Showing posts with label early repolarization. Show all posts
Showing posts with label early repolarization. Show all posts

Saturday, September 6, 2014

A 50-something year old with typical chest pain

A middle age male presented with chest pain.  Here is his ECG; there was no previous for comparison:
QTc is 380 ms. There is 3 mm of STE at the J-point in V2 and 2.5 mm in V3.  There is also slight STE in aVL with reciprocal ST depression in III. 

It is a rather scary ECG, very suggestive of proximal LAD occlusion (proximal would include the first diagonal, resulting in high lateral MI with STE in aVL and reciprocal ST depression in III).

What is it?
[There is also an upright T-wave in V1 and larger than the T-wave in V6 (some say this is a sign of STEMI - I have not found that it is a predictive independent variable)]





















I immediately knew when I saw this that is was early repolarization.  How?

First, what are the worrisome aspects?

1) what most catches the eye is the absence of an S-wave in V3.  Normally, this is called "terminal QRS distortion" and is a very good sign of STEMI. However, it is NOT QRS distortion because, even though there is no S-wave, there is a very pronounced J-wave (a wave at the J-point).

2) The STE in aVL and STD in III suggest STEMI, but this is minimal ST deviation, and not enough to prevent use of the LAD occlusion vs. early repol formula (see sidebar excel applet).

With QTc 380
STE at 60 ms after the J-point in V3 = 2.5
R-wave amplitude in V4 = 28
Result = 16.3, which is far less than the cutoff of 23.4

We did serial ECGs and there was no change.  He ruled out for MI with serial troponins.  (Ruling out alone is not proof, however -- This is a GREAT CASE)

The reciprocal relationship between aVL and III should still be bothering some.  Below is an explanation that is further elaborated upon in this post: 

Here is a post on True positive vs. false positive ST elevation in aVL, with illustrative cases

When there is ST elevation in aVL, with reciprocal ST depression in III:

1. Look for these signs of MI:
    a. Absence of J-waves 
    b. Other ST depression
    c. Large T-waves 
    d. Symmetric T-waves
    e. Down-Up T-waves
2. Compare with an old ECG
3. Use ED Echo if available 
4. Use formal Echo 
5. A positive troponin is helpful (a negative one is not if symptoms are of few hours duration or less)

Tuesday, July 22, 2014

Are these peaked T-waves the patient's baseline T-waves?

A middle-aged patient presented feeling moderately ill.  He had an ECG recorded.
QRS 102 ms.  There are peaked T-waves. See V4 especially.  The ST segment is horizontal until it abruptly rises to a very peaked T-wave.  The T-wave is "tented" to a point.  It is all but pathognomonic for hyperkalemia.

By history, the patient had no reason to have hyperK on history. A recent previous ECG, done at a K of 4.5 mEq/L, was sought by the residents:
The old ECG also shows very peaked T-waves.  The residents concluded that these were his baseline T-waves.  Were they correct? 
















No!  Notice the ST segments in the ECG at presentation are much more flat, and they then rise much more quickly to a peaked T-wave, especially in lead V4. 

Case Conclusion

Residents had already made the comparison and decided that it was not different.  Several minutes later, I saw these two ECGs and immediately saw the difference.   I could see that the new ECG was diagnostic of hyperkalemia, and told the residents that they must immediately start treatment.  As we were walking to his room, and before Calcium could be given, the patient had a v fib arrest while in his room, before his K returned from the lab.  This was a presumed hyperkalemic arrest.  He was immediately defibrillated and given Calcium.  His K returned at 7.0 mEq/L.

Some say you don't need to treat hyperK unless there is QRS widening, claiming that merely having peaked T-waves is not enough.  This is only one case, and anecdotal, but we found no other etiology of arrest in this patient.  The patient had new renal failure as the etiology of hyperK.


1.  Peaking of T-waves occurs in other conditions than hyperkalemia, such as early repolarization.  Comparison with the previous ECG must be done very carefully

2.  I always treat immediately if I think the ECG is affected by hyperK.  I do not wait for the laboratory results

Monday, June 10, 2013

4 mm of ST elevation in lead V2 (at the J-point) relative to PQ junction

A male in his 30's male complained of chest pain  while having a dental procedure, then became syncopal.  The patient is young and healthy, and thin.  He had no past medical history.  In the ED, he felt and looked fine, with normal vital signs and no chest pain.

Sinus rhythm.  High voltage.  The computerized QTc is 390 ms.  There is 4 mm of ST elevation in lead V2, and 1.5 mm in V3 (at J-point, relative to PQ junction).  There are straight ST segments in V2 and V3, which suggest STEMI.  However, the voltage is very high and the QT is relatively short.  

In this case, the ST elevation does meet the standard STEMI  "criteria" (see below) because there is 1 mm in V1 and 4 mm in V2, even though there is only 1.5 mm in V2.

Strictly speaking, the early repol vs. anterior STEMI formula should not be used because the ST segments are non-concave (i.e., straight, though not upwardly convex).  Nevertheless, if it is used, the result is 17.4, which is very low.

From reference 1: At least 2 Consecutive Leads With ST elevation of:

V1, V4-V6: 1 mm
V2, V3: for men over 40 yo: 2 mm
for men under 40 yo: 2.5 mm
for women, any age: 1.5 mm


A repeat ECG 2 hours later was unchanged.  The patient was discharged.

Diagnosis: Early repolarization with high voltage in young healthy patient with a thin chest wall.  Syncope due to vasovagal event (neurocardiogenic syncope) in dentist's chair.



1. Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized  Electrocardiology. J Am Coll Cardiol. 2009;53:1003-1011.

Thursday, April 25, 2013

Widespread ST Elevation. Activate the Cath Lab?

A 40 year old male with several chronic illnesses presented to the ED with decreased level of consciousness and hypotension.  He had an ECG recorded quite early and it was alarming:

When I was shown this ECG a day later, it took me about 1 second to say, "Cool case of Early Repol!"  A cardiologist who had been consulted had the same reaction.  How do we know that this is early repol in all 3 regions (inferior, anterior, lateral)?  That is hard to explain, but you can always use the early repol equation for anterior ST elevation (see sidebar, or the iPhone App "subtleSTEMI").  QRS duration 85 ms and Computerized QTc is 394 ms, STE at 60 ms after the J-point is 4mm, and R-wave amplitude in V4 is at least 22 mm.  Result = 20.85 (less than 23.4 is very unlikely to be an anterior STEMI).

But what about inferior and lateral STEMI?  Is it one or all of the above?   There appears to be ST depression in aVL, but, if you look closely, that is due to wandering baseline.  Without reciprocal ST depression in aVL, it is highly unlikely to be an inferior STEMI.

Certainly a widespread STEMI (anterior, inferior, lateral, from a large wraparound LAD) is consistent with hypotension, so we should not be quick to dismiss this possibility.

How about looking for a previous ECG?  There was an ECG available for comparison from 6 weeks earlier:

Computerized QTc = 359 ms.  This is quite different, and may make you more worried that the findings today are new, especially those that are inferior and lateral.
And another ECG from 4 months earlier was available, which I'm not sure that they saw:

Computerized QTc = 373 ms.  QRS 85 ms.  In this one, the anterior leads have some STE, but not as much as there is today.  And there is none in the inferior or lateral leads.

Not inappropriately, they activated the cath lab.  Then they did a bedside echocardiogram (this is a parasternal short axis view:
 

 (Right Ventricle is on the left, next to the septum, anterior wall is on the top of the image, inferior/posterior wall is at the bottom, and lateral on the right side of the image):
This shows a hyperdynamic heart with all walls functioning perfectly, and is not consistent with infarct.


Many of you are probably thinking "Widespread ST elevation! It must be pericarditis!"  And that is certainly high on the differential.  In my opinion, due to much researching for true pericarditis cases (with objective evidence such as effusion or rub or typical evolution of the ECG), I believe that pericarditis is a very unusual cause of ST elevation, and that benign (normal variant) ST elevation is much more common.

In any case, there is no PR depression anywhere on this ECG.  There was no rub or effusion.

The patient had sepsis and hypovolemia.

1) I do not think hyperkalemia was the etiology of the change.  I might be wrong.  It looks like early repolarization to me
2) Contrary to widespread belief, early repol may come and go; it is not always present in any given individual.  See article by Kambara below.
3) Tachycardia, or stress testing, may diminish the ST elevation of early repol.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.
 

Saturday, March 3, 2012

Anterior ST elevation with large broad T-wave: what is the diagnosis?

A 41 year old male presented to a clinic with chest pain.  Here is the ECG:

There are very large, scary T-waves, with significant ST elevation.  The computerized QTc is 398 ms.

The patient was sent home from the clinic.  Days later, the overread by the cardiologist was, appropriately, "ST elevation with hyperacute broad-based T-waves concerning for acute anterior MI."  The clinic physician was notified and the patient was called back to the ED and arrived 4 days later.

Here was his ED ECG:

There is little change, signifying that this was the patient's baseline ECG (Early repolarization).  The computerized QTc is 385 ms.

Answer below:













His troponin was normal, as were subsequent serial troponins.

How does the Smith equation fare on this ECG?  (See excel spreadsheet down the right side of this blog under the heading "The equation for differentiating the ST elevation (STE) of subtle LAD occlusion from early repol"). 

The clinicians in the ED calculated the value of the first one at 23.31, and the second at 22.8.  Both are below the cutoff for anterior STEMI of 23.4. 

I calculated them as well: 

1.  On the first, I get STE60V3= 4 mm, QTc = 398 ms, and R-wave V4 = 16.5 mm.  The calculator comes up with 22.89

2.  On the second, I get STE60V3 = 4 mm, QTc = 385 mm, and R-wave V4 = 20 mm.  The calculation comes to 20.98.

Again, both are < 23.4.

If I saw this patient in the ED, I would be scared by his ECG.  But the short QT and the tall R-wave in V4 make it less scary, and thus the equation value is < 23.4.

Would I then automatically dismiss this and say it is NOT anterior STEMI?

NO!  This ECG is scary.  The rule is about 90% accurate, but not perfect.

But I would also evaluate the patient more carefully before activating the cath lab.  I would  probably order (or do myself) an immediate cardiac echo to look for an anterior wall motion abnormality.  If none were seen, I would not activate.  If an anterior WMA were seen, I would activate the cath lab.


Sunday, December 4, 2011

Several Cases of ST Elevation from Early Repolarization

As I have pointed out in other posts, I have developed an equation to help in the electrocardiographic differentiation of anterior early repolarization from anterior STEMI.  If the equation [(1.196 x ST Elevation in mm at 60 ms after the J-point in V3) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in mm in V4)] has a value greater than 23.4, vs. less than 23.4, it is quite sensitive and specific for LAD occlusion.

Remember: when you are uncertain, look for old ECGs, do serial ECGs, then, if you still need to, you can get an immediate echocardiogram, and if you ultimately cannot be certain that it is not STEMI, then you may have to risk a false positive cath lab activation. That happens.

Case 1.  One of my partners phoned me when I was out.  He was worried about this ECG.  He used his iPhone to photograph it, then sent it to me by text message:



Computerized QTc was 391 ms, STE at 60 ms after the J-point is 2 mm, R-wave is 11.5. I looked at it at said I do not think it is STEMI.  If you apply the equation, the value is 21.7 (less than 23.4, so it is early repolarization).
 I told him that it is very unlikely to represent STEMI.

Here is a previous ECG from one year ago:
The new one looks different from this one, especially in V3, but this can happen in early repol
 This was recorded the next AM, after the patient had ruled out with serial troponins:

Here are all 3 side by side:

Case 2.
A Hennepin residency graduate called me to ask about an ECG.  I happened to be in the ED so I asked her to fax it.  She was worried about diffuse ST elevation and whether there was MI or pericarditis.

There is 4 mm of STE at 60 ms after the J-point (2.5 mm at the J-point) in V2, so it looks scary.  There is 1 mm STE in 2 consecutive of inferior and lateral leads.  So it meets "criteria" for fibrinolytic therapy in every coronary distribution.  But the computerized QTc is 370 ms, the STE at 60 ms after the J-point in V3 is only 2mm, and the R-wave in V4 is 19 mm.  Equation value is 21.08, so this is unlikely to be an anterior STEMI.  Is it lateral or inferior STEMI?  The pronounced J-waves make early repol in inferior or lateral walls much more likely than STEMI.  The absence of reciprocal ST depression in aVL makess inferior MI extremely unlikely.
 As for pericarditis: the ratio of ST elevation to T-wave in V6 is less than 25 percent, so pericarditis is unlikely.  Furthermore, there is no significant PR segment depression.

Case 3.  A 19 yo with stab wound to the chest.  After viewing the ECG, there was concern for LAD laceration.

Again, there is scary ST elevation.  In fact, the ST segments in V2 and V3 are straight, not concave.  In my study, I excluded ECGs with non-concave (straight or convex) ST segments because they are so specific for STEMI.  Nevertheless, if you apply the equation, the value is only 20.52.   The patient ruled out.  The heart was not affected by the stab wound.


Wednesday, October 12, 2011

ST elevation (Saddleback), is it STEMI?

This 56 year old male presented with atypical chest pain and left arm numbness off and on for one week, worse on the day of presentation:

There is saddleback type ST elevation in leads V2 and V3, and diffuse T-wave inversion.  But there is also very high voltage  especially in V4 (35mm, sorry it is cut off) and V5 (27 mm).  The QTc was 426 ms.



Answer is below:







This ECG was shown to me by a colleague, and I immediately said: "You thought it was a STEMI, but it is not."  He had, in fact, activated the cath lab, and the coronaries were clean and the patient ruled out.


Saddleback ST elevation, in my experience, is rarely due to STEMI.  I will not say it is never due to STEMI because I know of no research on this topic.  It is usually a form of early repolarization that also usually meets criteria for type II or III Brugada pattern (see this post).  I will post more on this topic later.  In this case, it may be related to the LVH or be simultaneous early repolarization and LVH.  The diffuse (both inferior and precordial) T-wave inversion is somewhat atypical of LVH. 

Echocardiography confirmed marked concentric LVH. 

In this case, you might want to try applying the early repol/anterior STEMI equation rule posted on the sidebar.  However, it is not validated in the presence of LVH).  You would get a value of 16.11, which is very low and argues strongly against LAD occlusion.

Wednesday, October 5, 2011

Inferior ST Elevation: what is the Diagnosis?


You can read this post here, or watch a video presentation of it:






I was handed this ECG, without any clinical information, while on my way to see another patient:
There is sinus rhythm.  There is ST elevation diffusely: 2 mm in V2, 3.5 mm in V3, 2.5 mm in V4, 1.5 mm in V5, and 1 mm in V6, 1.5 mm in lead II, 1 mm in leads III and aVF.  R-waves are well formed, and in fact there is high voltage.  T-wave to ST ratio is greater than 4 in lead V6, making pericarditis unlikely (also there were no symptoms of pericarditis).  The computerized QTc is 386 ms.   There are marked J-waves in II and V4-V6, with slurring of the R downstroke in III and aVF.  There is no reciprocal ST depression anywhere except aVR; in particular, there is none in aVL.  Not only is there no ST depression in aVL, there is actually a bit of STE in lead I.   These are all classic signs of early repolarization.
I immediately recognized this as early repolarization of inferior, lateral, and anterior leads, and went on my way. Some time later, I found out that the residents had initiated an aggressive workup because they were worried about the ECG.

It turns out that this was a 27 yo African American male who presented with pressure-like (non-pleuritic) chest pain and dyspnea.  He appeared very anxious and was hyperventilating and he had just had an episode of what sounds like carpal spasm.  Clinically, he was having a panic attack.  His ECG did not worry me.

Is there LVH on the ECG?  By voltage there does seem to be, but this was a young thin male and high voltage without LVH is common in this situation.


Most early repolarization is in precordial leads, where it is so common that it is considered normal to have baseline ST elevation on the ECG.  I have put up many posts on this topic, and on differentiating ER from LAD occlusion. But there is also early repolarization in inferior or lateral leads, and when present, it is virtually always present in anterior leads as well.


Here is a case of a 45 year old with chest pain:
There is ST elevation in inferior leads only, with no reciprocal ST depression in aVL.  There is a slight T-wave inversion in aVL.
Inferior MI was diagnosed by the emergency physician and the patient needed to be flown by helicopter to the cath lab.  The arteries were clean.  There was no MI.  This was the patient's baseline ECG.   It was a false positive.

How would you be able to know this from the ECG alone?  If there are no changes in aVL, it is highly unlikely to be inferior STEMI.  If there is simultaneous lateral MI, it is possible that aVL may be silent, but in this case V5 and V6 have very minimal ST elevation.  Would you be certain that it is not STEMI?  No, but you should suspect that it is a false positive.  If you have immediate echocardiography available, you could prove that it is early repolarization by showing good contraction of the inferior wall.  Serial ECGs may be useful.  Or perhaps you need to just activate the cath lab and risk a false positive.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

Is there danger to early repolarization itself?

Ha├»ssaguerre et al. performed a case control study of patients with idiopathic ventricular fibrillation, and found that many more of these patients than of controls had baseline inferior or lateral early repolarization.  Tikkanen et al. performed a longitudinal community study, following people for a mean of 30 years.  They found early repol pattern in inferior and/or lateral leads in 3.5% and 2.5% a , respectively, and in both locations in only 0.1%.  These patients had a small but significant increased long-term risk of death from cardiac causes (Relative Risk = 1.28 for 1mm, 2.98 for 2 mm of inferior STE). 

No one is certain what to do with this information, and it certainly does not impact emergency medicine, in which the problem remains: is it STEMI or not? 


1.  Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358(19):2016-23.
2.  Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009;361(26):2529-37.
3.  Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.

Sunday, September 25, 2011

ST elevation of early repolarization may vary with the rate

This 49 yo black male presented with sudden substernal non radiating pleuritic chest pain on the day prior to presentation.  Here is the presenting ECG:
There is ST elevation in anterior leads that is classic for early repolarization: there is excellent R-wave progression, QT is not long, T-waves are assymmetric (slower upstroke than downstroke), and well-formed J-waves.  The equation value [1.196 x (ST elevation at 60 ms after the J-point)] + [QTc x 0.059] - [R amplitude in V4) x 0.326)] is low [= (2.0 x 1.196) + (418 x 0.059) - (25 x 0.326)], which is equal to 18.9.  A value less than 23.4 is unlikely to be MI.  Interestingly, the presence of J-waves did not add value to the prediction rule equation. 
Bedside  ultrasound showed no wall motion abnormality.  A troponin drawn the next AM was negative.  A repeat EKG showed increased ST elevation:
Equation value is: (4.5 x 1.196) + (0.059 x 400) - (0.326 x 28)  = 19.9 (early repol)

Repeat echo again showed no wall motion abnormality.

Why is the ST elevation greater in the second ECG?  One must remember that the ST elevation of early repolarization diminishes with increased sympathetic tone, such as during exercise.  When the heart rate is faster, as in the first ECG, the ST elevation is likely to be less pronounced than when the heart rate is slower.

Kambara found in his longitudinal study of patients with early repolarization that, in 26% the ST elevation disappeared on follow up ECG and in 74% the degree of ST elevation varied on followup ECGs.


I do not have proof in this case, but I'm pretty certain that the difference in ST elevation is due to the difference in heart rate.

Learning point: The ST elevation of early repol is not constant.  In particular, it may be diminished with exercise, sympathetic tone, and heart rate, and may be increased when the heart rate is slower.

Thanks to Steve Dunlop for this case.

Here is a good review article on early repolarization:

Tuesday, January 12, 2010

HyperKalemia with Cardiac Arrest. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia



For more on hyperkalemia, click here (includes a great case of incessant ventricular tachycardia).
For more on early repolarization, see these cases:
For differentiation of early repol from LAD occlusion, click here.

Hyperkalemia resulting in cardiac arrest

Although there is little high quality data on differentiating these entities, some general insights are useful, and illustrated with the following cases:

The first ECG is one of a 27 y.o. patient who presented with ventricular fibrillation.

ECG #1, hyperkalemia


Because of the large T-waves, this ECG was interpreted as "hyperacute T-waves". However, these T waves are pathognomonic of hyperkalemia because they are peaked, "tented", come to point, have a very flat ST segment, and there is a long QRS (114 ms).

Conventional wisdom (with no hard data, to my knowledge) says that when hyperkalemia has a normal QRS that the QTc should be short. This idea conforms with the complex electrophysiology of hyperkalemia, but may not always be true in real life.

ECG #2, LAD occlusion

In this ECG#2 above, the T-waves are slightly more blunt at the peak, there is a normal QRS duration with a long QTc at 450 ms, the ST segment is straightened (less upward concavity, steeper ST segment) which results in an area under the curve (integral) that is larger than in either hyperkalemia or early repol (i.e., the T-wave is "fat")


Below (ECG #3) is a case of a patient who presented feeling moderately ill:

EKG #3, hyperkalemia, QTc 497 ms, QRS 102 ms (normal is less than 110ms)

See V4 especially.  The ST segment is horizontal until it abruptly rises to a very peaked T-wave.  The T-wave is "tented" to a point.
Due to the peaked T-waves, the physicians were immediately concerned for hyperkalemia and sought an old ECG, which they immediately found (shown below, ECG #4):

EKG #4, early repolarization, QTc 455 ms, QRS 82 ms
Notice the ST segments here are not nearly as flat, and the rise to a peaked T-wave, especially in lead V4, not nearly as steep
After viewing this previous ECG, and knowing that the K was 4.5 at the time it was recorded, the physicians believed that the peaked T waves in ECG #3 were this patient's baseline. It is true that early repolarization has tall and relatively peaked T waves, but not to the extent seen in ECG #3. Without seeing them side by side, it is hard to appreciate the difference, but the ST segment in V4 in EKG #3 is flat, making the base of the T wave much more narrow.

This patient, then did not get immediate treatment for hyperK.  He actually had a v fib arrest while in his room, before his K returned from the lab.  This was a presumed hyperkalemic arrest.  He was immediately resuscitated, then his K returned at 7.0 mEq/L.

Some say you don't need to treat hyperK unless there is QRS widening.  They claim that peaked T-waves are not enough.  This is only one case, and anecdotal, but we found no other etiology of arrest in this patient.  I always treat immediately if the ECG is affected by hyperK.

In addition, the QRS duration difference is important; the difference in QTc seems to defy conventional wisdom.

There is a definite difference, with EKG#3 pathognomonic for hyperkalemia.


Wednesday, December 31, 2008

Acute MI from LAD occlusion, or early repolarization?

3 hours of chest pain. Is it STEMI or is it normal (or early repolarization)?


 Read Answer Below



This ECG looks quite normal, with only moderate ST elevation, upward concavity, good R-wave amplitude.  There is no ST depression or T-wave inversion.

But one easily identified characteristic makes the ST elevation unlikely to be from early repolarization: the computerized QTc is 455 milliseconds. In my study of early repolarization (ER) (n=167), only 2 of 167 (2%) cases of ER had a QTc greater than 455ms. The mean QTc was 394ms, compared to 420ms for MI (n=125) from LAD occlusion. Conversely, only 4% of LAD occlusion, vs. 40% of ER, had a QTc less than 380 ms. These clues were not appreciated by the clinicians. A very astute interpreter would not that the T-waves are also too symmetric to be early repol, which should have a steeper downslope than upslope, as demonstrated here:


The clinicians did not appreciate these subtle differences.

The patient continued to have chest pain.  70 minutes later, they repeated the ECG, which is shown here:
Note that now there are tiny Q-waves in V2-V4, making this unequivocally diagnostic of acute STEMI.



These subtle Q-waves were not appreciated, but the clinicians were astute and ordered a stat echocardiogram, which confirmed anterior wall motion abnormality. The patient was taken to the cath lab and had a 100% LAD occlusion.

After reperfusion, the patients baseline ST-T complex was revealed. This is probably what they would have looked like prior to the LAD occlusion:



For those who want some more detail on differentiating ER from MI, see below:

Also useful was the mean (from V2-V4) R-wave amplitude, at a cutoff of 5 mm, with values less than 5 mm likely to represent MI. Interestingly, mean ST elevation (no matter how it was measured) was not as good a differentiator as the mean R-wave amplitude, but if mean R-wave was less than 5 mm OR the mean ST elevation (V2-V4, as measured at the J-point, STEJ) was greater than or equal to 2 mm, then it was very likely to be MI and very unlikely to be ER.

Even better was a formula derived with logistic regression, which also included the QTc :
(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc in milliseconds) - (0.326 x RA in V4 in mm), where RA is R-wave amplitude and STE60 is ST elevation at 60ms after the J-point relative to the PR interval.

If the value of the formula is greater than or equal to 23.4, it is MI (Sens, spec, accuracy all around 90%); if less, then it's ER.

For the first ECG, STE60, V3 = 2.5mm, QTc = 455, and RA V4 = 17, so: (1.196 x 2.5) + (0.059 x 455) - ( 0.326 x 17) = 24.29; this is barely greater than 23.4, thus consistent with MI but also further illustrating that this ECG is very difficult.