A 30-something with palpitations and lightheadedness

A 30-something male without any significant past medical history presented with palpitations and presyncope.

Here is his ED ECG:

Regular Wide Complex Tachycardia at a rate of 229

First: What do you want to do?

Next: What do you think is the ECG diagnosis?

First. Before getting into analysis, a regular wide complex tachycardia could be 

1. ventricular tachycardia (VT) or 

2. AV reciprocating tachycardia (AVRT, antidromic WPW) or 

3. SVT with aberrancy.  (SVT would usually be AVNRT or orthodromic WPW)

Since adenosine is safe in VT, and it works for AVRT and AVNRT, it is worthwhile trying adenosine.  Or, of course, you can always use electrical cardioversion.

Providers gave 6 mg of adenosine with no response, followed by electrical cardioversion.

This is what I texted back: "VT or AVRT. (Antidromic WPW).  I am sure you already shocked it, right?"

Next. ECG analysis: This is a regular wide complex tachycardia.  There are no P-waves.  The QRS onset is very slow. See magnified leads below.  The time from QRS onset to peak is approximately 110 ms.  

This is too long for either AVNRT or for Idiopathic VT.  Briefly, idiopathic VT is VT in an otherwise normal heart and initiates in conducting tissue and therefore has a rapid onset similar to SVT with aberrancy). See this post: Idiopathic Ventricular Tachycardias for the EM Physician.  

Such a slow onset is appropriate for VT in the context of myocardial disease, or for AVRT.

Here I put a lines, or arrows, at the onset (black) and end of the ONSET (blue) of the QRS.  I started in lead II at the bottom, where it is easiest to see the onset.  

The QRS in aVR starts with a 40 ms q-wave (see the dip after the blue arrow).  The onset of the QRS ends at the 2nd peak.  Thus, the QRS from onset to peak (the initial depolarization takes about 110 ms).  

This is prolonged and would not be so slow if it were through conducting tissue, as it would be with AVNRT or with idiopathic VT.

Here is the post cardioversion ECG (texted to me):

This what I texted back: "Could be WPW. You don’t always see Delta waves."

After cardioversion, echo showed excellent LV function.

Final analysis:

1. Good LV function means that if this is VT it would likely be idiopathic VT

2. But idiopathic VT should have a rapid onset

3. This has a slow onset, so it is unlikely to be either type of VT.

4. Finally, Right ventricular outflow tract VT, which responds to adenosine, has an LBBB morphology and inferior axis, which is not present here.

5.  Therefore AVRT is most likely, even though there are no delta waves.

This was the note of our electrophysiologist:

“… Although the morphology is consistent with ventricular tachycardia, we cannot completely rule out antidromic AVRT originating from LV base insertion site of an accessory pathway.  The EKG during sinus rhythm does not show robust preexcitation, but we will keep in mind that for left-sided accessory pathways may not show robust preexcitation during sinus rhythm since this is essentially dependent upon relative conduction of the AV node versus accessory pathway (if any).”

Outcome

Electrophysiologic study showed an accessory pathway (WPW, antidromic AVRT)

Why did adenosine not work?  6 mg often does not work, but especially in low flow states.  Our electrophysiologist, Rehan Karim, explains: "At this HR in general one might expect overall transit time for any IV drug to be very slow to reach the heart. Adenosine as you know has very short half life so a small dose like this probably would fade away before it would reach the target area."

Dr. Karim wrote some further key take away points are:

1. Degree of pre-excitation (“WPW”) during sinus rhythm is dependent on competition between the AV node and pathway - and is also impacted by relative location of pathway. If I live in West Suburbs of Twin Cities, I’ll probably take I-35 W rather than I-35 E unless it is blocked for whatever reason.

So if you don’t see pre-excitation during sinus rhythm, it doesn’t mean there can’t be any - as sinus node is right atrial structure and left sided pathways may not show robust pre-excitation if someone has fast conducting AV node!

2. Antidromic AVRT morphologically will meet the criteria for “VT” originating from “insertion site” of the accessory pathway- because essentially that’s where Ventricular activation is originating. Now it can NEVER have negative concordance though - because the accessory pathways usually insert at base of the heart rather than apex!

===================================

MY Comment by KEN GRAUER, MD (5/14/2022):

===================================

What I liked most about today's case — was the skillful use of bedside Echo in the ED by Dr. Smith to facilitate rhythm diagnosis! I'd add the following comments to his excellent clinical decision-making strategy.

• As per Dr. Smith — the initial rhythm in today's case is a regular WCT ( = Wide-Complex Tachycardia) at ~230/minute, without clear sign of atrial activity. Dr. Smith suggested the following Differential Diagnosis for this WCT rhythm: i) VT; ii) Antidromic AVRT (in a patient with WPW); and/or, iii) SVT with aberrant conduction.
• 
  
• I'd add: iv) SVT with preexisting BBB (Bundle Branch Block) to the above differential diagnosis — as instead of an initially narrow QRS complex (that manifests aberrant conduction as a result of the rapid rate) — the etiology of this regular WCT rhythm could be an SVT in which the QRS was already widened (ie, "preexisting" BBB).
• 
  
• Dr. Smith narrowed the likely differential for aberrantly-conducted SVT to either AVNRT or orthodromic AVRT. This is because the ventricular rate of ~230/minute for today's tracing is too fast for sinus tachycardia in an adult — it is slower-than-would-be-expected for 1:1 AFlutter — and — faster-than-would-be-expected for 2:1 AFlutter. While Atrial Tachycardia could be possible at this rate — ATach is far less common in practice than either of the reentry SVT rhythms (which are AVNRT and AVRT).
• 
  
• Dr. Smith highlighted delay in the initial conduction time (perhaps seen best in the slow upslope for the R wave in leads V1-thru-V4 — as well as measured in Dr. Smith's magnified view of lead aVR that is shown above). This delay in initial conduction of the QRS makes it much less likely that a supraventricular mechanism is operative (since initial conduction with AVNRT and orthodromic AVRT is usually fast, being transmitted over the normal AV nodal pathway).

At this point — the patient was electrically cardioverted, and a post-cardioversion Echo in sinus rhythm showing normal LV function was obtained.

• PEARL #1: Getting an Echo when your arrhythmia patient is stable can sometimes prove highly insightful for determining the rhythm. For example, in today's case — Knowing that the Echo obtained after conversion to sinus rhythm revealed normal LV function — allowed Dr. Smith to deduce that ischemic VT was unlikely (since this entity is almost always associated with at least some impairment of LV function). 
• Use of Echo therefore narrowed diagnostic considerations for today's rhythm to 2 entities: i) Antidromic AVRT (in a patient with WPW) — vs — ii) Idiopathic VT (ie, that group of ~10% of all VTs that occurs in patients who do not have underlying heart disease).

PEARL #2: I favor addition of QRS morphology features in my considerations to enhance prediction of the rhythm etiology.

• While exceptions exist — supraventricular conduction with QRS widening (ie, from either aberrancy — or from preexisting bundle branch block) — tends to resemble some form of conduct defect (ie, either RBBB, LBBB, or RBBB with LAHB or LPHB). QRS morphology in today's initial tracing does not resemble any known form of conduction defect because: i) The uniformly amorphous and slurred complexes in leads V1-thru-V4 are completely lacking in the triphasic appearance that RBBB typically shows in lead V1 — and — lacking in the usual progression of an RBBB pattern as one moves across other anterior leads; and, ii) The multiphasic (fragmented) and virtually isoelectric complex in lead III is not consistent with any known hemiblock pattern.
• 
  
• QRS morphology in today's initial tracing is not consistent with either of the 2 most common forms of idiopathic VT — which are RVOT VT (Right Ventricular Outflow Track VT) and Fascicular VT. I've reproduced the summarizing Table from my discussion of this topic in the February 14, 2022 post in Dr. Smith's Blog in Figure-1. Today's initial tracing is not RVOT VT — because it does not have an LBBB-like appearance in the chest leads. This initial tracing is also unlike Fascicular VT because it is too wide, too amorphous in its anterior lead shape, and too fragmented and isoelectric in lead III. While a small percentage of the idiopathic VTs manifest a less recognizable QRS morphology — the initial delay in conduction (as per Dr. Smith), marked QRS widening, and other morphologic features described above make idiopathic VT highly unlikely as the diagnosis.
• 
  
• In contrast — the very rapid rate of today's reguar WCT rhythm — in association with the initial slurring of the wide positive complexes in most chest leads would seem perfectly consistent with antidromic AVRT.

BOTTOM Line Regarding Today's CASE: 

Determining the precise etiology of today's initial tracing is not needed for appropriate initial management. As Dr. Smith said in his initial comment, "I am sure you already shocked this rhythm, right?" While brief trial of medical therapy (ie, with use of Adenosine) may be reasonable if the patient is hemodynamically stable — the chances are high that electrical cardioversion will soon be needed.

• PEARL #3: It is not always possible to distinguish between VT vs antidromic AVRT from an initial ECG showing a regular WCT rhythm. Statistically — over 95% of such rhythms will turn out to be VT. Clinically — this distinction is not essential, since appropriate initial management considerations are usually similar (ie, both rhythms will respond to electrical cardioversion).
• 
  
• That said — today's case is insightful for illustrating how use of Echo and assessment of QRS morphology may guide diagnostic considerations. Knowing that the probable etiology of the very rapid WCT in today's case is antidromic AVRT can help expedite definitive therapy — which will be EP referral for ablation of the patient's "culprit" accessory pathway.

Figure-1: Review of KEY features regarding Idiopathic VT (CLICK HERE — for the source of this Summary).

Quiz post - which of these, if any, are OMI? What is the South African Flag Sign? Will you activate the cath lab? Can you tell the difference on ECG?

 Written by Pendell Meyers, additions and edits by Grauer, Smith, McLaren

Below we have 5 cases of adults (ranging from 40-70 years old) who all presented to the ED with acute nontraumatic chest pain that sounded at least somewhat like potential ACS to the provider. 

You should look at each ECG and decide if it is OMI, not OMI, or something else.

Our goal in this post is to compare and contrast OMIs with false positives that mimic them. In this post we will examine the anterolateral distribution that has been described as the "South African Flag Sign." (SAFS)

It is very hard to describe why an ECG expert can easily differentiate these 5 cases. Some of these cases will appear to violate some rules of thumb that are commonly given in rudimentary ECG education. In the end, what matters is accuracy - can you tell which are "real" and which are "fake"? For now, the only thing that can tell the difference is expert human interpretation by someone who has spent much time to memorize these ECG patterns and correlate them with patient outcomes.

Think about faces: you can recognize your friend instantly.  But can you describe why?  Did you measure her nose?  The size of her eyes?  No.  An EKG is like a face and you need to get to know them so you can recognize them.  This is what we hope to teach to artificial intelligence. 

A short discussion of the SAFS pattern will come at the end for review.

Case 1

 - this case had a prior ECG available, here:

Case 2

Case 3

Case 4

Case 5

Scroll down for answer key and discussion.

Case 1 - Normal variant (Not OMI, False Positive STEMI criteria)

With no clinical information at all, I sent this to Dr. Smith who immediately said "Not OMI." I responded: "Correct. But you can see why well meaning learners who are trying to learn to find hyperacute T waves and the south african flag sign are so upset when I told them that!"

ECG: Sinus rhythm. QRS grossly within normal limits. STE in I and aVL and V2, reciprocal STD in III and aVF. The T waves are tall in I and aVL, but not "fat." They are not hyperacute, because they are not "inflated with air" in my opinion. The morphology of the STD and TWI in III is especially specific for NOT OMI, and it has the appearance of LVH with "strain pattern." It is fake, not OMI.

Clinical info: 40s year old woman presented to the ED for off and on chest pain over a week or so, with an episode today that woke her from sleep and wouldn't go away. There was associated cocaine use, but unclear if recently.

Here is an example of a prior ECG on file:

STEMI was activated. Cardiology refused and cancelled the cath lab activation, reportedly stating that they believed that her ECG findings were consistent with prior episodes of cocaine use. I am not quite sure what that means or what exactly their reasoning was, but regardless no angiogram happened.

The patient was admitted to medicine for high risk chest pain.

Three serial troponin I measurements were each 9 ng/L.

Potassium level was 4.1 mEq/L.

She checked out against medical advice before any further workup was done.

Case 2 - D1 OMI (STEMI[-] OMI)

ECG: Sinus rhythm, QRS grossly normal. Subtle STE in I and aVL, with tiny terminal T wave inversion in aVL. Reciprocal STD in II, III, aVF. V2 has the slightest suggestion of STE with convex ST segment. This one matches many prior cases of true SAFS in my experience, and the morphology looks like acute OMI at least affecting the high lateral leads. The slight terminal TWI in aVL may suggest that it is starting to reperfuse.

Clinical info: 70s year old M with chest pain for 1 hour. 

Initial high sensitivity troponin I = 27 ng/L (below the URL; i.e. normal)

Given ASA, morphine, NTG for ongoing pain.

Repeat trop 233, then 14,000, then greater than 25,000 ng/L

As this was not recognized as OMI, cath was done too late and showed 100% thrombotic acute D1 occlusion, stented. 

EF 35%, WMA mid-apical anterior, lateral, and apical myocardium.

Post PCI ECG:

Case 3 - D1 OMI (STEMI[-] OMI)

Sent to Dr. Smith with no information at all, who immediately responded with: "This one is OMI."

ECG: Sinus rhythm. QRS grossly within normal limits. Similar to case above with STE in I and aVL with reciprocal STD in III and aVF. Similar V2 as case above. This time the T waves are upright in I and aVL. Leads III and aVF have a very concerning "down-up" morphology that is specific for reciprocal STD from OMI in lead aVL. 

Clinical info: 50s year old man with tobacco use presents for acute substernal chest pain just prior to arrival.

Initial troponin less than 6 ng/L (less than limit of detection).

Repeat troponin 17 ng/L.

Echo shows hypokinesis of the anterolateral myocardium.

Repeat trops: 2740, 5835, 7077 ng/L. None further ordered.

Cath shows acute thrombotic occlusion of D1, deemed small and not suitable for PCI. 

No further ECGs recorded.

Note: the first 2 troponins were negative; if you rely on troponin to make this difficult diagnosis, you will lose a lot of time and all of the myocardium at risk!

Case 4 - Normal variant (Not OMI, False Positive STEMI criteria)

Sent with no information to Dr. Smith, who said "Not OMI."

ECG: Sinus rhythm. QRS shows relatively high voltage, but maybe not meeting clear LVH criteria. Could also be simply healthy young high voltage. There is STE in I, aVL, and V2, with convex ST segments and reciprocal STD in II, III, aVF with TWI. I strongly suspect these T waves are not hyperacute (unless a baseline ECG later proves me wrong), but instead a confusing baseline variant. There is also terminal T wave inversion in V3-V6, which reminds me somewhat of benign T wave inversion pattern (another normal variant). This ECG simply does not look like OMI in my experience.  

See here for many examples of "benign T-wave inversion", just like what you see here in V3-V6

Clinical info: A 50s year old man presented with acute chest pain of several hours duration. 

Two ED troponins were less than 6 ng/L.

Many prior ECGs on file over years, including this one:

No other dangerous cause of chest pain was found. He was discharged.

Case 5 - mid LAD OMI (the easiest one of all 5, but still STEMI[-] OMI)

ECG: Sinus rhythm. QRS grossly within normal except poor R wave progression and left axis (possibly could describe as LAFB). Hyperacute T waves in I and aVL and V2, STE in aVL and V2. Reciprocal STD in II, III, aVF (from high lateral OMI) and STD in V3-V6 (appears to become maximal in V6, likely indicative of a component of subendcardial ischemia). Terminal QRS distortion in aVL. This one is OMI.

Clinical info: 50s year old man presents with chest pain waking him from sleep 6 hours ago.

STEMI activated, at cath lab: total mid LAD occlusion, stented.

First trop 12,960 ng/L, none further measured.

Post cath ECGs:

South African Flag Sign:

This is a particular ECG pattern found in OMI cases affecting the anteroseptal / anterior / high lateral walls. It has been described as a territory corresponding often to the first diagonal artery, but of course there is substantial coronary variation and any artery in the anterior and or lateral areas can cause this pattern. See the diagrams above from Littmann et al. (referenced below) for the visual explanation of why the pattern of ECG changes can be remembered using the image of the South African flag.

Here is a diagram by Ken Grauer of the South African Flag sign, from this prior post:

References:

Durant E, Singh A. Acute first diagonal artery occlusion: a characteristic pattern of ST elevation in noncontiguous leads. Am J Emerg Med. 2015; 33:1326.e3-5

Littmann L. South African flag sign: a teaching tool for easier ECG recognition of high lateral infarct. Am J Emerg Med. 2015; 34.

DOI: https://doi.org/10.1016/j.ajem.2015.10.022

Images from google search.

Learning Points:

If you use the STEMI criteria to decide which patients need emergent reperfusion, YOU WOULD GET ALL 5 OF THESE CASES WRONG. You would falsely activate the cath lab for 2 patients, and withhold treatment of OMI in the other 3!

It can be difficult to determine OMI from OMI mimics, but this is possible with experience and practice, in which you learn based on memorizing the patterns that correlate with the proven outcomes of OMI.

Expertise can correctly overrule many ECg "rules of thumb." Some of the OMIs above have concave ST segments, and some of the false positive ones have convex ST segments! Many of the false positive cases above indeed have reciprocal findings in inferior leads. Reciprocal findings occur regardless of the reason for focal primary findings. If you learn by seeing many cases and their outcomes, you can see which are true positives and false positives.

The South African Flag sign is a nice teaching tool for the anterolateral OMI distribution.

=======================================

MY Comment by KEN GRAUER, MD (5/11/2022):

===================================

As I worked through the 5 tracings selected for today's "Quiz Post" by Dr. Meyers — I found myself asking, "What is it about each case?" — that makes me favor OMI or not favor OMI?

• As per Dr. Meyers — "It is very hard to describe why an ECG expert can differentiate these 5 cases". Words on paper do not suffice — since "the rules" are not always followed.
• Instead — there is an intuitive (unspoken) form of "pattern recognition" that just "happens" — in the same way that an experienced clinician can look at a patient, and in a matter of seconds know the likely diagnosis.
• Clearly — seeing the patient and knowing the history would help in your interpretation of these ECGs. But Drs. Meyers and Smith instantly arrived at the correct interpretation in each case without the benefit of any history.

MY Approach:

• As I contemplated each of these 5 cases without the benefit of any history — I found myself looking for 1 or 2 leads that I knew were either not normal — OR — that I really thought looked like a benign repolarization change.
• Then I looked for neighboring (or reciprocal) leads that supported that impression.
• 
  
• NOTE: The South African Flag Pattern described below by Dr. Meyers adds to the challenge (For more on this pattern — See My Comment at the bottom of the page in the April 8, 2022 post of Dr. Smith's Blog). This is because acute occlusion of the 1st or 2nd Diagonal Branch of the LAD will typically only result in ST elevation in 1 chest lead ( = lead V2) — so you lose the potential benefit of seeing similar abnormal ST elevation in neighboring anterior leads.

I picked 2 of the 5 Cases to comment on. For clarity — I've put these 2 tracings together in Figure-1 — and have labeled the findings that I focused on.

Figure-1: I've reproduced Case #2 and Case #3 from today's post.

What Is It About these 2 Cases?

Beginning with Case #2 — the rhythm is sinus with a PAC.

• The lead in Case #2 that caught my eye — was lead aVL. The shape of the subtle-but-real ST elevation in this lead is not normal. Adding to my concern is the small q wave, and hint of beginning T wave inversion. This is not the appearance of a repolarization change.
• In view of the abnormal appearance in lead aVL — the subtle ST elevation in lead I (above the dotted RED line in this lead) suggests a similar ongoing process in this other high-lateral lead.
• Confirmation that the lead aVL appearance is likely to be acute — is forthcoming from reciprocal changes in all 3 inferior leads (II,III,aVF). The ST segment straightening that we see in these leads (as per the RED lines) — that then leads up into clearly disproportionately tall T waves (considering the modest R wave amplitude) is not normal.
• Normally — there is slight (1-2 mm) upward concavity ST elevation in leads V2 and V3, that is usually accompanied by an upright T wave. The ST segment coving with slight elevation that we see in lead V2, with hardly any T wave (within the dotted RED rectangle in this lead) — is definitely not a normal appearance for lead V2. Raising suspicion more — is the finding of a QS pattern in both leads V1 and V2.
• T waves in leads V3-thru-V6 all look disproportionately tall and peaked considering the modest R wave amplitude in each of these leads. Support that this finding is abnormal is forthcoming from straightening of the ST segments (RED lines).
• 
  
• BOTTOM LINE: Awareness that acute occlusion (OMI) of the 1st or 2nd Diagonal may cause ST elevation in lead aVL (sometimes also in lead I) — and only in 1 chest lead ( = lead V2) should prompt this diagnosis for Case #2 until proven otherwise. My suspicion that an acute process was ongoing until proven otherwise in this case — was supported by the finding that ST-T waves in no less than 10/12 leads are clearly abnormal! 

What about Case #3?

Once again the rhythm in Case #3 is sinus.

• Once again — lead V2 caught my eye, as the shape of the subtle-but-real ST elevation in this lead (within the dotted RED rectangle) — is simply not normal.
• Although a small-but-present initial r wave is seen in leads V1 and V2 of Case #3 — there is no doubt that the ST segment flattening in leads V3-thru-V6 is not normal (especially given the contrast in shape between the subtle ST elevation in lead V2 — and the definite ST straightening in lead V3).
• As opposed to the shape of the elevated ST segment in lead aVL of Case #2 — I was not initially certain in Case #3 from looking at lead aVL alone, that the ST elevation represented OMI.
• That said — the 2 limb leads that caught my eye in Case #3, were leads III and aVF. In both of these leads, in addition to ST depression — was a "down-up" terminal T wave which is distinctly abnormal — and which strongly suggested recent (if not acute) reciprocal change to the ST elevation in lead aVL.
• In view of the definitely abnormal ST-T wave appearance of leads III and aVF in Case #3 — the much more subtle-but-present ST segment straightening that we see in lead II completes the inferior lead pattern of "reciprocal changes".
• Similarly — in view of now knowing that the shape of ST elevation in lead aVL of Case #3 is abnormal — the similar ST-T wave shape in lead I doubtlessly reflects the same ongoing process.
• 
  
• BOTTOM LINE: Although the "look" of Case #3 is not quite the same as what we saw in Case #2 (Note especially the reduced T wave amplitudes in multiple leads) — the "theme" of Case #3 is similar. That is — Case #3 manifests ST elevation in leads I, aVL and V2 — ST depression in leads III and aVF, with an acute "down-up" T wave pattern — and in total, no less than 10/12 leads with clearly abnormal ST-T waves. Once again — the diagnosis should be acute OMI of the 1st or 2nd Diagonal until proven otherwise.

What about the Non-OMI Tracings?

I wish I had easy answers for how to quickly recognize the 2 tracings in Dr. Meyers' Quiz that were not OMIs.

• Here — the History really helps! Even marked ST elevation is often benign when a young adult is either asymptomatic or presents with atypical symptoms. On the other hand — a worrisome history is clear indication of need for more information plus diagnostic testing (ie, stat Echo during chest pain — troponin — repeat ECGs — search for a prior ECG for comparison). IF in doubt — it is best to be prudent until you can rule out an acute event.

The more non-OMI variants that you see — the better you get at recognizing them! There are numerous examples throughout Dr. Smith's ECG Blog.

• See the April 8, 2017 post — for a nice review by Drs. Smith and Dunbar of some normal variants with T wave inversion.
• See My Comment at the bottom of the page in the September 11, 2020 post — showing lots of ST elevation in a young adult.
• The August 22, 2020 post — Even repolarization variants may sometimes show "dynamic" ST-T wave changes.
• See My Comment in the November 14, 2019 post — regarding distinction between T-QRS-D (Terminal QRS Distortion) vs repolarization variants.
• 
  
• There are many others — and we continue to post more!

Unstable Angina Still Exists in Era of high sensitivity troponin, with a short lesson on troponin interpretation

42 y.o. male with no past medical history presented for chest pain of onset 2 weeks prior.  It is not constant, but lasts only a couple minutes.  It is substernal without radiation, and is associated with SOB.  Onset of chest pain was 2 weeks.  States it is not constant. 

He has PMH of HTN, hyperlidemia, DM2, 1/3 ppd smoking (4 risk factors).

A few days prior, his chest pain was intense and lasted about 10 minutes and it made him sweat. 

On the day of presentation, he was walking to the ED from the parking lot and the chest pain recurred and lasted about 2 minutes.   

Here is his ED ECG:

There are non-specific down-up T-waves in I, aVL

Some nonspecific T-wave inversion in V4-V6

Here is a previous ECG:

The T-wave changes were not present at that time.

T-wave changes like this can come and go for no apparent reason, so these differences may, or may not, be due to ischemia/MI.  Given that the top ECG is recorded in an aysmptomatic state, it is unlikely that it represents active Occlusion MI, but it could represent a Non-Occlusion MI (NOMI).

The first high sensitivity troponin I returned at 32 ng/L.  The 99th percentile upper reference limit (URL) is 34 ng/L for men, and 16 ng/L for women; since this patient is a man, this level does not quite qualify for acute MI.  

4th Universal Definition of Myocardial Infarction requires:

1) a rise and/or fall in cTn with at least one value above the 99 the percentile occurring in appropriate clinical circumstances consistent with acute myocardial ischemia. AND

2) 1 or more of the following: a) ischemic symptoms, b) development of pathological Q waves in the 12-lead ECG, c) ECG changes indicative of new ischemia, d) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality, or e) identification of an intracoronary thrombus by angiography or autopsy.)

Since this troponin is not above the 99th percentile URL, it is not acute MI (yet).  But perhaps the next one will be higher and we can make the diagnosis of MI?

Educational interlude on troponins:  Why is 32 ng/L normal, and not high?  

The manufacturer determines normal from a population of asymptomatic "normal" people without known heart disease who are without symptoms.  The value below which 99% of normals are measured is defined as the URL.  For this Abbott Architect high sensitivity troponin I, that value is 16 ng/L for women and 34 ng/L for men.  However, individuals with measurable values below the 99th percentile (below the URL but above the limit of detection - LoD) have ＞3x the incidence of adverse outcomes at 180 days compared to those whose values are reported as below the limit of detection (LoD), which is 1.9 ng/L (Europe).  [U.S. FDA only allows reporting the LoD at 4 ng/L].  This date comes from our publication in Circulation.

Dr. Fred Apple and others studied many assays in individuals who are even more certain to be "normal." (Clinical Chemistry, Volume 66, Issue 3, March 2020, Pages 434–444) as proven by a normal GFR, normal Hemoglobin A1C, and normal BNP.  In this asymptomatic group with no evidence of serious illness, the values for this Abbott Architect assay (he studied several other assays also) were 13 ng/L for women and 20 ng/L for men. 

So for a very healthy patient, a value of 32 ng/L is actually high!!  Nevertheless, strictly speaking, it cannot be used to make the diagnosis of acute MI.  But it sure can make you suspicious that ACS is the etiology, and thus the diagnosis is Unstable Angina.  

How about this patient?  His A1C = 9.2, GFR is normal, and BNP is normal.  It is uncertain what the 99th percentile for a group of patients with normal GFR, normal BNP, but elevated A1C would be. 

Another ECG was recorded:

Not very helpful.  

The 2nd troponin returned at 33 ng/L.  So the "delta" is an insignificant 1 ng/L (this difference is within laboratory imprecision).  Our data and our protocol would say that if both troponins are below the 99th percentile URL (34 ng/L) and the delta is < 3, then the patient would not rule in for MI if more troponins (e.g., at 6 or 12 hours) were to be measured.  Thus he is eligible for discharge.

However, patients with a classic history, as here, must not be discharged, regardless of the ECG or troponin!

Let's do a HEART score:  worrisome history, 4 risk factors, and nonspecific ECG = 5 (moderate risk)

How about EDACS score: = 15 (< 16 is low risk)

So the patient was admitted.  

-------An alternative would be a CT Coronary Angiogram, but this is only available 8AM - 4 PM on weekdays.  Also, since this patient's symptoms were provoked by exertion, a stress test is a very good test for him.

Next day he had a stress echo, which was positive and is interesting:

The patient exercised for 7:25 minutes on the standard Bruce protocol and achieved a peak heart rate of 153 bpm representing 86% of age predicted maximum heart rate and an estimated work load of 9.1 METs. Test was terminated because of chest pain and dyspnea.

 

Abnormal stress echocardiogram with a high degree of certainty--evidence for ischemia in the LAD territory.

 

1. Inducible wall motion abnormality with stress--apical septal, mid anteroseptal, mid to apical anterior, apical lateral, and apical inferior akinesis with stress.

2. Left ventricular function normal at rest, severely decreased with stress.

3. Left ventricular dilatation with stress.

4. Ischemic ECG response with stress (up to 2 mm of flat ST depression in the inferior leads, most severe 3:00 minutes into recovery).

5. The patient reported angina with stress.

6. Exercise capacity was fair (85% METS for age and gender).

7, Hypertensive response to exercise (peak BP 215/111 mmHg).

Angiogram:

Severe 3 vessel disease.

Required 5 vessel CABG.

Learning Points:

1. Unstable Angina still exists.

2. A troponin beneath the diagnostic threshold for myocardial infarction is not always normal.

3. A strong history should supercede a negative ECG and troponin.

===================================

Comment by KEN GRAUER, MD (5/8/2022):

===================================

As an Attending in Primary Care who taught Exercise Stress Testing ( = EST or ETT) to Family Medicine residents for many years — one of the most common areas of confusion I saw was in distinction between MI "Rule Outs" — with the decision to follow-up ED or hospital discharge with evaluation for potential presence of underlying coronary disease.

• Just because a patient rules out for an acute event — in no way rules out the possibility that this patient might still have underlying coronary narrowing.

I found it interesting that the 42-year old man in today's case presented to the ED. He literally walked into the ED! 

• The history that this previously healthy patient gave, was of chest pain that began 2 weeks earlier. The pain was not constant. It lasted only minutes (by his account — never more than 10 minutes). The pain was substernal, without radiation — and associated with shortness of breath. He did report one 10-minute episode of more severe chest pain associated with diaphoresis — but that was several days earlier. Other than on the day of admission — there was no mention in the history provided of exacerbating or alleviating factors.
• From the history given — we do not know WHY this patient chose the particular day that he walked into the ED. The only mention of chest pain on that day was walking from the parking lot, and that episode lasted only 2 minutes. 
• NOTE: It is true that "deniers" often minimize (or completely deny) symptoms — but at least on paper — the history we are given did not sound to me like the history of an acute event. That said — of obvious concern in this 42-year old man with no prior history of chest pain, were his 4 significant coronary risk factors (ie, smoking, hypertension, hyperlipidemia and diabetes).
• 
  
• KEY Point: The literature suggests that for a patient of a "certain age", who presents with new chest pain to the ED — that cardiac risk factors play a minor role in influencing the likelihood of whether the patient is having an acute cardiac event. In contrast — the likelihood of underlying coronary disease is greatly influenced by the presence of multiple cardiac risk factors (such as those described for today's patient).
• 
  
• Editorial NOTE: In my experience — there is a unconscious "self-selection" that chest pain patients intuitively make at the time they decide whether to go to their family physician's office, to an Urgent Care Center — or to the ED. By this I mean, that given the identical history and risk factors — statistical likelihood that a patient is having an acute event is much greater for those patients who come to the ED, compared to those patients who decide to go to the office. In my 30 years of seeing ambulatory patients and precepting countless residents — it was exceedingly uncommon for a patient with an acute MI to present to our office. Instead, almost all of our patients who had acute MIs "self-selected" and went to the ED.

How Does the Above Relate to Today's Patient?

Despite a history not suggestive of an acute cardiac event — today's patient did present to the ED. This fact alone is enough to justify sufficient evaluation to rule out acute OMI (Occlusion-based Myocardial Infarction).

• As per Dr. Smith — although this patient's Troponin values of 32 ng/L and 33 ng/L were slightly below the acute MI "cut-off" — these values were clearly higher-than-expected when compared to a healthy population. I would not call these Troponin values "completely normal".
• 
  
• That said — even IF this patient's serum Troponin values and his serial ECGs were totally normal — this in no way would rule out the possibility of underlying coronary disease. On the contrary, given this patient's 4 cardiac risk factors and his history of new symptoms — some form of Stress Testing is clearly indicated.
• IF instead of presenting to the ED, this patient had presented to our Primary Care Clinic — We would have followed the identical approach that was followed after ruling out an MI ( = Risk stratification by some form of Stress Testing).

Were the ECGs in Today's Case "Negative"?

The 3 ECGs shown above clearly do not suggest acute OMI. That said — I interpreted this series of tracings as abnormal, and potentially consistent with "dynamic" ST-T wave changes.

• For clarity — I've reproduced the 3 ECGs from today's case in Figure-1. I've rearranged the sequence that I show these 3 tracings to facilitate comparison between this patient's initial ECG ( = ECG #1) — with his "baseline" tracing ( = ECG #2) — and then between his initial ECG with the repeat ECG done a little bit later in the ED ( = ECG #3).

Figure-1: Comparison between the 3 ECGs in today's case.

MY Thoughts on these 3 ECGs:

• ECG #2 ( = the "Baseline" tracing) — The rhythm is sinus tachycardia at the fairly rapid rate of ~115/minute! There is a Q wave of uncertain significance in lead III. There is no chamber enlargement. R wave progression is normal. There is some nonspecific ST-T wave flattening in a number of leads — but nothing that looks acute. KEY Point: Given the significant tachycardia — true comparison of ECG #2 with the 2 ECGs done the day the patient presented can not be accomplished until we understand the circumstances causing this tachycardia.
• 
  
• ECG #1 ( = the initial ECG in Today's Case) — The rhythm is sinus. The heart rate varies (ie, sinus arrhythmia) — but overall, the rate is clearly slower than it was in ECG #2. There is no significant change in either frontal plane axis or precordial lead QRS appearance — so other than the change in heart rate, comparison of ST-T wave change between ECG #1 and ECG #2 should be valid. As noted earlier by Dr. Smith — there is now shallow T wave inversion in lateral chest leads V4,5,6 that was not present in ECG #2.
• 
  
• ECG #3 ( = the tracing done after ECG #1 in the ED) — A regular sinus rhythm at ~80-85/minute is seen (the rate slightly slower than for ECG #1). There has been a change in frontal plane axis (ie, the QRS is now predominantly negative in lead III — whereas it was positive in ECG #1). This may make it more difficult to evaluate any "true" change in limb lead ST-T wave morphology. I thought there was a slight-but-real change in ST-T wave appearance in the chest leads (ie, the T waves in V1,V2 are smaller — and there was a bit more T wave inversion in other leads).

IMPRESSION: Clearly there is no indication from these ECGs of acute OMI. But despite some difference in heart rate and frontal plane axis — I thought that there was a change compared to the prior ECG — and perhaps also slight change in ST-T wave appearance in ECG #3 compared to ECG #2.

• Acute OMI has essentially been ruled out.
• This 42-year old man with new symptoms + 4 cardiac risk factors + 2 serum Troponins that are at least suspicious + subtle but-I-think-real ECG changes — is clearly in need of Stress Testing.
• The abnormal Stress Echo — especially in view of development of chest pain with exercise in association with both Echo and ECG evidence of ischemia — dramatically increases the post-test likelihood of significant coronary disease. I would have been surprised if significant coronary was not found on cath.

Final EDITORIAL NOTE: As I alluded to earlier — many patients (especially males, in my experience) — either minimize or deny anginal symptoms. I found being the one there to do the Exercise Stress Test on our patients gave me a unique opportunity to watch and question the patient during exercise. This provided me with tremendous insight as to the nature and severity of whatever symptoms the patient was having

• I strongly suspect the 42-year old man in today's case was a "minimizer" of symptoms. I would not be at all surprised if after doing the Stress Test — a longer duration and much more typical history for anginal symptoms could have been obtained.