 2019

Should Troponin be a Vital Sign? Perhaps, but only if Interpreted Using Pre-test Probability.

An 80-something non-english speaking patient complained of vertigo.  He was asked multiple times about chest pain or dyspnea, but repeatedly denied any such symptoms.

His vital signs were all normal.  His exam was normal.

He had a triage ECG at time 0 (ECG-1):
Computer read, with Physician overread:
Sinus rhythm.  Possible right ventricular conduction delay.

What do you think?

When I saw this without any other information, I said it was very suspicious for a high lateral MI.  In aVL, there is a tiny QRS with 0.5 mm of STE, and there is reciprocal ST depression in inferior leads.  If you see this, you must very closely question the patient about any chest symptoms, and even if no relevant symptoms, to be certain to look for old ECG, and to do serial ECGs and troponins.

There actually was an old ECG from about 4 years prior (ECG-2), which I'm not sure anyone saw:
Here the limb leads have much higher QRS voltage, without a correspondingly larger ST-T voltage.
This means that the ST-T is out of proportion to the QRS on ECG-1

The clinicians did not see the finding on ECG-1.

The clinicians later stated they had had no suspicion of ACS, but that the faculty wanted a troponin anyway.  So troponin was ordered, and it returned some time within the next few hours (uncertain exactly when they saw it):

Troponin I = 27 ng/mL (900 x the upper limit of normal)

A 2nd ECG was recorded at 3 hours (ECG-3):
Computer, and physician overread: 
Minimal ST depression
What do you think?

The STE in aVL and STD in III and aVF is more pronounced, and now there is STD in V2 and V3.  This makes it diagnostic of a posterolateral OMI (especially with the troponin!).

A 3rd ECG was recorded at 3.5 hours (ECG-4):
Computer, and physician overread: 
Minimal ST depression
This is about the same.
This was in the chart:
"Troponin found to be elevated to 27. Patient denied chest pain on initial review of symptoms. Was now endorsing chest pain which began 30 minutes ago. Upon further questioning, he states that he has had intermittent chest pain since yesterday. Pain worsens when lying flat and improves with sitting up. Given 324 mg aspirin. Repeat ECG shows modest ST elevation in I and aVL and depression in inferior leads."

The cath lab was activated.

LM 30% ostial.
LAD 80% mid
LCx occluded mid (acute infarct lesion)
RCA 80% mid. distal stent patent.
PCI mid LCx

So this is an OMI (Occlusion Myocardial Infarction), but not a STEMI

Decreased left ventricular systolic performance, mild/moderate.
The estimated left ventricular ejection fraction is in the range of
Regional wall motion abnormality (WMA):
Regional WMA: Inferobasal (this is another name for posterior), akinetic, small.
Regional WMA: Lateral, large, hypokinetic.

The patient went into cardiogenic shock and ultimately died of this MI.


There are many, cardiologists especially, who think that Emergency Physicians order too many troponins.  Many come back "positive" and trigger many often unnecessary downstream tests.  In our UTROPIA study (NCT02060760), from which there are many publications, 85% of "positive" troponins (at least one value above the 99th %-ile upper reference limit (URL), were either type II MI or non-MI myocardial injury (acute or chronic myocardial injury).

Sandoval Y et al. Type 1 and 2 Myocardial Infarction and Myocardial Injury: Clinical Transition to High-Sensitivity Cardiac Troponin I.  American Journal of Medicine 130(12): 1431-1439, Dec. 2017.

Important: this was not due to high sensitivity troponin; the number of troponins greater than the 99% URL was lower with high sensitivity troponin I than with contemporary troponin I.

We published another study (see below) showing that, as expected, patient selection greatly influences the positive predictive value of troponin.

My opinion on this:

It is not that we necessarily order too many troponins.  However, we use the 99th percentile cutoff as a cutoff for diagnosis of type I MI, and too often assign a diagnosis of type I MI simply because there is a troponin above that URL.  It is this interpretation of the test which is often inappropriate, not necessarily the ordering of the test.  Only in the right clinical context is a slightly elevated troponin highly suspicious for type 1 MI.

However, no matter the clinical context, a troponin that is 30x, 100x, or 500x the URL is indeed most likely to be type I MI.

This figure comes from the Diamond T study (all type 1 MI were NSTEMI, not STEMI):
Notice that the 6 hour value (far right) is very low for type 2 MI.
Sandoval Y.  Nelson SE.  Smith SW.  Schulz KM.  Murakami M.  Pearce LA.  Apple FS.  Cardiac Troponin Changes to Distinguish Type 1 and Type 2 Myocardial Infarction and 180-Day Mortality Risk.  Acute Cardiovascular Care 2014;3(4):317-325.

The following study, of which I am also a co-author, could be interpreted to conclude that one should not order troponins unless there is a very high pretest probability of type 1 MI.  

I would interpret the study in the following way:

When pretest probability is low, then the troponin must be very high in order to suspect type 1 MI.  

When pretest probability is very high, the troponin need not be so high.

I have the same approach with ECGs:

If the patient has a low pretest probability and the ST elevation or T-wave is not clearly diagnostic, then don't call it OMI without further testing.  If the presentation for MI is classic, then the highly suggestive ST-T has a much higher post-test probability.

Learning Points:

1. It was wise to order a troponin on this patient who does not speak English and is very old and at high risk of MI, even though his chief complaint is not suggestive of MI.  Had his troponin come back only a bit elevated, then it would not be diagnostic of type 1 MI.  But it returned so high that type I MI is by far the most likely diagnosis.

2. Of course, recognition of the ECG findings would be ideal, but this is very difficult.


Shah A.  Sandoval Y.  Noaman A.  Sexter A.  Vaswani A.  Smith SW.  Gibbins M.  Griffiths M.  Chapman AR.  Strachan FE.  Anand A.  Denvir MA.  Adamson PE.  D'Souza MS.  Gray AJ.  McAllister DA.  Newby DE.  Apple FS.  Mills NL.  Patient selection for high-sensitivity cardiac troponin testing and the diagnosis of myocardial infarction.  BMJ 2017;359:j4788 doi: 10.1136/bmj.j4788 (Published 2017 November 07)


Objective To evaluate how selection of patients for high sensitivity cardiac troponin testing affects the diagnosis of myocardial infarction across different healthcare settings.
Design Prospective study of three independent consecutive patient populations presenting to emergency departments.
Setting Secondary and tertiary care hospitals in the United Kingdom and United States.
Participants High sensitivity cardiac troponin I concentrations were measured in 8500 consecutive patients presenting to emergency departments: unselected patients in the UK (n=1054) and two selected populations of patients in whom troponin testing was requested by the attending clinician in the UK (n=5815) and the US (n=1631). The final diagnosis of type 1 or type 2 myocardial infarction or myocardial injury was independently adjudicated.
Main outcome measures Positive predictive value of an elevated cardiac troponin concentration for a diagnosis of type 1 myocardial infarction.
Results Cardiac troponin concentrations were elevated in 13.7% (144/1054) of unselected patients, with a prevalence of 1.6% (17/1054) for type 1 myocardial infarction and a positive predictive value of 11.8% (95% confidence interval 7.0% to 18.2%). In selected patients, in whom troponin testing was guided by the attending clinician, the prevalence and positive predictive value were 14.5% (843/5815) and 59.7% (57.0% to 62.2%) in the UK and 4.2% (68/1631) and 16.4% (13.0% to 20.3%) in the US. Across both selected patient populations, the positive predictive value was highest in patients with chest pain, with ischaemia on the electrocardiogram, and with a history of ischaemic heart disease.
Conclusions When high sensitivity cardiac troponin testing is performed widely or without previous clinical assessment, elevated troponin concentrations are common and predominantly reflect myocardial injury rather than myocardial infarction. These observations highlight how selection of patients for cardiac troponin testing varies across healthcare settings and markedly influences the positive predictive value for a diagnosis of myocardial infarction.

Comment by KEN GRAUER, MD (2/5/2019):
Excellent case by Dr. Smith — both for emphasizing important clinical concepts regarding optimal use of Troponin in the ED — and — for a number of insightful subtleties on interpretation of serial tracings, with comparison to a prior tracing on the patient. I focus my comments on these ECG subtleties.
  • For clarity — I have combined in Figure-1 the first 2 ECGs done in the ED, as well as the prior tracing done on this patient.
Figure-1: The first 2 ECGs done in this case, together with a prior tracing done 4 years earlier (See text).
Clinical presentation of this case was especially challenging = an elderly, non-English speaking patient who initially denied any hint of chest pain. The prior ECG ( = TOP tracing in Figure-1) was not available at the time the patient was first seen — so initial assessment was based solely on the 1st ECG = MIDDLE tracing in Figure-1. My thoughts regarding this initial ECG done in the ED were the following:
  • As per Dr. Smith — there is a tiny QRS complex in lead aVL, with what appears to be 0.5 mm of coved ST elevation. There is an equally tiny QRS complex in lead III, with subtle-but-real scooping depression that looks to be the “mirror-image” of the subtle ST elevation in lead aVL. Similar suggestion of reciprocal change is seen in lead aVF — but not in lead II. While I thought these changes were far from definitive — I agree with the excellent point emphasized by Dr. Smith = this clearly could represent OMI (high-lateral MI?), and the case needs immediate attention.
  • Additional Thoughts about this 1st ECG: There is an RSr’ in lead V1 — with a QRS complex of normal duration. The question arises as to whether this represents incomplete RBBB? Technically, it does not — because there is no terminal s wave in lateral leads I and V6. I generally acknowledge this finding by simply writing, “RSr’ in lead V1”. Of note — transition is early (a prominent R wave is already forming by V2, and the R wave becomes predominant by lead V3). Of note — T waves are upright in all 6 chest leads. Often with complete or incomplete RBBB — there is ST-T depression in lead V1, and sometimes also in V2 and V3. Given our concern about possible subtle high-lateral OMI — this raises the question whether the upright T waves in leads V1 and V2 of this 1st ECG might be abnormal and reflect ischemia. I wasn’t certain of the answer to this from assessment of this single tracing.
  • There are tiny initial q waves in multiple leads — including leads I, II, III, aVL, aVF, and V4,5,6. I suspected these small and narrow q waves seen in multiple leads were not significant.
A Prior ECG (done 4 years earlierwas found TOP tracing in Figure-1. It is interesting to compare this prior ECG with the initial ECG done in the ED.
  • As per Dr. Smith — QRS amplitude in the limb leads was greater on the prior tracing. In addition — there is slight axis shift (ie, the QRS complex is almost entirely negative in lead III of the prior tracing — whereas it appears to be isoelectric in the 1st ECG). This is relevant — because the T wave inversion that we see isolated to lead III in the prior tracing is not necessarily abnormal (ie, T wave inversion may be normal when isolated to either lead III or aVF if the QRS complex in the same lead is predominantly negative).
  • We do not see any hint of ST coving or elevation in lead aVL in the prior ECG. That said, given the axis shift that has occurred, with different QRS morphology now seen in aVL, I wasn’t sure about the significance (if any) of this change.
  • A monophasic R wave, equal in amplitude to the thin S wave in lead V1 is seen in the prior tracing. There was no hint of the RSr’ seen in the 1st ECG. Transition was again early in the prior tracing (R=S by V2, with a predominant R wave by V3). Of note — the T wave was also positive in all 6 chest leads on this prior tracing — so this T wave positivity in all 6 chest leads is not a new finding.
  • BOTTOM LINE — I didn’t think the prior tracing clarified the situation. We were still left with potential concern regarding the changes noted above for the initial ECG.
My primary purpose in commenting on this case arises from the 2nd ECG = BOTTOM tracing in Figure-1. When assessed by comparing this 2nd ECG to the 1st ECG — definitive diagnosis of OMI can now be made!
  • In the 3 hours that passed since the 1st ECG was done — there is now clearly more coved ST elevation in lead aVL — and — more mirror-image ST depression (reciprocal changein leads III and aVF. In addition, the 3rd inferior lead ( = lead II) now shows suggestion of reciprocal ST depression.
  • In the anterior chest leads, since the 1st ECG was done — there is now J-point ST depression in leads V2 and V3 that was not previously present.
  • In the lateral chest leads — there now appears to be slight-but-real ST elevation, with beginning T wave inversion in leads V5 and V6. Although admittedly difficult to assess because of baseline artifact in leads V5 and V6 in both tracings — I do think the new ST elevation in these leads is real.
  • BOTTOM LINE  Even without the markedly increased Troponin in this case — the sequential ECG changes described above that developed between the time the 1st and 2nd ECGs were done (a time span of 3 hours) are diagnostic of acute postero-lateral OMI.
SUGGESTION  The ECG findings and sequential ECG changes described for the 3 tracings shown in Figure-1 are subtle! That said, they are perfectly consistent with the clinical history and cath findings. It is worth another look if you did not confidently diagnose acute OMI after seeing the 2nd ECG, and comparing it to the 1st ECG done 3 hours earlier.

P.S. As per Arron Pearce, instead of a sinus rhythm in the 1st ECG (MIDDLE tracing in Figure-1) — there is probably a Low Atrial Rhythm, because a clear upright P wave is lacking in lead II — the P wave appears to be negative in leads III and aVF — and, the P wave is upright in leads I and aVL. Note how sinus rhythm returns in the 2nd ECG done 3 hours later (the P wave now is upright in lead II, as well as in the other inferior leads)
  • Lack of a long lead II rhythm strip, baseline artifact and very low amplitude atrial activity all contribute to making rhythm assessment of the 1st ECG quite challenging. That said — a low atrial rhythm clearly appears to be present.
  • Clinically — the clinical significance of a transient, non-accelerated low atrial rhythm is minimal.
  • Our THANKS again to Dr. Smith for presenting this case.

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