A Young Man with Sharp Chest pain

Suppose this patient had chest pain.  What would you diagnose?

What is the diagnosis?

OK.  I lied, just so you could assess your reaction to this ECG.

In fact, this patient did NOT have chest pain.  But some day he may show up in an ED with chest wall pain, and he might erroneously be diagnosed with pericarditis.

This is just classic early repol.  This was recorded in an 18 year old otherwise healthy young man who just had a seizure.  There were no chest symptoms at all.  This was his baseline ECG.

Notice:

1. There is diffuse ST elevation, in all myocardial territories.
2. STE is greater in lead II than III
3. There is no reciprocal ST depression, especially none in aVL
4. There is some PR depression, but less than 0.5 mm
5. Spodick's sign is present
6. There are prominent J-waves in almost every lead.

ECGs like this are often attributed to pericarditis, when the vast majority of the time they are simply normal early repolarization.

Here is a great case where such bias led to poor management:

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

It is true that early repolarization, as defined by J-waves in inferior and lateral leads, is associated with a higher long term risk of ventricular fibrillation.  But it has no bearing on ED management.

Long-Term Outcome Associated with Early Repolarization on Electrocardiography

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Comment by KEN GRAUER, MD (4/19/2019):

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My initial impression on seeing the ECG posted in this case (which I’ve reproduced for clarity in Figure-1) — was that despite the history we were given ( = chest pain) — that the tracing most probably represented Early Repolarization. That said — I was admittedly not 100% certain of this. I’ll explain my thought process by use of 4 words: i) History; ii) Rub; iii) Proportionality; and, iv) Superimposition.

Figure-1: The ECG posted in this case (See text).

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My thought process:

• The HISTORY: There’s a lot to the history when considering acute pericarditis — including age of the patient — clinical likelihood of acute viral pericarditis ( = by far, the most common cause of acute pericarditis in an ED or out-patient center) vs pericarditis secondary to some other underlying disorder — and, the specific nature of the type of chest pain that the patient is having. I’ve summarized some factors to consider in this regard in Figure-2.

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Figure-2: Factors to consider in obtaining the history in a patient who might have acute pericarditis (Excerpted from Grauer K: ECG-2014-ePub).

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• The RUB: During the past 9+ years that I’ve been interpreting too-numerous-to-count ECGs on a daily basis on various internet ECG forums — the overwhelming majority (I’d estimate well over 90%) of ECG cases posted in which acute pericarditis is a diagnostic consideration, fail to even mention cardiac auscultation in listening for detection of a pericardial friction rub. When the pertinent negative of “No rub heard” is not even mentioned in the clinical presentation — it usually means that the clinician did not specifically listen for a rub. While true that acute pericarditis may not necessarily manifest an audible rub at the time you examine the patient — sometimes it does !!! And, IF you are able to hear a definite pericardial friction rub — then you have made a definitive diagnosis within seconds.

Figure-3: Factors to consider regarding physical examination in a patient who might have acute pericarditis (Excerpted from Grauer K: ECG-2014-ePub).

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• PROPORTIONALITY: The numerical amount of ST elevation seen in multiple leads in Figure-1 is impressive (many leads showing ≥3-4mm of ST elevation). That said — when you consider the markedly increased QRS amplitude evident in so many leads (which I have counted and noted in BLUE letters) — proportionally, the relative amount of ST elevation in Figure-1 is not that great. Together with the prominent J-point notching we see in so many leads — the appearance of ST-T waves in this tracing could be perfectly consistent with a repolarization abnormality.
• SUPERIMPOSITION: One factor that I see all-too-often-ignored — is that a patient may start out with an early repolarization picture — and superimposed on this, then develop a case of acute pericarditis. I have NO idea how to rule out this possibility simply by looking at the ECG shown in Figure-1. Finding a prior ECG on the patient may help — but the caveat exists that ST-T wave changes of early repolarization may vary when serial ECGs are obtained. This is why without considering the other factors mentioned above — I would not be 100% certain that the ECG in Figure-1 was simply a repolarization variant. This ECG certainly has many features consistent with a repolarization variant — and acute pericarditis is a far less common entity. But more than just a single ECG is needed when the goal is to be sure that the patient does not have pericarditis.

Tachycardia, fever to 105, and ischemic ST Elevation -- a Bridge too Far

A near 60 year old male called 911 for increasingly severe fever and SOB.  A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI.

He presented very tachycardic with a very high fever.

Here was his initial ED ECG:

There is sinus tachycardia at a rate of about 140
There is profound ST Elevation across all precordial leads, as well as I and aVL.
QTc was 374, and the formula value was quite high, consistent with LAD occlusion.

A previous ECG from 4 years prior was normal:

This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.

If a patient presents with chest pain and a normal heart rate, or with shockable cardiac arrest, then ischemic appearing ST elevation is STEMI until proven otherwise.

But when the clinical presentation is sepsis, one must entertain the possibility that the ST elevation is due to demand ischemia, or some other process, and exacerbated by tachycardia.

It is prudent to treat the other conditions, get the heart rate controlled, and repeat the ECG.

Case continued

A bedside echo was done:

Although the quality is suboptimal, it appears to me to show a hyperdynamic heart and possibly and apical wall motion abnormality.

Case Continued

The patient was treated for sepsis and had another ECG 35 minutes later:

Heart rate is still fast at 120
The QTc = 410 ms
There is still scary STE
The formula is still positive

The patient continued to improve and had another ECG at 65 minutes:

QTc = 419
It looks a lot better, though the formula is still marginally positive:
STE at 60 ms after J-point in V3 (STE60V3) = 3.5
R-wave amplitude in V4 (RAV4) = 10
Total QRS amplitude in V2 = 26
Formula value = 18.9
Any value greater than 18.2 should be assumed to be LAD occlusion until proven otherwise.

Tough case.

Cardiology was consulted and they did not think there was an indication for emergent cath lab activation.

He was admitted and serial troponins were measured:

Because of elevated troponins, a next day echo was done:

The estimated left ventricular ejection fraction is 50%.

The estimated pulmonary artery systolic pressure is 37 mmHg + RA pressure.

Normal estimated left ventricular ejection fraction lower limits of normal.

Regional wall motion abnormality-distal septum anterior and apex akinetic

Here is a repeat ECG:

Looks like a reperfused LAD lesion (Wellens' morphology)

The resident asked me what I thought about this case after the fact but before the angiogram.

I said I think there is a fixed stenosis in the LAD and the tachycardia and stress caused a type 2 STEMI.

In this abstract from 2011, we found that 4%(4 of 99) type 2 MI and 38% of type 1 MI had ST Elevation.
https://www.annemergmed.com/article/S0196-0644(11)00829-8/fulltext


An angiogram was done:

It showed no culprit and no coronary disease, but did show a myocardial bridge in the mid LAD.

An excellent review of myocardial bridging, with full text:

https://academic.oup.com/eurheartj/article/26/12/1159/524878

Myocardial bridging is when the coronary artery, usually the LAD, dives into the myocardium.  

Here is an excerpt from the article:

"Normally, only 15% of coronary blood flow occurs during systole, and because myocardial bridging is a systolic event on angiography, its clinical significance and relevance have been questioned. The presence of tachycardia could unmask the ischaemic effect of a myocardial bridge by shortening the diastolic period and increasing the importance of systolic blood flow. Also, tachycardia may worsen ischaemia because of a decrease in diastolic filling time and in coronary flow reserve (a measure of the ability to augment coronary blood flow under stress).  According to one hypothesis, systolic kinking of the blood vessel may cause trauma to the intima and damage to the endothelium, especially at high heart rates. This, in turn, could produce platelet aggregation and vasospasm and result in an acute coronary syndrome."

Summary of the pathophysiology of this case and the ECGs:

This was a type 2 LAD STEMI.  In other words, there was transmural ischemia during the tachycardia due to both demand (high heart rate) and to the effect of myocardial bridging, which would mimic near occlusion.  Then when the heart rate comes down, demand is decreased and full perfusion is restored, just like it is in Wellens’ syndrome.  So the ECG findings are the same as if the patient had an anterior STEMI with reperfusion.  Thus, there is a wall motion abnormality in the distribution of the LAD (not global apical dyskinesis, as in takostubo).  This wall motion abnormality will almost certainly resolved with time (myocardial stunning).

Takotsubo stress cardiomyopathy is also a possibility, but the echo did not have the typical global apical hypokinesis, and the ECG, especially the reperfusion ECG, is more consistent with LAD ischemia.

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Comment by KEN GRAUER, MD (4/15/2019):

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There are 3 aspects about this case that I love: i) It reminds us about the clinically (but not anatomically) uncommon, but very important entity of Myocardial Bridging; ii) It illustrates the concept of a Type 2 MI, with an example in which there was marked diffuse ST segment elevation; and, iii) It illustrates the influence that tachycardia may have on the amount of ST elevation that will be seen.

• Autopsy studies suggest that Myocardial Bridging may be found in as many as 1/3 of adults. But because most cases result in little or no restriction of coronary flow — the condition usually goes unrecognized, unless there is occasion to perform cardiac catheterization. Emergency providers will encounter this condition — so it is good think about it! — CLICK HERE — for my Review on Myocardial Bridging in discussion of another case.
• It is important to remember that not every acute MI with ST elevation is the result of acute coronary occlusion. With a Type 2 MI, despite no acute coronary atherothrombosis — there will be positive Troponin with either new cardiac chest pain — and/or new ischemic ST-T wave ECG changes — and/or new Q waves on ECG — and/or objective demonstration of new wall motion abnormality. The mechanism responsible for Type 2 MIs is oxygen supply & demand imbalance — which may result from a variety of causes including sustained tachycardia, severe bradycardia, coronary spasm, severe anemia, respiratory failure, hypotension/shock — all of which may be exacerbated by significant underlying coronary disease that had been compensated prior to the appearance of the precipitating cause. —  CLICK HERE — for the ESC/ACC/AHA/WHF 2018 Consensus Document on the 4th Universal Definition of MI, in which these concepts are discussed and illustrated.
• Finally — I selected the 1st and 3rd ECGs done in this case to illustrate the difficulty assessing acute ST segment elevation in association with marked tachycardia (Figure-1).

Figure-1: The 1st and 3rd ECGs in this case (See text).

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Discussion of Figure-1: As per Dr. Smith — ECG #1 showed marked sinus tachycardia at ~140/minute — with diffuse ST segment elevation.

• I often find it difficult to determine the precise amount of ST elevation when the heart rate is very fast. For clarity — I’ve added short horizontal RED lines in Figure-1 to show what I took as the “baseline” for assessing the amount of J-point ST elevation for the 2 ECGs in this figure.
• It may be especially difficult when there is marked tachycardia to identify the J-point that defines the number of millimeters of ST elevation. This is because of the tendency for the ST segment to be curved rather than showing a distinct J-point when the heart rate is fast. For clarity — I’ve added BLUE arrows in ECG #1 to show what I took as the J-point in various leads. I accept that others may differ with the location of my arrows. Suffice it to say that there appears to be ≥4-5 mm of ST elevation in leads V2-thru-V5, with a lesser amount of ST elevation in leads I, aVL, V1 and V6.
• Clinical Context is everything! Given the tachycardia + the lack of chest pain in this patient who was thought to have septicemia — I was not convinced that ECG #1 was the result of an acute cardiac event. Tachycardia may sometimes produce a surprising amount of ST elevation — that greatly decreases (or even goes away) when the heart rate slows. As per Dr. Smith — It is prudent to treat the other conditions, get the heart rate controlled — and then repeat the ECG!
• By the time ECG #3 was done — the patient’s condition had significantly improved, and his heart rate had decreased to ~90/minute (Figure-1). Note how at this slower rate — it becomes much easier to make out the change in slope within the ST segment that defines the J-point (PURPLE arrows). It should be clear that the amount of ST elevation is now significantly less.

BOTTOM Line: It’s impossible to be certain how much of an effect the reduction in heart rate between ECG #1 and ECG #3 had in reducing the extent of ST elevation. We simply can’t tell if the degree of flow restriction produced by the myocardial bridge changed during the course of treatment — since many factors may influence to what extent myocardial briding obstructs flow (including disproportionate shortening of the period of diastolic ventricular filling that occurs at faster heart rates). Regardless, comparison of the 2 ECGs in Figure-1 highlights the wisdom of treating other conditions and, then repeating the ECG as the heart rate slows.

• Qualitatively — I thought the straight ST segment take-off in lead V6 of ECG #1 was the most suspicious shape suggesting more than just tachycardia was going on in the initial ECG. And as the heart rate slowed (in ECG #3) — the amount of persistent ST elevation with abnormal ST coving in leads aVL, V6 + the uncharacteristically straight ST segment take-offs in leads V3, V4, V5 all strongly favored an acute ongoing cardiac event. As per discussion above by Dr. Smith — other tests confirmed the diagnosis of myocardial bridging and Type 2 MI.

The delay between OMI and STEMI claims yet another patient's anterior wall

Written by Pendell Meyers with edits by Steve Smith

An elderly woman with HTN presented with L sided chest pain, intermittent over the past week but worse over the past hour, associated with shortness of breath. She had no known history of CAD.

Here is her presenting EKG at 2210:

What do you think?

This is quite an obvious anterior OMI, with STE in V2 with hyperacute T-waves in V2-V3, however it unfortunately does not meet STEMI criteria as there is insufficient STE in either lead V1 or V2 to have two consecutive leads. There is a small amount of coved, convex STE in aVL with a terminal T-wave inversion. There is also the beginning of a Q-wave in V2-3.

First ECG stretched out vertically to magnify the QRS:

Here I have stretched the image vertically (the entire image, waveform and gridlines alike). This highlights the principle of proportionality - now that hte QRS is closer to normal size, the same proportion of STE strikes you as obvious.

A consult for emergent catheterization was placed, however the cardiologist was not convinced of the EKG findings. Emergent catheterization was not performed, and the patient was instead admitted to the CCU. Heparin and other antiplatelet medication was not started at this time for unclear reasons.

Initial troponin T returned significantly elevated at 0.51 ng/mL.

One hour later, at 2322, here is her ECG:

Persistent STE in V2-V4. Although there is a terminally inverted T-wave in V2 (which by itself may suggest reperfusion), V3 shows persistent STE with upright, hyperacute T-wave. Q-waves are present in V2-V6.

Serial troponins continue to rise. However the patient is not taken to the cath lab because these ECGs were interpreted as not meeting STEMI criteria.

It is unclear whether pain is continuing at this time, however it is extremely unlikely for serial ECGs to be recorded in an asymptomatic admitted patient overnight who has already had a cardiologist decide against emergent catheterization. The patient was also given morphine, which seems unlikely in an asymptomatic patient. Therefore there was likely ongoing chest pain.

Another repeat ECG at 0351 when another troponin continued to increase:

Persistent STE in V2-V5. The T-wave in V2 is now upright, signifying reocclusion of that territory's blood supply. Q-waves becoming slightly more prominent, and there is no longer any R wave in V2.

Heparin is finally started at this time, around 4am.

Another repeat at 0536:

Clearly meets STEMI criteria in I and aVL, with reciprocal changes in the inferior leads. Persistent STE and upright T-waves in anterior leads as before. This correlates with aVL on the first ECG, and suggests that there was some ischemia of D1 that has now become complete occlusion of D1.

Because the ECG finally meets STEMI criteria, the patient is finally taken to the cath lab.

A 100% thrombotic mid-LAD occlusion was discovered and stented open, with pre and post TIMI flow 0 and 3.


Here are angiogram images:

Same image with arrows showing the point of occlusion. The small branch overlaid in this image extending past the arrows is a small side branch that took off before the point of LAD occlusion. 

Arrows showing the site of former occlusion, showing the territory beyond the site of occlusion which had been ischemic.

Here is her ECG immediately post cath:

Reduced but persistent STE in anterior and high lateral leads, indicating reperfusion. It may take hours or longer for the residual STE to disappear, or it may persist indefinitely ("LV aneurysm morphology).

ECG later that day:

The STE in lateral leads has resolved, while the anterior leads have QS waves with persistent STE, likely indicating full thickness completed infarction. 

Peak troponin T was roughly 3.5 ng/mL. QS waves with such a high troponin (in my most recent study, the average peak troponin T of clear cut STEMIs was 3.19 ng/mL) are very unlikely to represent myocardial stunning, and much more likely to represent full thickness irreversible infarction.

Echocardiogram the next day showed wall motion abnormalities of the anterior, lateral, septal, and apical regions. EF at that time was 38%.

Learning Points:

There is commonly a significant delay between the first ECG diagnostic of Occlusion MI and the presence of STEMI criteria, during which the patient loses a significant amount of myocardium.

Ongoing evidence of ischemia (whether ongoing chest pain, rising troponins, ongoing ECG evidence of ischemia) despite maximal medical management mandates emergent catheterization by our current NSTEMI guidelines.

You must advocate for your patients with Occlusion MI, because our current paradigm does not.

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Comment by KEN GRAUER, MD (4/12/2019):

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One would think that there should no longer be a need for cases like this one = Wishful thinking … The fact that in 2019, a consulting cardiologist would deny the need (and potential benefit to accrue) from prompt cardiac catheterization of the elderly woman in this case — despite her initial ECG, in association with a history of recent-onset chest pain over the past week (clearly worse over the previous 1 hour) + new dyspnea tells us how much work still needs to be done among clinicians charged with recognizing acute OMI (including cardiologists! ).

• I focus my comments on ECG interpretation of the first 2 tracings in this case. For clarity — I’ve put them together in Figure-1.

Figure-1: The first 2 ECGs in this case (See text).

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The elderly woman in this case had NO known history of coronary disease. Her symptoms of “intermittent” chest pain began over the previous week — clearly becoming worse over the hour just before she arrived in the ED.

QUESTION: Looking at ECG #1 in Figure-1 — Is there anything on this tracing to suggest that she may have had a 1st event (ie, infarction) earlier during the week — and is now presenting with extension of an earlier infarction?

• HINT: How many leads in ECG #1 manifest Q waves?

ANSWER: The reason I favor use of the memory aid, “Q-R-S-T Changes” as part of my Systematic Approach to ECG interpretation — is that doing so prevents me from overlooking which leads have Q waves — and — it prevents me from overlooking whether R Wave Progression is normal or not.

• In ECG #1 — small Q waves are present in leads I, II, III; aVF; and V2-thru-V6 (ie, in no less than 9 of the 12 leads! ).
• While true that small and narrow q waves may normally be seen in one or more lateral leads (ie, leads I, aVL; V4, V5, V6) — and sometimes normally in one or more of the inferior leads (ie, leads II, III, aVF) — the Q waves that we see in leads V2 and V3 in ECG #1 are definitely not normal!
• In addition to their anterior location — reasons why the Q waves in leads V2 and V3 are not normal include: i) There is loss of r wave as one moves from lead V1-to-V2; ii) In these 2 leads, which manifest predominant negativity — there is a triphasic (qrS) complex, the shape of which strongly suggests there has been infarction at some point in time; and, iii) Given the tiny QRS amplitude in these 2 leads — the Q wave in leads V2 and V3 is both relatively deep and relatively wide!
• BOTTOM Line: While important to appreciate a point repeatedly emphasized by Dr. Smith = that new infarction Q waves may sometimes develop VERY soon after acute coronary occlusion (ie, as soon as within the 1st hour after acute occlusion!) — it clearly is possible that the patient in this case had a 1st event (infarction) days earlier when her symptoms began — and is now showing signs of acute extension of that initial MI. — Personal Note: As a primary care Attending physician for 30 years — I saw many cases of older patients who only presented to our out-patient medical center days (or longer) after the onset of symptoms that they initially ignored — with an ECG indicative of a recent (but not acute) event.

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Regardless of whether numerical criteria for acute STEMI were satisfied — and regardless of whether this patient had an initial event earlier during the week — the new-onset aggravation of her symptoms (which according to the case description required morphine for relief) + the ECG signs of acute ischemia that we see in ECG #1 should be more than enough to merit prompt cardiac catheterization with the goal of acute reperfusion (See the 2nd Learning Point at the bottom of Dr. Meyers discussion).

• There is just NO way that the coved ( = “frowny”-configuration) ST segment in lead V2 of ECG #1 is not acute. And because of how rounded the initial part of this elevated ST segment is — there may be as much as 2 mm of J-point ST elevation (which considering the tiny QRS amplitude, is as much as the R wave in V2 is tall).
• In a certain sense, lead aVL is “contiguous” with lead V2 (ie, there is overlap in the area of the heart viewed by these 2 leads) — and, we see similar ST coving with slight ST elevation in lead aVL of ECG #1.
• The 3 QRS complexes we see in lead V3 all manifest a slightly different ST-T wave shape. Which shape is the “real” one? Regardless — the T wave for each of these 3 complexes is obviously hyperacute (dysproportionately tall) given the tiny r wave amplitude for each of the complexes in this lead.
• FINAL Point: I suspect there is some lead malposition in one or more of the anterior chest leads in ECG #1. I say this because: i) Given ST coving in contiguous lead aVL — I would expect a similar shape to the ST segment in neighboring lead V3 (unless there was acute occlusion of the 1st diagonal branch of the LAD — in which case leads aVL and V2 may be the only leads showing ST elevation); ii) The finding of an R wave = 2 mm in lead V2 — that then decreases to <1 mm in V3 — but then increases again in lead V4 (to 5 mm) is counterintuitive to a physiologic R wave progression; and, iii) The P wave is non-existent in lead V2 — but shows reasonable amplitude in neighboring leads V1 and V3 — and this also does not make “physiologic sense”. NOTE: It is relevant that there may be lead malposition of one or more chest leads in ECG #1 — because a “lack of numeric criteria” for acute STEMI was apparently the reason the attending cardiologist did not promptly perform cardiac catheterization in this case — and — it is possible that immediate repeat ECG after verifying accurate chest lead placement might have resulted in an ECG that would meet numeric STEMI criteria.

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COMMENT on ECG #2: One hour later — ECG #2 was obtained. Although difficult to tell if the slight change in QRS morphology in lead V2 between ECG #1 and ECG #2 is the result of somewhat different chest lead placement — there does appear to be some ECG signs of acute evolution:

• The ST segment in lead V2 of ECG #2 is less elevated, and T wave inversion is developing.
• It looks like there may be slight increase in the amount of J-point ST elevation in leads V3 and V4 of ECG #2 compared to ECG #1.
• Despite virtually NO change in QRS morphology/axis in the 6 limb leads between these 2 tracings — the T waves in lead III especially, but also in lead aVF look more hyperacute in ECG #2 (relatively taller and fatter-at their peak given the small R wave amplitude in these respective leads).
• Ideally — the 2nd ECG should have been obtained sooner than 72 minutes after the 1st ECG, since clinicians should have been contemplating whether or not acute cath is indicated. Acute evolving ECG changes often occur much sooner than one hour later.

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BOTTOM Line: The Learning Points put forth by Dr. Meyers (above) tell the story:

• The ECG diagnosis of acute OMI will often be possible hours before “accepted” acute STEMI criteria become evident. IF your consulting cardiologist is among those who fail to recognize (or acknowledge) acute OMI on ECG in a patient with new chest pain — even when there is evidence of acute ischemia — it falls on YOU to advocate for your patients with ECG evidence of acute OMI — because (as per Dr. Meyers) — our current paradigm still does not!
• I’ll ADD this Learning Point: If working with a cardiologist who fails to accept acute OMI ECG findings because "numeric criteria" for acute STEMI are not met — Be ALERT to signs suggesting possible chest lead malposition — since immediate repeat ECG after verifying accurate chest lead placement might NOW satisfy STEMI criteria that were not manifest when lead placement was off ...

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FOR MORE:

• For “My Take” on use of the Systematic Approach to ECG Interpretation — CLICK HERE.
• Regarding ST segment Shape (ie, “smiley” vs “frowny” configuration) — CLICK HERE (Please see My Comment at the bottom of the page).