Wednesday, November 15, 2017

A male in his 50s with chest pain. What is your interpretation?

Written by Pendell Meyers, edits by Smith:

A male in his 50s with no significant past medical history complained of several episodes of chest pain over the course of the past 24-48 hours, which became acutely worse and persistent approximately 1 hour prior to arrival.

Here is his presentation ECG:
What is your interpretation?

Sinus rhythm. Normal QRS morphology with the exception of possibly high voltage. There is minimal elevation of the J point in III and aVF, with significant reciprocal ST-T depression in aVL and I, as well as ST-T depression in V2 with minimal J-point depression in V3. The large, symmetric, bulky T-waves in the inferior leads are highly suspicious for hyperacute T-waves, and this suspicion is confirmed in aVL by the massive area between the baseline and the ST-T depression/inversion compared to the QRS complex, making this definitively consistent with a reciprocal hyperacute T-wave. This ECG even without knowing the appropriate clinical history has extremely high probability of acute coronary occlusion in the inferior and posterior distributions. Additionally, there is ST elevation in V1, indicating RV involvement. The ST depression of posterior MI sometimes attenuates the ST elevation of concomitant RV MI, but in this case there is clear ST elevation in V1 even in spite of the fact that there is ST depression in V2.

The physicians were able to look up a baseline ECG:
All findings on the presentation ECG are new compared to this baseline ECG. Specifically, notice the negative T-waves in the inferior leads with positive T-wave in aVL at baseline, which are "pseudonormalized" in the presentation ECG above. These differences again confirm acute coronary occlusion. 

The physicians were highly suspicious of the findings on the presentation ECG. They did not immediately activate the cath lab but instead called the interventionist on call who was also worried and together they decided to activate the cath lab. He was moved to the critical care area of the Emergency Department and a repeat ECG was performed:
Findings in the inferior leads are not much changed, however there is even more ST elevation in V1, confirming concomitant right ventricular MI. The ST depression is somewhat attenuated, likely because it is being caught between the anterior/rightward vector of the RV MI and the posterior vector of the posterior MI.

Smith comment: We have a manuscript under consideration in which we found that ST elevation in V1 in an inferior MI is very specific for RV MI, especially when there is ST depression in V2.  However, STE in V1, in inferor MI, is not sensitive enough (about 85%) to rule out RV MI.  Therefore, I recommend a right sided ECG for every patient with inferior MI, unless it will delay coronary intervention.  No right side ECG was recorded.

Initial troponin T was undetectable.

The patient was taken for angiography:
Before intervention: there is a proximal to mid RCA occlusion. The angiogram report states it was a total thrombotic occlusion with TIMI-0 flow.
The tortuous vessel appears to be a right ventricular marginal branch.
This is surprising because it indicates that there may not be a right ventricular infarct.
On the other hand, sometimes there is a second branch to the RV.

After PCI of the RCA: TIMI-3 flow through the entire RCA.
Here you see a more distal branch that appears to supply the RV.

Without right sided ECG, and without typical RV physiology of hypotension, and without an echo showing RV dysfunction, it is impossible to tell from the information we have whether, in fact, an RV MI was present.
Repeat ECGs ordered after cath:
J-points all nearly back to baseline. There is terminal T-wave inversion in leads III and aVF, with reciprocal terminal upright T-waves in aVL and V2. This confirms reperfusion in the inferior and posterior distributions. 

Further T-wave changes indicating progression of reperfusion findings.

Peak troponin T was 2.68 ng/mL (large MI) at approximately 12 hours from presentation. Echo showed an inferior and posterior wall motion abnormality.

Learning points:

Lead aVL often has the most definitive and most easily noticeable evidence of inferior acute coronary occlusion.

Serial ECGs make difficult decisions easier.

Comparison with old ECG can make the diagnosis.

Initial contemporary troponin within the first few hours of onset of acute coronary occlusion will usually be negative.

ST elevation in V1 in the right context is indicative of acute coronary occlusion of the right ventricle, especially in the context of ST depression in lead V2.

Record a right sided ECG in cases of inferior MI.

Here is an interesting case with ST elevation in V1:

RV MI diagnosed by ST elevation in V1

Tuesday, November 14, 2017

Is this acute coronary occlusion? Simple ACS? Where is the culprit lesion?

This was sent by Brandon Stein.

This patient presented with chest pain:
What do you think?

There is "inferior" ST depression.  When you see this, especially with down-up T-waves, as in III and aVF, it is reciprocal to barely visible ST elevation in aVL.  Then look at V2 and V3.  Both have hyperacute T-waves, which suggests the LAD.  The combination of STE in aVL and V2 is typical of a first diagonal occlusion (the first lateral branch off the LAD).

It was described in the below article.  They called it a "mid-anterior" or "mid-anterolateral" infarction without involvement of the septum or apex.

Brandon was very astute and recognized the acute coronary occlusion.  The cath lab was activated and there was a first diagonal 100% occlusion.

Here is the post cath ECG:

Compare to the presentation ECG:
The post cath ECG has significantly small T-waves in V2-V5
All of the STE in I and aVL is resolved.
All of the inferior ST-T ischemia is resolved

Peak troponin I was only 1.36 ng/mL, thanks to immediate recognition and rapid reperfusion!!

Learning Points:

1. Coronary occlusion need not have "diagnostic" levels of ST elevation.
2. NonSTEMI frequently needs the cath lab NOW.
3. First diagonal occlusions have their own footprint that is recognizable.  Its sensitivity and specificity are really unknown, however.  But every time I see it, I recognize it and have not been wrong yet.


Friday, November 10, 2017

A middle-aged woman with chest pain and a "normal" ECG in triage

This was sent to me by a former resident from a community hospital:

A middle-aged woman complained of chest pain and was seen in triage.

She had a ECG recorded.

The computer interpreted the ECG (GE Marquette 12 SL) as:

"Sinus Bradycardia.  Normal ECG."

It was not seen by a physician.

Here it is:
Computer interpretation: 
"Sinus bradycardia. Normal ECG"

--This ECG does, at first glance, appear normal

--It is sinus rhythm.
--The QRS is normal

--There is possibly an abnormal Q-wave in lead III, and non-specific T-wave in aVL, but the computer did not see it.

--All the intervals are normal, including the PR, QRS, and QTc at 455 ms
--There is ST elevation in V2-V4, but it is within normal limits.

That is, it appears to be normal ST Elevation and the computer thinks it is normal STE.

There is one thing that is clearly abnormal, but computers are not programmed to detect it:

When there is ST Elevation in V2-V4, it is only normal when there is:
1) high R-wave voltage and 
2) a short QTc
3) relatively high QRS voltage in V2

This ECG has a relatively long QTc, low R-wave amplitude, and low QRS amplitude

That is why the formulas work.

STE60V3 = 2.5 mm, QTc = 455 ms, RAV4 = 6 mm, QRSV2 = 11
3-Variable formula = 27.9 (very high, diagnostic of LAD occlusion)
4-Variable formula = 23.05 (very high) 

To my knowledge, no computer algorithm has yet been programmed with the formulas

The ECG was not shown to a physician.

Later, the patient collapsed in triage and became unresponsive.  She was in full arrest with ventricular fibrillation.

Fortunately, she was resuscitated.

She had a 100% LAD occlusion.

She survived neurologicially intact.   I don't know what her subsequent cardiac function was, but that is not the point of this post.

But it could have been a disaster.


This paper has received some press recently:

Safety of Computer Interpretation of Normal Triage Electrocardiograms

The algorithm used was also the GE Marquette 12 SL.

It purports to show that you don't need to read the ECG if the computer says "normal".   That it saves you from pesky interruptions.   Many on Twitter seem to agree.

222 of 855 (26%) were interpreted as normal.  The confidence intervals were 97-100%.  Would you like to be 97% sure you're not missing an emergency?

Neural Networks are coming:

We compared a new deep neural network (DNN) machine learning artificial intelligence algorithm from Cardiologs technologies(DNN) to Veritas conventional algorithm in the interpretation of 1473 ED ECGs:

Veritas: Of 364 ECGs (24% of total) that it interpreted as "normal," is missed 5 emergencies.
DNN: Of 493 ECGs (33% of total) that it interpreted as "normal," it missed 2 emergencies.

As you can see, it had both fewer false positives and fewer false negatives. That is powerful, and it will only get better as it learns from more and more ECGs.
So things will get better as technology advances.

By the way, this deep neural network algorithm does calculate the 3-variable "Smith score" and displays it for the physician.  It did not use machine learning for this task; it was programmed.

Learning Points:

1. It is hazardous to trust the computer, even when it interprets "Normal"
2. I never trust a computer interpretation.  I only look at it after I have read the ECG, and only in order to see if it found something that I overlooked.
3. If the computer says "normal", it takes very little time to confirm this with visualization (at least for me, and anyone can get good at it with practice)
4. Learn to recognize LAD occlusion.  It is not always obvious.  And the computer will not help you.

Here are some previous posts in which the computer interpreted the ECG as "normal."

Chest Pain Diagnosed as Gastroesophageal Reflux

Another case of arrest:

Another case of arrest:

It is easy to be led astray by the computer....

Wednesday, November 8, 2017

Anterior ST Elevation with Elevated Troponin, but with low T/ST ratio, 2 Cases

Case 1

This case was sent by Michael Masias (EMCurious, Twitter handle: @EMedCurious), an ultrasound fellow in the Department of Emergency Medicine at UC San Diego.

He sent this ECG with the following inquiry:  

"What do you think about this? 21 year old with chest pain. I am getting a result of "STEMI" by using the 3-variable formula, and "no STEMI" with the 4-variable."
Computerized QTc = 418

Here was my immediate answer:
"Tough one! There is a very low T/ST ratio. That is to say, the J-point is very elevated in V3 and V4 but without a tall T-wave. That is unusual for both early repol and LAD occlusion, and suggests myo- pericarditis. But I do think it is early repol.  I don't think it is STEMI. Tell me more."

I should also have added that tachycardia does not fit with anterior MI unless there is cardiogenic shock.

More Analysis:
There is ST Elevation in V2-V5 that meets "criteria" for anterior STEMI.
There is over 3 mm of STE (at J-point, relative to PQ jct.) in V3 and V4.
In a 21 year-old, only 2.5 mm in V2 and V3 is required, and only 1 mm in V4.
So there are 2 consecutive leads with STE that exceeds "critieria."

3-variable formula = 24.56 (above 23.4, indicating LAD occlusion)
4-variable formula = 12.96 (very low due to high QRS voltage in V2)
This formula is meant to help differentiate early repol from LAD occlusion.
It does not differentiate other etiologies of STE elevation!

The 4-variable formula is more accurate, but this is not validated.

More information:
"21 year old with 3 days of sharp left sided chest pain. He had a pharyngitis 1.5 weeks prior. He was transferred to me for STEMI but when he arrived he was very comfortable and the tachycardia didn’t fit, in my opinion. So I did a bedside echo and he was hyperdynamic with no signs of heart failure, and all walls looked good to me. I did speak with the interventionalist on call and they thought it was early repol."

Smith comment: this was a very astute evaluation. Anterior MI will not have hyperdynamic cardiac function with excellent ejection fraction!

We recorded another ECG 45 minutes later:
There is less ST elevation now.

"The first troponin I returned at 4 ng/mL. The patient remainded comfortable in the ED and cardiology just recommended observation so I admitted him for formal echo and serial troponins."

"The patient never underwent angiogram, but echo did not show a wall motion abnormality and this rules out STEMI."

Case 2

Medics came into the ED and showed me this prehospital ECG on a 40-something patient with chest pain:
My opinion was that this was normal ST Elevation, not LAD occlusion.

There is ST Elevation in V2-V5.  The STE meets STEMI criteria.
There are prominent J-waves in V4-V6
There is a saddleback in V2
Saddleback STE in V2 is rarely due to MI in my experience.
Computerized QTc was 414 ms.
I did the formulas and came up with values that were quite high, indicating LAD occlusion.

Why do I think it is not STEMI?
Because the ST elevation is more pronounced than the T-wave is hyperacute (low T/ST ratio).  The ST segment is either downsloping (saddleback) or almost flat.  This ST segment shape is a result of the relatively low T-wave voltage.  When a T-wave is tall and large (not this case), the ST segment by necessity slopes steeply upward to the tall T-wave.  When a T-wave has comparatively low voltage, as do these T-waves, the ST segment is relatively flat.

I went to talk with the patient.  He had been having a cough and fever for about a week, and had gone to a clinic for dyspnea 3 days prior.  The pain had been intermittent for the previous 3 days and there seemed to be some positional component to it, but he really could not describe it well and was holding his chest.

We recorded this ED ECG:
Approximately the same.

I was not convinced, even by my formulas.  We sent a troponin I, which returned quite elevated, at 4.80 ng/mL, within an hour of arrival. 

That caught my attention, but I thought, due to the symptoms and the ECG, that this was probably myocarditis. 

I repeated the ECG:
Not much different

I did a bedside echo and was worried for an anterior wall motion abnormality (WMA).

Unfortunately, this is common in myocarditis.  Absence of WMA would confirm myocarditis. Presence of WMA does not differentiate.

However, I was not willing to bet the patient's life on it.  I talked with the interventionalist and we arranged for the patient to go to the cath lab, but did not actually "activate" the cath lab as one would with a STEMI.

A repeat troponin was 4.9 ng/mL

The coronaries were clean.

Next day formal contrast echo was normal.

Diagnosis: myocarditis.

Next day, a friend at another hospital found a previous ECG on this patient:
The same kind of ST elevation was not present previously.
This shows that the findings were NOT due to early repol, but a consequence of myocarditis.

Monday, November 6, 2017

How can you persuade your cardiologist to take a Non-STEMI patient to the cath lab emergently?

This case was sent by Joseph Ryan (@DocJoseph08), chief resident from Corpus Christi's EM residency program.  

This middle-aged patient complained of acute chest pain and called 911.

He had the following 12-lead ECG in the ED at time zero:
There is ST depression diffusely.
This is diagnostic of ischemia.
There is a Q-wave in V2 and a possible hyperacute T-wave.
It is now clear the patient has acute coronary syndrome.
It is not clear that there is, or is not, a complete coronary occlusion.

The patient was treated with aspirin and sublingual NTG on arrival, which did not relieve his pain.

Cardiology was called but they were not interested in taking the patient to the cath lab.

First troponin I returned at 0.65 ng/mL.  This confirms myocardial infarction.

After that, another ECG was recorded one hour after the first one:
The ST depression appears a bit worse.
There is a touch of ST elevation in V2.

The patient had unrelieved pain, so again cardiology was called, but they stated that the case did not warrant emergent angiography, as it "did not meet STEMI criteria."  The resident pleaded with them to take him, but they would not.

He was given Plavix 600 mg, heparin with infusion, and a nitroglycerine infusion.  His pain continued.

2 hours later (3 hours after onset)
Now there is ST elevation in aVL, aVR, and more in V2 (but the T-wave is less hyperacute). 
The ST depression in more profound.
This is very concerning for proximal LAD occlusion.

17 minutes later
About the same

2 minutes later
About the same

6th ECG, only 4 minutes later
Increasing ST elevation in V1, V2, aVL and aVR, with worsening ST depression.

2nd Troponin I returns at 3.34 ng/mL.

At this point, the cardiologist was convinced and the patient went for PCI and had a 100% proximal LAD occlusion opened and stented, with an approximate 4 hour door to balloon time.

Here is the post PCI ECG:
Beginnings of Reperfusion T-waves in V2 and aVL.
These are identical to Wellens' waves, except that there is no R-wave in V2.

And one day later:
Evolution of T-wave inversion

Echo was performed right after cath lab and showed:
1.  Left ventricular systolic function is impaired.  Left ventricular ejection fraction is 40-45% with anteroapical akinesis. 
2.  Concentric left ventricular hypertrophy.
3.  Mild mitral insufficiency.

Peak Troponin I was over 50 (they do not quantify above that.)

Peak Troponin T was 4.50 (this correlates with a very large myocardial infarction)

Smith commentary:

Learning Points

1. The purported dichotomy between STEMI and Non STEMI is a false one.
2. Patients without ST elevation, or with ST elevation that does not meet diagnostic "criteria,"  may have total coronary occlusion and may have a lot of myocardium at risk, which may infarct without immediate treatment.  This patient had a very large anterior infarction but never, even after 3.5 hours, was there ST elevation that met diagnostic "criteria."
3. Both the American Heart Association/American College of Cardiology guidelines (1) and the European Society of Cardiology Guidelines (2) recommend less than 2 hour intervention on patients with refractory angina from ACS.  I have quoted those documents below.

Also: if you think that this represents Left Main occlusion, you are incorrect.  Read this post, which explains all: STE in aVR, with diffuse ST depression, does not represent left main occlusion 

Anecdotally, by my conversations and emails with people all over the world, this recommendation appears to be ignored by many cardiologists/interventionalists.  Why is it ignored?  One reason, I believe, is a misunderstanding of the results of randomized trials of emergent vs. delayed, angiography and PCI for NonSTEMI.  It is erroneously believed that these trials were negative.  However, patients with refractory pain were excluded from these trials.  In the largest such study, the TIMACS trial in NEJM (3), they found no difference between "immediate" and "delayed" angiography and PCI except for in patients with a high GRACE score of 140 or more.  But "immediate" was a mean of 16 hours, which is not immediate!  Furthermore, they excluded patients with ongoing chest pain; this exclusion was not stated in the methods.  But I know they excluded these patients because I emailed the first author, Dr. Mehta, and he replied that "I doubt investigators would have enrolled pts with ongoing CP in this NSTEACS trial."

Many readers of this blog, and providers who attend my ECG talks, ask me:

"How can I get my interventionalist to take these patients to the cath lab?"

My answer:

Tell them "Your own guidelines state that these patients with refractory pain should go within 2 hours."

The only caveat is that you must be certain that the symptoms, ECG findings, and elevated troponin are due to acute coronary syndrome, and not another etiology of type II MI, such as hypotension, tachy- or bradycardia, anemia, aortic stenosis, hypoxia, etc.

Guideline quotes


4.4.4. Early Invasive and Ischemia-Guided Strategies: Recommendations
Class I
1. An urgent/immediate invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients (men and women) with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures) (42, 44, 138, 338). (Level of Evidence: A)

European Society of Cardiology:
5.6.3 Timing of invasive strategy Immediate invasive strategy (less than 2 hours):
Very-high-risk NSTE-ACS patients (i.e. with at least one very-high-risk criterion: hemodynamic instability, Recurrent or ongoing chest pain refractory to medical treatment, life threatening arrhythmias or cardiac arrest, mechanical complications of MI, acute heart failure, recurrent dynamic ST-T wave changes, particularly with intermittent ST elevation) according to Table b) have been generally excluded from RCTs.  Owing to a poor short- and long-term prognosis if left untreated, an immediate (i.e. less than 2 h from hospital admission, analogous to STEMI management) invasive strategy with intent to perform revascularization is recommended, irrespective of ECG or biomarker findings.


1.  Roffi M, Patrono C, Collet JP, et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). European heart journal 2016;37:267-315.

2. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;130:e344-426.

3. Mehta SR, Granger CB, Boden WE, et al. Early versus delayed invasive intervention in acute coronary syndromes. The New England journal of medicine 2009;360:2165-75.

Friday, November 3, 2017

12 Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

Here are 12 Cases using the 3- and 4-variable formulas, which help to distinguish normal ST elevation in leads V2-V4 from that of subtle LAD occlusion.

Instructions for using free subtleSTEMI iPhone app for the 3-variable formula.  4-variable version still to come.

Here is a video lecture of subtle LAD occlusion: One hour lecture on Subtle ECG Findings of Coronary Occlusion

The 3-variable formula comes from this paper:

It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. Thus, there must be ST Elevation of at least 1 mm in any of leads V2-V4. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves, or ST Elevation of 5 mm or more), then the formula MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI.
--QTc is the computer measurement.
--RAV4 = R-wave amplitude, in mm, in lead V4.
--ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PR segment, in millimeters.

Formula: (1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).
A value greater than 23.4 is quite sensitive and specific for LAD occlusion.
A value greater than 22.0 is more sensitive, has fewer false negatives, but specificity drops to 80%.

4-variable formula (slightly more accurate than 3-variable):

Uses the same measurements, but adds the total QRS amplitude (both R- and S-waves) in lead V2:

Formula: (1.062 x STE at 60 ms after the J-point in V3 in mm) + (0.052 x computerized QTc) - (0.151 x QRSV2) - (0.268 x R-wave Amplitude in V4 in mm).
A value greater than 18.2 is quite sensitive and specific for LAD occlusion.

The 4-variable formula is based on this paper:  

Driver, BE et al.  A new 4-variable formula to differentiate normal variant ST segment elevation in V2-V4 (early repolarization) from subtle left anterior descending coronary occlusion - Adding QRS amplitude of V2 improves the model.  J Electrocardiology 50(5):561-569; September/October 2017.

Go here to find excel applets. you enter the

Case 1

Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)?

This is the initial ED ECG of a 46 year old male with chest pain:
The QTc was 420
ST Elevation at 60 ms after the J-point in lead V3 = 2.5 mm
R-wave amplitude in V4 = 2
QRS V2 = 19 mm
3-variable formula = 27.11 (above 23.4, consistent with LAD occlusion)
4-variable formula = 21.09 (above 18.2, consistent with LAD occlusion)
This patient was misdiagnosed with normal variant STE.  He was admitted for a "rule out MI." He ruled in for acute MI with a peak troponin I of 130 ng/mL.

Next day angiogram showed a 100% proximal LAD occlusion.  He had a convalescent anterior wall motion abnormality.

Case 2

Acute MI from LAD occlusion, or early repolarization?

The QTc was 455
ST Elevation at 60 ms after the J-point in lead V3 = 3.0 mm
R-wave amplitude in V4 = 17
QRS V2 = 16 mm
3-variable formula = 24.89 (above 23.4, consistent with LAD occlusion)
4-variable formula = 19.87 (above 18.2, consistent with LAD occlusion)

This was not recognized, repeat ECG at 69 minutes showed new Q-waves in V2-V4 that were not appreciated, and patient waited for a prolonged period in the emergency department before STEMI was diagnosed.

100% LAD occlusion.

Case 3

I was reading a stack of ECGs yesterday, and saw this one, with no clinical information....

The QTc was 400
ST Elevation at 60 ms after the J-point in lead V3 = 1.5 mm
R-wave amplitude in V4 = 4.0
QRS V2 = 22 mm

3-variable formula = 24.1 (above 23.4, consistent with LAD occlusion)
4-variable formula = 18.0 (below 18.2, consistent with Normal STE)
The 3-variable formula is positive, but because of a 22 mm QRS in V2, the 4-variable formula is barely negative.  Whenever the value comes close to the cutoff, it is very hazardous to call it negative.  Appropriately, the physicians repeated the ECG 20 minutes later and it was diagnostic of anterior STEMI.

100% LAD occlusion.

Case 4

Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 ng/ml)

A 45 year old male called 911 for chest pain:
The QTc was 400
ST Elevation at 60 ms after the J-point in lead V3 = 3.5 mm
R-wave amplitude in V4 = 13
QRS V2 = 18 mm

3-variable formula = 23.54 (above 23.4, consistent with LAD occlusion)
4-variable formula = 18.315 (above 18.2, consistent with LAD occlusion)

It was not diagnosed. Fortunately, it spontaneously reperfused and subsequent ECGs show resolution of ST Elevation.  All troponins were below the level of detection.

Angiogram showed a critical LAD thrombotic stenosis.  He underwent CABG.

Case 5. False Negative for both formulas.

Male in early 40's with 1.5 hours of chest pain

This was sent to me for my interpretation without clinical data:
This was my response: 
"Tough one.  Probably is acute LAD occlusion, needs serial ECGs/echo."


The QTc was 410
ST Elevation at 60 ms after the J-point in lead V3 = 2.5 mm
R-wave amplitude in V4 = 14
QRS V2 = 16 mm
3-variable formula = 22.6 (below 23.4, consistent with normal STE)
4-variable formula = 17.8 (below 18.2, consistent with normal STE)
At a cutoff of 23.4 (my typically recommended cutoff), the sensitivity for LAD occlusion among subtle cases is 86% (much higher if all LAD occlusions are used as the denominator), with a specificity of 91%.

At a cutoff of 22.0, the sensitivity was 96% but with decreased specificity of 81%.  I get worried about any value greater than 22.

To me, the T-waves looked too fat to be normal.  And even though the formula was not greater than 23.4, at 22.6 or 23.2, it is close enough to be worried.

At 7 hours after presentation, after several positive troponins, the patient went for an angiogram and had a 100% LAD occlusion.  Peak Troponin T was very high at 2.11 ng/mL.

Case 6.

A 75 year old woman who complains of "Reflux."

Incredible Case Demonstrating the Value of Frequent Serial ECGs

The QTc was 400
ST Elevation at 60 ms after the J-point in lead V3 = 2.5 mm
R-wave amplitude in V4 = 4.5
QRS V2 = 6 mm
3-variable formula = 25.12 (above 23.4, consistent with LAD occlusion)
4-variable formula = 21.17 (above 18.2, consistent with LAD occlusion)
This prompted serial ECGs:
These dynamic changes confirmed ACS

There was a large obtuse marginal 100% occlusion (surprisingly not LAD!  But, in reality, the formula only tells you that the wall under leads V2-V4 is involved; it cannot actually specify the artery involved).

Case 7.

A 60 year old male had resolving chest pain
There is minimal ST elevation and there are subtle T-wave inversions in V2-V5, highly suggestive of Wellens' syndrome.  
Is the ST Elevation normal? Very low R-wave amplitude suggests NOT.  See formula here:

The QTc was 380
ST Elevation at 60 ms after the J-point in lead V3 = 1.5 mm
R-wave amplitude in V4 = 2.5
QRS V2 = 15.5 mm
3-variable formula = 23.4 (equals cutoff of 23.4, consistent with LAD occlusion)
4-variable formula = 18.34 (above 18.2, consistent with LAD occlusion)
So this, along with the resolving chest pain, appears to be a reperfusing LAD occlusion.

In Wellens' syndrome, the artery is open.  T-wave inversion is indicative of reperfusion of the infarct-related vessel.

BP was elevated, pulse lowered to 45.  He received ASA, Plavix 600mg, Heparin, and a Nitro drip.

Another ECG 15 minutes later, pain free, had more T-wave inversion.

Then 15 minutes after that, the pain recurred and the T-waves pseudonormalized.  The ST elevation remained subtle, but the formula value was even higher.

The patient went to cath and had a distal LAD 99% stenosis with thrombus and TIMI-2 flow.

Initial troponin I returned at 1.5 ng/ml.  Peak was 8.1 ng/ml.

Case 8.

Formula positive for LAD occlusion. But echo shows no wall motion abnormality! What is it?

A 35 year old male complained of chest pain:
The QTc was 405
ST Elevation at 60 ms after the J-point in lead V3 = 4.0 mm
R-wave amplitude in V4 = 12.5
QRS V2 = 12.5 mm

3-variable formula = 23.95 (above 23.4, consistent with LAD occlusion)
4-variable formula = 19.53 (above 18.2, consistent with LAD occlusion)

This was sent to me without any clinical information, asking for my opinion.  I was worried about LAD occlusion. The clinicians thought it was normal, but due to elevated troponins, thought it was myocarditis.  There was no wall motion abnormality.  After many hours, the decided that it was appropriate to do an angiogram and they found a distal LAD occlusion which was opened and stented.

100% distal LAD occlusion.

Case 9.

Patient presentation is important

This was a 60-something with acute chest pain:
There is sinus bradycardia at a rate of 44. 

There is 2 mm of ST elevation in V2 and V3 (at the J-point, relative to the PQ junction), which is below the "criteria" for men under 40 (2.5 mm). 

There is upward concavity
There is no ST depression
There are no Q-waves
There is no terminal QRS distortion

So early repolarization is a possibility.

The cardiologists were not impressed by the ECG.

However, there is very suspicious STE in III and aVF, with ST depression in aVL.    To me, this makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III and aVL, so it is a bit confusing.  Unless you consider a wraparound LAD to the inferior wall. 

There is also an upright T-wave in V1, larger than V6.  This is a very soft sign of LAD occlusion, and did not add any diagnostic improvement over our formula model for diagnosing LAD occlusion vs. early repol.  In that study, this finding was present in 39% of LAD occlusion and 15% of early repol.

The measurements are:

RA V4 = 6.5
STE60V3 = 3.0
QRSV2 = 12.5
QTc = 362 ms

The formula values are thus:

3-variable: 22.83 (less than 23.4; the most accurate, but not most sensitive, cutoff).  I still worry when the value is above 22.0 (still misses 4% of LAD occlusion when below 22.0)

4-variable 18.38 (greater than 18.2; the most accurate, but not most sensitive, cutoff). So this is strongly indicative of LAD occluson.

Computerized QTc = 362 ms (this is VERY short for LAD occlusion, but is so short because of correction for slow heart rate; the measured QT was 413 ms.)  This is the main reason the formula value is not very high.

Thus, the ECG is early repolarization by the old 3-variable formula and is LAD occlusion by the new one.

Even though the ST Elevation is not diagnostic, and T-waves of this size can be seen in early repolarization, but low QRS and R-wave amplitude is not. 

The inferior ST findings also make this ECG diagnostic.

In case you were wondering about the T-waves and bradycardia, the K was normal.

Why bradycardia?  Think about that inferior ST elevation.  Maybe there is also inferior MI from wraparound LAD with associated sinus bradycardia.


The cath lab was activated by the emergency physician. The patient had a 100% LAD occlusion and a peak troponin I of 51 ng/mL.  

Case 10.

A 50-something with chest pain and minimal precordial ST elevation

This ECG was recorded at 1350, with pain decreasing after nitroglycerine:
There is 1 mm of ST elevation at the J-point in both V2 and V3 (within normal limits). 
Computer interpretation is normal
Cardiologist overread is normal
What do you think?

More description: There is also poor R wave progression, with small R waves in V4. The T waves are slightly broad and large, but probably could not be called hyperacute. There is minimal STD in aVF.

One of our interns had texted this ECG-1 to me, with the message:

"3 hours of chest pain, QTc = 415 ms, 3 variable formula is 25.3.  What do you think?"

[The 3-variable formula for differentiating normal variant ST elevation from the ST elevation of subtle LAD occlusion can be accessed by clicking on the link at the top of the page and entering the values into the online excel applet.  Values are: 1. ST elevation at 60 ms after the J-point in lead V3.  2. R-wave amplitude in V4. 3. computerized QTc.  See also the free iPhone app "SubtleSTEMI".  See also MDcalc.]

A value greater than 23.4 is very worrisome for LAD occlusion.

[The 4-variable formula adds the entire QRS amplitude in lead V2 and is more accurate than the 3-variable formula.  It is: (1.062 x STE at 60 ms after the J-point in V3 in mm) + (0.052 x computerized QTc) - (0.151 x QRSV2) - (0.268 x R-wave Amplitude in V4 in mm).  It can also be accessed at the top of the page, with value entry into the excel applet.]

The publication of the formula can be found here: A new 4-variable formula

A value greater than 18.2 is quite sensitive and specific for LAD occlusion. 

The calculated value was 19.2 (highly suggestive of occlusion)

I suggested serial ECGs, which were done as the patient had diminishing pain after nitroglycerine:

Here are the successive ECGs, V1-V3
The first image is of an earlier ECG, of which the providers were unaware.

                   1300               1350, pain decreasing               1430                  1700, pain free       1800, still pain free
This shows that the T-waves (which never were quite hyperacute), are deflating and may have been hyperacute prior to arrival.


The third troponin I, drawn 4.5 hours after presentation, returned at 4.2 ng/mL.

The patient went for angiogram and had an 80% mid-LAD thrombotic stenosis and proximal LAD disease, as well as a 90% diagonal lesion.  He went for Coronary bypass (CABG). 

This outcome is perfectly consistent with all the ECGs.

Learning points:

1. Pay attention to diminishing T-wave amplitude during diminishing pain.

2. The formulas are very accurate.  I have always thought that I can do better than my formulas, but now I'm in doubt.

3.  Some patients have near zero ST elevation at baseline. Any ST elevation in these patients is abnormal.  In such patients, LAD occlusion may result in very subtle ST elevation.

Case 11.

A Male in his 40's with Decreasing Chest pain - what do you think?

A male in his 40s presented with decreasing chest pain.  Here was his first ECG:
There is sinus rhythm. 
The QTc is 379 ms. 
There is ST elevation in V2-V4 that does not meet STEMI "criteria" of at least 1 mm in 2 or more leads (except V2 and V3, which require 2.0 mm of more for men over age 40).

So it looks like early repolarization. 
The clinicians used the subtleSTEMI formula.  I am not sure exactly what numbers they used, but they told me the value they arrived at was 21.2.

Let's examine that:
The computerized QTc was 379 ms.
The R-wave amplitude in lead V4 is from 11-14 mm, depending on the complex used.
Here is a magnification of V3 in order to measure ST elevation at 60 ms after the J-point in lead V3:
The black arrow shows the J-point.  The red arrow is at 60 ms (1.5 small boxes) after the J-point.  The lower edge of the upper green line is where one should measure from.  The upper edge of the lower green line is at the PQ junction.  The distance between these two is 4 mm.  Some might say 3.5 mm

If we put these values into the formula, using QTc of 379, we get 6 different values depending on the measurements:

                                   RAV4 = 11 (min)                     RAV4 = 12.5 (avg)                  RAV4 = 14 (max)
STE = 3.5 mm                   22.96                                       22.5                                             22.0

STE = 4.0 mm                   23.56                                       23.1                                             22.6

Only one of these 6 values is very specific for LAD occlusion (23.56, greater than 23.4)

All the rest are greater than 22.0, above which one should definitely be worried and get serial ECGs.

QRS V2 = 15.5 mm; the 4-variable formula is at the very least 17.6 and at most 18.9. With the most accurate cutpoint at 18.2, this is also ambiguous.

So a second ECG was recorded 12 minutes later:
QTc is now 383 ms.  STE 60 V3 = 2.5 mm.  RAV4 = 11-12 mm. 
3-variable formula = 21.7
4-variable formula = 17.0
Thus, values of both have fallen
Formula value is now slightly lower. 

These two ECGS are significantly different, but it was not noticed the treating physicians.

Look at the ECGs side by side.  And remember the pain is waning.
The first is on the left, the follow up is on the right.
The T-wave amplitude in V3 is 10 mm on the earlier and only 7 mm on the later one.
This changed the ST elevation at 60 ms after the J-point from 4.0 to 2.5.

This makes it almost certain that the ST elevation on the first one is due to ischemia.

Although the clinicians were uncertain and obtained a very low formula value for both, they were worried about the patients symptoms and appropriately activated the cath lab.

The angiogram showed a 99% thrombotic occlusion with TIMI-II flow (enough coronary flow to prevent outright ST elevation).

It is probable that the artery was fully occluded at the time of maximal chest pain.

Learning Points:
1. Hyperacute T-waves diminish in size as the artery reperfuses
2. The formula is more likely to be falsely negative when there is a reperfusing artery.
3. A value less than 23.4 but still greater than 22.0 may still be due to LAD occlusion or near-occlusion.
4.  Serial ECGs are critical but they must be scrutinized for changes, which may be very subtle (see below).

This was a 30-something woman with bilateral trapezius pain.
There are hyperacute T-waves
There is 1 mm of STE in V3, so the formula can be used to find if this is normal STE or not
QTc is 444 ms.
STE 60 V3 = 1.5 mm, R-wave amplitude V4 = 15 mm
Formula value is 23.1, which is close to being an LAD occlusion value of 23.4.  It is below the cutoff of 23.4, but above my safe value of 22.0

4-variable formula value = 19.38 (consistent with LAD occlusion)
The QRS amplitude in V2 is very small for early repolarization, and that is why the formula gets this right.

This was missed by the physicians, even with a bedside speckle tracking ultrasound: no wall motion abnormality was seen.

The first troponin I was below the level of detection.

She was admitted for rule out MI, but the 2nd troponin was elevated, so she had another ECG recorded: 
This demonstrates what normal T-waves look like for this patient, and that she has zero ST elevation at baseline.
Fortunately for her, the artery had spontaneous repefusion.  '


She went for angiogram immediately after this and had a thrombotic LAD that was open with TIMI-3 flow.  It was stented.

Case 10.

A 25 year old with Epigastric Discomfort, Worse Supine, Better Sitting Up.

STE60V3 = 2.5 mm
 computerized QTc = 437 
(notice how it lengthened from the earlier values of 372 and 402 ms!)
R-wave amplitude V4 = 9 mmQRS = 26
3 variable formula = 25.839 (greater than 23.4 is all but diagnostic of LAD occlusion)
4-variable formula = 19.0 (greater than 18.2 is all but diagnostic of LAD occlusion)

The cath lab was activated, and angiogram showed a 90% distal LAD lesion with thrombus.  The post PCI ECG showed reperfusion T-waves.  

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