New STEMI in the same location as previous Q-wave MI may also have deep QS-waves,

but also has tall T-waves and an increase degree of STE.

In contrast to LVA, patients with acute STEMI who have Q-waves have a larger T-wave. See
figure 5 for an example of a patient with QS-waves but with hyperacute T-waves, such that the
T/QRS ratio is high. It was an acute LAD occlusion.

Figure 5. There are QS-waves as one would see in LV aneurysm, but there are large T-waves, as
is seen in acute STEMI. The T/QRS ratio is high. It was an acute LAD occlusion.
29 year old, healthy, with pleuritic chest pain

A 29 year old male presented with 6 hours of stuttering chest pain, constant for the last hour,
worse with breathing. He had no medical history.

What is the diagnosis?

Diagnosis: There are Q-waves, ST elevation, and hyperacute T-waves in V2 and V3, diagnostic
of acute LAD occlusion (STEMI).

Take home point here: Obtain an ECG on anyone with chest pain. Sometimes you will find an
obvious STEMI.

Clinical Course: He was taken for immediate PCI of a 100% LAD occlusion with thrombus;
door to balloon time was less than 60 minutes and symptom onset to balloon time was
approximately 2 hours.

Nevertheless, he suffered a large infarction with peak troponin of 110 and the following ECG the
next AM:

There are now deep QS-waves, with persistent ST elevation in precordial leads. The shallow T-
wave inversion is typical of completed transmural infarction, and contrasts with the deep T-wave
inversion seen with quick reperfusion of an MI with much remaining viable myocardium.

He did not regain his R-waves after reperfusion. Whether he will do so over the next months or
not is uncertain now. He has persistent ST elevation. This may resolve over a couple weeks; if
it does not, then he is at high risk of developing an LV aneurysm, or diastolic dysfunction of the
anterior wall. He is also at risk of a mural thrombus.

Q-waves in acute MI:

1) QR-waves are common early in anterior MI.

2) QS-waves are uncommon early in anterior MI; they are common in late presentation.

3) Q-waves are independently associated with worse outcomes (78% relative increase in 90-day
mortality in Armstrong et al.)

4) Q-waves alone do not necessarily imply irreversibly infarcted myocardium; they should not
dissuade from reperfusion therapy.
Classic LV aneurysm (persistent ST elevation after previous MI)

70 yo with h/o MI, recent CABG, has acute onset of chest pain.

What are the worrisome EKG findings, and what is the differential diagnosis? What is the most
likely diagnosis? What info would you like to have to make a decision?

Answer

There are deep QS waves in V1 and V2, and tiny R-waves in V3 and V4. With ST elevation in
V1-V3, one must always entertain the possibility of acute MI in this patient with CP. The
differential is wider, however, and mostly includes "old MI with persistent ST elevation,"
otherwise known as "left ventricular aneurysm morphology". This morphology is very common
after an old and completed or nearly completed anterior MI. By complete, that is to say that there
was no early reperfusion (spontaneous or therapy related). It was, in the old terminology, a
"transmural" infarction. More accurately, there was a substantial mass of myocardium that died
(infarcted, meaning irreversibly). Very often, such large anterior MI result in persistent ST
elevation and they may or may not have a demonstrable "LV aneurysm" by echo.
Echocardiographically, this is called "diastolic dyskinesia", meaning that the infarcted territory is
thinned out and bulges even in diastole. Much of the time, there is only "akinesis", meaning no
contraction of that territory. The important point is that old MI frequently has persistent ST
elevation.

This is an example of "old MI with persistent ST elevation". So how do you differentiate old MI
from acute MI? First, there are deep QS waves. Although anterior MI may have Q waves very
early after onset, these are always QR waves (Q waves followed by an R-wave). The fact that
there are zero anterior forces should lead you to think that there is no remaining anterior wall left
to infarct. Second, in acute MI, as long as there is significant viable myocardium, the T wave is
usually upright; remember that acute MI has large T waves. Lastly, acute infarction should have
not only an upright T wave, but a prominent one. The "hyperacute T wave" is not simply a
phenomenon of early infarction; it is simply more visible early on.
If you want a rule, I derived one a few years ago (AJEM 23(3):279-287; May 2005). Comparing
proven acute LAD occlusion to patients with proven old MI and diastolic dysfunction and ST
elevation, I found that the T/QRS ratio in any one of leads V1-V4 was almost always higher than
0.36 in acute MI, and almost always lower in LV aneurysm. Better was a T amplitude
(V1+V2+V3+V4) / QRS amplitude (V1+V2+V3+V4) <> 0.22. The only acute MI's missed by
this rule had at least 6 hours since symptoms onset.

I cannot tell from this ECG if it is 12 hours or 12 years since the MI. But looking through the
records, I found that he had an old anterior MI with anterior apical akinesis.

He did have improvement of pain on a nitro drip, so we admitted to the CCU. He ruled out for
MI.
Stuttering thrombus in the LAD, dynamic hyperacute T-waves, Q-waves, full resolution at
3 months

A 70 y.o. woman who presented with L arm pain that started at 6:45 in the morning when she
woke up. Pain was also in the upper back with some discomfort in the L chest. Described as
"Achy" pain. She initially thought she must have slept wrong. No associated SOB, diaphoresis,
or dizziness. No similar pain previously. No h/o CAD. She sat and rested but the pain got
stronger, so she took 2 ASA. She felt a little "clammy." The pain went away after ~15 min. She
lay down for ~20-25 min and while lying down the pain returned and persisted x 10 min prior to
resolving again. She called 911.

She was pain free when the medics recorded 3 ECGs over 40 minutes. They all were similar to
the first:

V6 is missing. There are Q-waves in leads V3 and V4, with ST elevation and a large T-wave.
Normally, one might think this ST elevation and T-wave is early repolarization, but early repol
like this should 1) not occur in a 70 yo woman 2) never have Q-waves. Therefore, this is old MI
with acute ischemia or acute STEMI.

In the ED she was pain free. This was her ECG at presentation:

QTc 442 ms. The T-waves in V3 and V4 are still large, but definitely smaller than in the
prehospital ECGs. This is typical of hyperacute T-waves during reperfusion. You can compare
the T-waves with her baseline (next ECG below). Additionally, there are new Q-waves in V2
and V3.

These ECG indicate that, at the time the patient was having pain, her LAD was occluded or
nearly occluded. Old ECG from 3 years prior:

QTc 405 ms. Normal previous ECG. No Q-waves. No ST elevation. No large T-waves.

So the patient has a spontaneously reperfused LAD. Antiplatelet and antithrombotic therapy was
begun.

At 113 minutes after presentation (first troponin was less than 0.04):

QTc 447 ms. T-waves continue to diminish. Q-wave in V2, V3.

Just before cath, time = 240 minutes:

QTc 447 ms. T-waves very diminished now

Here is a composite of V4-V6 from previous to prehospital to ED:

2 hours after LAD intervention (80% stenosis with hazy LAD thrombus):

QTc 450. T-waves begin to invert. If this was the first ECG you had recorded in the ED, it
would be Wellens' syndrome.

Next Day. Troponin I peaked at 2.28 mcg/L. The septum, anterior wall, and apex are akinetic
on echo (myocardial stunning):

T-waves evolve to become deeper and more symmetric

3rd day, 48 hours.

T-wave evolution continues

6th day, 120 hours: Normal echocardiogram now:

T-wave evolution continues

7 weeks later:

R-waves present, T-wave inversion gone

3 months later:

Complete recovery of ECG

Summary:

1) With a large amount of myocardium at risk, there is a large wall motion abnormality

2) Hyperacute T-waves are a sign of a large amount of myocardium at risk and that it is still
viable

3) With minimal actual myocardial cell death (infarction), as shown by a low peak troponin, the
myocardium will recover:

a) The myocardial function (as shown by echo) will recover (this may take weeks)

b) The ECG will recover (this may take months, as in this case).
Dyspnea, resp failure, DNR/DNI, what to do?

79 yo patient with no known previous history of MI and a history of severe dementia presented
with acute dyspnea, pulmonary edema, BP 110/70 and tachycardic, requiring noninvasive
ventilatory support. CXR confirmed pulmonary edema. Bedside echo showed severe anterior
wall motion abnormality and very poor EF. Here is the ECG:

Obvious Acute Anterior STEMI. There are wide and deep Q-waves, with some R-wave
preservation (QR-waves). Is this previous MI with persistent ST elevation (LV aneurysm
morphology)? No! The presence of an R-wave makes this very unlikely. More important, the
T/QRS ratio is very high. We have shown that a high T/QRS ratio is very unlikely in LV
aneurysm. Only acute MI has such a ratio. However, subacute MI (duration > 6 hours
commonly has a low T/QRS ratio). It is also possible that this is an acute STEMI superimposed
on old MI.

A previous ECG was found from 3 years prior:

No evidence of anterior MI

After exhaustive inquiry, it was determined definitively that this patient would not want to be
intubated under any circumstances. He could not undergo PCI without intubation and paralysis.
We considered fibrinolytic therapy, heparin, GP IIbIIIa inhibitors, but decided to give aspirin
alone.

Interestingly, the next AM he was much better, he was no longer SOB, his troponin peaked at
only 2.7 ng/ml. A formal echo showed severe anterior wall motion abnormality with dyskinesis
and EF of 15%. Dyskinesis usually implies LV aneurysm and is unusual in acute STEMI, so it is
quite possible that he had a previous undiagnosed anterior MI since 2008, and that he now has a
superimposed STEMI.

He never had a subsequent ECG, but I can only surmise that he had spontaneous reperfusion
(occurs in up to 25% of STEMI). If he indeed underwent reperfusion, and does not re-occlude,
his ejection fraction will mostly recover.

When we are certain that our therapy saved the patient, cases like this should give us a bit of
humility!
A 50-something male with Dyspnea

A middle-aged male presented with dyspnea. An ECG was recorded.

What is going on? See below.

There is sinus rhythm. There is notable ST depression in V1-V4, maximal in V2 and V3. At
first glance, it appears to be a posterior STEMI.

But one must always read ST and T-wave abnormalities in the context of the QRS. There is a
large R-wave in V1-V3. One can see a large R-wave in posterior MI, and so one feels as if one's
first impression is confirmed.

However, Right ventricular hypertrophy (RVH) also results in large right precordial R-waves
and secondary ST and T-wave abnormalities that mimic ischemia.

One should always look for an S-wave in lead I. And there it is. There is right axis deviation.
All this is strongly suggestive of RV hypertrophy.

So a cardiac ultrasound was done:

-Pulmonary hypertension: The estimated pulmonary artery systolic pressure is 72 mmHg + RA

pressure.

-Right ventricular enlargement .

-Decreased right ventricular systolic performance .

-Right atrial enlargement but the inferior vena cava is small in size.

-Left ventricular hypertrophy concentric .

-The estimated left ventricular ejection fraction is 75 %

--There is no left ventricular wall motion abnormality identified.

The patient ruled out for MI.

Also, the the workup for PE was done and was negative. Etiology was airway disease. McGinn
(S1Q3T3) is present here but is a very soft sign of PE. In a large group of dyspneic patients
worked up for PE, those without PE had a 3% incidence of S1Q3T3 and those with PE had an
incidence of 8%, for very low positive and negative predictive values. Also, PE does not give
large R-waves in right precordial leads.

Learning Point:

1. Abnormal ST elevation and/or depression, and/or T-wave inversion (abnormal

repolarization), may be primary (due to ischemia, for instance), or these may be secondary to
abnormal depolarization (an abnormal QRS, such as LVH, RVH, LBBB, RBBB, and others).
Thus, one must always closely examine the QRS to be certain that it does not harbor
abnormalities that explain the repolarization abnormalities.

2. Right ventricular hypertrophy often results in right precordial ST depression and T-wave
inversion that mimics ischemia. In particular, it mimics posterior STEMI.
This shows diffuse ST depression (diffuse subendocardial ischemia) in leads I, II, aVF an V3 to
V6, with reciprocal ST elevation in aVR and V1. This is diagnostic of subendocardial ischemia
or injury.
Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-
equivalents.

Here are some basic concepts before we get into the ECGs:

 STEMI and NonSTEMI are arbitrary terms that may confuse the clinician.
 "STEMI" should mean "coronary occlusion" (or near occlusion, without good collateral
circulation -- in other words, it needs thrombolytics or emergent angiogram with PCI).
 NonSTEMI should mean "MI without occlusion."
 "STEMI-equivalent" is a good term for "coronary occlusion".
 Many STEMI-equivalents have no significant ST elevation, as you may have seen from
many of my posts.
 In some STEMI-equivalents (posterior STEMI, lateral STEMI, posterolateral STEMI),
ST depression is the only, or most visible, feature of the ECG.
 So how do we tell if ST depression represents a STEMI-equivalent or
NonSTEMI/subendocardial ischemia?
 As I see it, there are 5 primary patterns of ST depression. I outline them below and
demonstrate them to show which are STEMI equivalents and which are NonSTEMI.
 NonSTEMIs/subendocardial ischemia may need immediate angiogram and PCI (or
emergent CABG) if the patient is hemodynamically unstable or if the ischemia (as
measured by chest pain and ECG findings) cannot be controlled medically (aspirin, GP
IIb IIIa inhibitor, antithrombotic, nitroglycerin).
 NonSTEMIs should never get thrombolytic therapy.
 Clopidogrel should probably be avoided in NonSTEMIs that have a high likelihood of
needing CABG (ST elevation in aVR)

ST elevation axis (vector) is the opposite of the ST depression vector, though not necessarily the
same magnitude (millivolts or millimeters). Once you understand this, it makes everything
simple. It is worth a few moments to concentrate and learn it.

First, there are countless ways ischemic ST depression (STD) presents. Check here, for
instance.

But I like to classify 5 primary STD patterns in ACS in which there is ST depression without any
significant ST elevation. Some are STEMI-equivalents, and some are Non-STEMI. The
diagnosis depends on the ST axis. Which direction does ST elevation go? Sometimes it is better
to ask: what is the opposite of the ST depression vector?
If the ST depression is directly anterior (V1-V4), then the ST elevation axis is directly posterior,
and there is a high likelihood of posterior STEMI.

If the ST depression vector is inferior and leftward, there is a lot of ST depression in inferior and
left lateral leads, and corresponding ST elevation in aVR (superior and rightward), towards the
base (top) of the heart. (There may also be ST elevation in right sided leads but NOT due to RV
MI). Unless there is a concomitant anterior STEMI (high occlusion resulting in STEMI of
anterior and basal walls), STE in aVR is not a STEMI in lead aVR; rather the STE in aVR is
reciprocal to a leftward and inferior ST depression axis caused by diffuse subendocardial
ischemia.

Thus, an ST elevation axis that is anterior, posterior, inferior, or left lateral is likely to be a
STEMI-equivalent. Anterior-Superior axis (anterior STE + V1 and aVR) is also STEMI

An ST axis which is rightward (ST depression V3-V6) or superior (ST elevation in aVR) is
likely to be a NonSTEMI.

In all this, it is important to realize that ST depression does not localize subendocardial
ischemia. On the other hand, reciprocal ST depression does help to localize the area with ST
elevation. For instance, if there is ST depression in V4-V6, it does not necessarily mean that the
ischemia is of the lateral wall. The ischemia might be in that location, but not necessarily.

This is a mystery I cannot explain, but has been proven by comparing ECG findings to
angiography.

Examples

1. Severe subendocardial ischemia, nonlocalized: Diffuse ST depression, including leads I, II,

aVF, III, V3-V6, with STE in aVR. This one was severe acute left main stenosis. One might
also find this in severe 3 vessel disease with ACS.

A patient who lives through Left Main Occlusion is not common. Acute left main ACS with
critical stenosis is the much more common issue, and this causes subendocardial ischemia. So
no thrombolytics. Both severe 3 vessel ACS and acute left main ACS are likely to need CABG
and thus you might want to avoid clopidogrel. So the fact that 3 vessel ACS and left main
cannot be differentiated on the ECG is not so important.
ST elevation is in aVR. The ST axis is towards aVR, but this does not mean there is STEMI in
aVR! Instead, this elevation is reciprocal to global subendocardial ischemia with the negative
ST axis inferior and lateral, towards the apex (I, II, aVF, III, V3-V6). There is no occluded
artery here. There is no STEMI. The precordial ST depression is not maximal in precordial
leads V1-V4, therefore there is no posterior ST axis and no posterior STEMI.

2. Isolated posterior STEMI: Leads V1-V4 primarily

ST depression is limited to precordial leads and is maximal in V2-V4 precordial leads. Thus the
ST axis is posterior.

Posterior ECG: Leads V4-V6 replaced by leads V7-V9:

ST elevation in V7-V9 confirms posterior STEMI. There was a circumflex occlusion.

3. Posterolateral STEMI: Precordial leads V1-V3 +/-V4 with STD in II, III, aVF, but no ST
depression in I and minimal STE in aVL

Example 1:

The ST axis is away from inferior and anterior leads, and so is posterior and superior. With a bit
of ST elevation in aVL, it is also lateral.

Example 2:

There is ST Elevation here, in aVL, but it is much less obvious than the ST depression in
inferior leads and in V2, V3.
4. Subendocardial ischemia, non-localized, usually not as severe as #1 above: ST Depression in
V3,V4-V6. ST axis is rightward, with little posterior or inferior components.

77 yo presented with pulmonary edema. Troponin I peaked at 6.7 ng/ml. There was an
inferoposterior wall motion abnormality. All arteries were diseased but there was no obvious
culprit. This is not a posterior STEMI. This is a NonSTEMI.

In this case, the ST axis is perpendicular to III and aVF and towards aVR, and away from I and
II (leading to ST depression in I and II). So it is upward and rightward. If this were inferior
STEMI, the ST axis would be towards III and aVF (which also give ST depression in I and aVL).

5. Isolated High Lateral STEMI: II, III, aVF only (ST Depression is reciprocal to minimal STE
in aVL)

Example 1.

Acute Circumflex occlusion (also old inferior MI with Q-waves, and early repol giving anterior
STE)
Example 2.

Acute First Diagonal Occlusion.

Example 3.

This patient presented with DKA and an acute STEMI with first diagonal occlusion. The peaked
T-waves are due to hyperkalemia, which was immediately treated. Notice that the ST elevation
in aVL is far less obvious than the reciprocal ST depression in II, III, aVF. The ST axis is
towards aVL and away from inferior leads; thus there is ST depression in inferior leads. There
was a 100% acute occlusion of the first diagonal, with peak troponin I of 110 ng/ml, new lateral
wall motion abnormality, and ejection fraction decreased to 55%.
Inferior ST depression in ACS is reciprocal to ST elevation in aVL

This 72 yo male with h/o HTN, hyperlipidemia, and CAD, and h/o 4-vessel CABG 17 years
prior presented with 8 hours of substernal chest pain radiating to upper back.

Here is his initial ECG:

Notice there is ST segment depression in II, III, and aVF. The QRS is normal, so any ST
segment abnormality cannot be blamed on the QRS (i.e., ST depression is "primary", not
"secondary," and the ddx of this is ischemia, hypokalemia, digoxin, and normal variant). The ST
depression is somewhat "scooped" in appearance, suggesting hypoK or digoxin, but the QTc is
423 ms, so hypokalemia is unlikely (usually > 450 ms) and the patient was not taking Digoxin.

ST depression of subendocardial ischemia does not "localize". That is to say, for example, that
"inferior" ST depression does not represent inferior subendocardial ischemia. When there is
inferior ST depression from ischemia, it is invariably reciprocal to ST elevation in aVL (i.e., the
high lateral wall). So if we look at aVL, there is indeed some ST elevation, about 0.5 mm. This is
actually a significant amount of ST elevation because the R-wave is only 2 mm, and this is
common in aVL.

Furthermore, there is subtle ST depression in lead V3 (0.5 mm). There should NEVER be ST
depression in leads V2 and V3, there is usually some amount of ST elevation. 0.5 mm of ST
depression is likely to be 1.0-1.5 mm of relative ST depression.

A colleague showed me this and I said that, because there is ST elevation in aVL and ST
depression in V3, it is probably an obtuse marginal (OM) branch (of the circumflex) or near-
occlusion.

Appropriate management is to treat maximally for ischemia with ASA, heparin or enoxaparin
(depending on institutional preference), clopidogrel if institutionally acceptable and epitifibatide
if not. If the pain does not resolve, go urgently to the cath lab. If the pain and ECG findings
resolve, then next day cath is acceptable.
The patient had initial symptom control and was put in the ICU, but symptoms recurred and were
refractory, so he was taken urgently to cath and was found to have ACS of the saphenous vein
graft to the obtuse marginal. This was stented, and flow was TIMI-III after the procedure. Pre-
procedure flow was not documented, but pain was resolved afterwards. Troponin I peaked at 8.5
ng/ml. Post-procedure ECG showed prominent T-wave inversion in aVL (analogous to Wellens'
T-waves in the anterior leads). Notice the ST depression in V3 is gone, but the ST elevation in
aVL is more pronounced, as is the reciprocal ST depression.
40-something with severe CP. True + vs. False + high lateral MI. ST depression does not
localize.

This post presents one new case, then reviews some interesting aspects of high lateral MI and of
ST Depression in "inferior" leads. Down below are 3 more cases and a discussion of how to
differentiate false positive isolated STE in aVL from True positive.

Case: A 47 year old male called 911 for severe chest pain. He was clammy and looked unwell.
He had a previous MI with cardiac arrest 2 years prior.

This is his prehospital ECG:

There is very subtle ST elevation in I and aVL, with very subtle ST depression in III and aVF.

Is this due to coronary occlusion?

Jason asked me if I thought it is due to occlusion (without either of us knowing the outcome),
and this was my answer:

This is a posterolateral MI. Probably due to occlusion of the circumflex or one of its obtuse
marginal branches.

Why did I say this?

1. The inferior ST depression is reciprocal to high lateral subtle STE

2. There is a down-up T-wave in aVF. Down-up T-waves in inferior leads are almost always
reciprocal to ischemia in the territory underlying aVL.

3. ST segment in V2 has minimal ST elevation and is very flat, and the one in V3 is actually
subtly downsloping. This is not normal and is a tip off that there is posterior ischemia
accompanying the ischemia in aVL. Together they strongly suggest a circumflex lesion.
The medic activated the cath lab but was refused by the interventionalist, who did not believe
that this ECG represented acute coronary occlusion.

Later, the patient was taken to the cath lab. The artery was occluded. It was opened and stented.
I could not get details on which artery, but I'm sure it was the circumflex.

Important Learning Point:

"STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet.
Therefore it is not a STEMI. But what we truly care about is coronary occlusion, for which
STEMI is just a surrogate that is only about 75% sensitive for occlusion.

"Inferior" ST Segment Depression

It is important to understand that "inferior" ST Depression is not due inferior wall ischemia.

When there is ischemic ST depression localized to the "inferior" leads, it is more likely to be
reciprocal to ST elevation that localizes to the high lateral wall (aVL), even though that ST
elevation may be nearly invisible. The ST depression may be the most visibly obvious sign of
STEMI.
True Positive ST elevation in aVL vs. False Positive ST elevation in aVL

Case 1.

A woman in her 60s with no prior history of CAD presented with 3 hours of sharp, centrally
located chest pain with radiation to the anterior neck, with associated nausea. She had known
HTN and DM. She appeared to be in distress. She was given sublingual NTG with
improvement, but there was not complete resolution.

Here was here initial ECG:

There is ST elevation in I and aVL, with inferior reciprocal ST depression in all of II, III, and
aVF, and a down-up T-wave in aVF (a sign that is very specific for ischemia). There is also ST
depression in V3-V6. This ECG is diagnostic of ischemia.
Case 2: Another subtle lateral MI, from this post:

A male in his 60's presented 30 minutes after the onset of crushing substernal chest pain. Medics
recorded 2 ECGs, one before and one after sublingual NTG, and both are similar to the first ED
ECG. The patient had never had pain like this before. The pain improved from 9/10 to 3/10
after NTG. Here is the initial ED ECG:

There is subtle ST elevation in I and aVL with subtle reciprocal ST depression in III. Look at
aVF. There is a downsloping reciprocal ST segement followed by an upright T-wave ("down-
up" T-wave). This morphology is highly suspicious for ischemia. There are also symmetric
anterior T-waves with very poor R-wave progression. T-waves in V4-V6 are taller than normal
(compare to ECG in case 3 below)

This ECG, especially along with the very typical history, was very worrisome, but not absolutely
diagnostic of, ischemia. Several serial ECGs showed no change, even after the pain finally
resolved to 0/10 after NTG.

He was given aspirin, clopidogrel, IV nitroglycerine, and heparin, the general cardiologist was
called and notified that this patient was very high risk and needed close attention. He readily
agreed, and the plan was to admit for close observation, serial ECGs and troponins, and to
scrutinize for any recurrence of pain or change in the ECG.

The first troponin I then returned at 0.063 ng/ml (upper limit of normal = 0.025 ng/ml). Repeat
ECG remained unchanged.

- He remained pain free and the plan remained to admit with a diagnosis of Non-STEMI on
medical therapy with plan for angiogram in the morning.

- Just before admission to the hospital, the patient admitted to recurrent pain and appeared
uncomfortable. Therefore, the cath lab was activated urgently.

- The suspicion was for a circumflex (or obtuse marginal branch) or diagonal artery occlusion or
subtotal occlusion.
- At cath, there was a 95% proximal LAD stenosis with TIMI-II flow, proximal to a large
diagonal. A stent was placed and the patient became pain free.

Case 3: False positive

And here is a similar one that is NOT MI. How do we tell the difference?

There is ST elevation in I and aVL, with reciprocal ST depression in lead III.

Just so you don't think I'm cheating by using a retrospectoscope, this was sent to me without any
outcome, and I read it as "no MI" with a high degree of certainty. This is because:

1. The remainder of the ECG is normal. No poor R-wave progression, no other ST depression,
no symmetrical T-waves, no large T-waves, no down-up T-waves, typical early repol in anterior
leads

2. The reciprocal ST depression is in lead III only. Not in leads II and aVF.

3. There are distinct J-waves in the two leads with ST elevation. This is highly suggestive of
early repolarization in these leads.

4. The T-waves in I and aVL are not large (this was also true with the MI case 1 at the top, but
that case had many other suspicious findings (many leads with ST depression and no J-waves)

5. There is ST elevation in V2-V4 that is clearly due to early repol. Early repol in aVL should be
accompanied by early repol in the "anterior" leads.
Lessons:

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

1. Look for:

a. 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)

6. Angiogram if necessary. You don't want to miss an occlusion.

ST depression does not localize: 2 cases of "inferior" ST depression diagnostic of high
lateral STEMI

Case 1: This is a 72 yo male with h/o CABG who presents with 5.5 hours of sudden onset,
constant, substernal chest pressure. Here is the initial ECG:

This shows "inferior" ST depression. But stress testing shows us that ST depression does not
localize. In other words, when the stress test shows ST depression in an apparent distribution, it
does not correlate with the echo, nucleide imaging, or cath. Thus, subendocardial ischemia, for
an unknown reason, does not localize. When there is ACS with ST depression due to
subendocardial ischemia, it is diffuse (II, III, aVF, V4-V6). If it is focal, one should suspect that
it is reciprocal ST depression, reciprocal to ST elevation elsewhere. This is most commonly seen
with high lateral STEMI, with reciprocal depression in II, III, aVF. In fact, this ST depression is
usually the most obvious finding on the ECG because ST elevation in aVL is rarely pronounced
(most commonly because the QRS voltage in aVL is usually very low, and ST voltage cannot
exceed QRS voltage).

Thus, this ECG is diagnostic of occlusion of a vessel supplying the high lateral wall.

It does not meet the definition of STEMI because there is not 1 mm of STE. However, this
definition is arbitrary. The purpose of the definition is to diagnose coronary occlusion.

The first troponin was 0.82 ng/ml. The findings were not recognized. Subsequent ECGs did not
change. The patient was admitted and did not get cath until the following day, at which time the
Obtuse Marginal was found to have 90% stenosis with TIMI I-II flow.
The post cath ECG is shown here:

There is now a new Q-wave in aVL, with T-wave inversion. This is diagnostic of completed high
lateral MI. Echo showed a new wall motion abnormality. Peak troponin I was 8.6 ng/ml.

Case 2.

This patient presented very ill in DKA and with depressed mental status. He was intubated.

There are peaked T-waves diagnostic of hyperkalemia, but there is also suspicious ST depression
in II, III, and aVF. The hyperkalemia was immediately recognized and appropriately treated.
However, the significance of the ST depression was not.

.
It is reasonable to hypothesize that the ST depression is related to demand ischemia (though in
such as case it should be diffuse, not localized). If that is the case, it should resolve with therapy
and improved hemodynamics and slower heart rate.

A second ECG, after stabilization, was recorded:

The peaked T waves have resolved, and there is less tachycardia, but the ST depression in II, III,
aVF persists. There is definite ST elevation in aVL.

This was not acted upon.

[There is also precordial T-wave inversion which was present on previous ECGs and is
consistent with "Benign T-wave Inversion (BTWI)" -- I can't remember if I have posted on
BTWI before, but will if I have not]

Outcome: the patient had a peak troponin of 110.00 ng/ml (very large) and was taken for
angiogram the next day. It showed an occluded first diagonal. Echo showed a lateral wall motion
abnormality and the EF was 55%.
ST Elevation and Positive Troponin. Is it STEMI? No. And it is not even ACS.

A male in his 60s complained of constant chest pain for 12 hours. He has a h/o DM and HTN
and has been off his meds, including clonidine, for 3 days. His first two BP measurements were
176/108 and 191/126, with a pulse of 100-112. Here is his initial ECG:

ED ECG with pain:

There is sinus tach at a rate just above 100. There is profound LVH, with deep S-waves in V1-
V3 and a large R-wave in V6. There is left atrial enlargement, with a very large negative
deflection of the P-wave in V1, also supporting LVH. There is 3-4 mm of ST elevation in V1-
V3: this is classic for the pseudoSTEMI pattern of LVH: 1) location: V1-V3 and 2) preceded by
a deep, high voltage S-wave. Armstrong et al., concluded that an ST/S ratio of less than 0.25 in
the presence of LVH is very unlikely to be due to STEMI. There are small Q-waves in III and
aVF that suggest, but are not diagnostic of, old inferior MI.

Although this ECG is abnormal, I see no evidence of ischemia on this ECG. It is nondiagnostic.
There certainly could be ischemia hidden in this ECG. But there is nothing specific for
ischemia. And it is not an ECG that should result in cath lab activation.

Just to prove the point, I will show his previous ECG when he was symptom free:
It is very similar but at a higher heart rate. But there are also clearly inferior Q-waves, strongly
suggesting that he had a pre-existing inferior MI. This proves that the baseline ECG has high ST
elevation in V1-V3. But you did not need to see this previous ECG to know that the ST
elevation on the presenting ECG was due to LVH! This amount of ST elevation is
APPROPRIATE for an ECG with such deep S-waves. In LVH, as in LBBB, the ST elevation in
precordial leads is appropriately discordant, but if it is baseline, it should be proportionally
discordant. As indicated before, Armstrong's research suggests that an ST/S ratio of 0.25 is an
appropriate amount of proportional discordant ST elevation.

The hypertension and tachycardia could be due to, among other things, clonidine withdrawal: the
abrupt withdrawal of clonidine can result in rebound central sympathetic outflow, with increase
in both blood pressure and heart rate. The patient was administered clonidine which resulted in a
modest improvement in his vital signs.

The initial troponin I returned at 0.155 ng/mL, all but diagnostic of Acute MI (I say "all but"
because, strictly speaking, there must be a rise and/or fall of troponin to confirm Acute MI). It
was confirmed with a rise to 0.222 ng/mL on the next). But acute MI does not necessarily mean
ACS (plaque disruption, thrombus, need for anti-platelet and antithrombotic therapy). Is this
patient having a type I or type II MI? That is to say, is there demand ischemia due to the
increased O2 demand of hypertension and tachycardia? Or is there ACS? There is no way to tell
for certain without an angiogram showing a culprit or not. In either case, as long as there is
good cardiac function and no contraindications, beta blockers are indicated. (For explanation,
see this case posted this week on the use of anti-ischemic therapy, including metoprolol, in ACS)

The patient was not started on metoprolol in the ED, but was (appropriately) given
Nitroglycerin. Nitro may lower the BP, but won't lower the heart rate, and both cause increased
oxygen demand with ischemia. His pain continued.
An echocardiogram was ordered and done in the ED just before the patient was transported
upstairs. The report returned as a large inferior wall motion abnormality (WMA) with extension
to the lateral wall. (There was also "Abnormal left ventricular diastolic performance grade 3,
Severe restrictive pattern)" This is consistent with the LVH on the ECG.

It was unknown for certain if the WMA was new or old. He was started on carvedilol 25 mg po
bid at admission. His pain abated and he was taken to cath the next morning, at which time a
100% occlusion of a small dominant distal circumflex was found (to the inferior wall). It could
not be crossed with a wire. It appeared to be a chronic total occlusion. There was good
collateral circulation and it was a very small vessel. The peak troponin was only 0.270 ng/mL.

This was recorded 24 hours after presentation:

Now the heart rate is slower and there is only 2-3 mm of ST elevation in lead V2. It is very
common for tachycardia (ECG above) to result in more ST elevation than is present at baseline.
There is still no sign of an infarct.

Interpretation:

1. Type II MI (demand ischemia) from hypertension and tachycardia due to clonidine withdrawal

2. Right Precordial ST Elevation from LVH

3. Inferior Q-waves due to old inferior MI

3. Dense inferior wall motion abnormality due to old MI

Follow Up: He was taken off clonidine and started on lisinopril and carvedilol.
Lessons:

1. MI is not necessarily due to a coronary event. It may be due to increased demand (Type II
MI)

2. MI and ischemia due to a coronary event is usually subendocardial ischemia and the ECG is
usually nondiagnostic, or has ST depression of subendocardial ischemia. ST elevation is
possible, but very unusual.

3. A large amount of ST elevation may be due to pseudoSTEMI patterns such as LVH. A

positive troponin may have nothing to do with the ST elevation

4. When there is Hypertension, don't forget beta blockade such as metoprolol. Again, see here
for details. An alternative is esmolol: if you are worried about the potential adverse effects of
beta blockade, esmolol is very short acting. It is given as a bolus and drip, and its effect wears
off very quickly after discontinuation of the drip
Hyperacute T-waves? Anterior STEMI? No, LVH with PseudoSTEMI pattern!

A woman in her 30's with h/o HTN presented with atypical chest pain after a stressful event.
Here is her ED ECG:

There is sinus tachycardia. There are very large anterior T-waves, with ST elevation. However,
there is also very high voltage. Criteria for LVH is clearly reached in aVL, with tyical
repolarization ("strain") in aVL. The ST elevation and tall T-waves are discordant to deep S-
waves in V2 and V3.

I took care of this patient and was concerned about the ST-T waves in V2 and V3, but thought
that they were almost certainly a result of LVH. One should not apply the LAD occlusion vs.
Benign Early Repol Formula if the patient has LVH. Had I done so, with a QTc of 375ms, the
formula value would have been 26.1, indicating anterior STEMI. Here is another example of
LVH resulting in a falsely positive formula value.

I think that the formula would be more accurate if it took into account the entire QRS, not just
the R-wave. I will be using all the original ECGs to study this hypothesis.

There were no previous ECGs for comparison.

We did a bedside cardiac echo which showed concentric LVH and a well functioning anterior
wall. A repeat ECG 30 minutes later was identical. We recommended admission for further
evaluation but the patient signed out against medical advice.

Her heart rate came down with IV fluids.

I am quite certain that this is the patient's baseline ECG.

Lesson:

1. LVH can result in PseudoSTEMI patterns of various morphologies. Here are some others.

2. The formula may give false positives in LVH

Male in his 40's with chest pressure: what is the diagnosis

This 40-some year old patient complained of chest pressure and had this ECG recorded:

See comments and diagnosis below:

The providers were a bit worried about this ST elevation and I was in the department, so they
showed it to me: my answer took 2 seconds and was unequivocal: LVH and early repolarization,
no STEMI.

How did I know this? Primarily because:

If inferior MI, there would be significant ST depression in aVL.

If anterior MI, there would not be such high voltage, especially in lead V4.

Though the early repol/anterior STEMI formula may give false positives in LVH (I'm actually
not sure of this), the value obtained after plugging in STE60V3 = 5 mm, QTc = 400 ms, and R
wave V4 = 33 mm = 18.2 (far less than 23.4, strongly arguing against anterior STEMI). I did not
use the formula, but one could do so and be reassured.

My colleagues appropriately did a bedside ultrasound and found completely normal function.
They did admit him for "rule out" and all troponins were negative.

Diagnosis: Anterior and "inferior" ST elevation due to LVH and early repolarization
Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH)

A 52 year old male presented with epigastric pain, continuing in the emergency department. He
has a history of hypertension, and is on amlodipine. Thinking that epigastric pain might be an
anginal equivalent, this ECG was recorded:

There is LVH. There are T-wave inversions in aVL and V3-V6.

The physicians were worried about Wellens' syndrome and treated for ACS. He was placed on a
nitroglycerine drip. Initial troponin was negative. A followup ECG was done 3 hours later.

Perhaps slightly less T-wave inversion. Nonspecific.

He was admitted. All troponins were normal. A formal echo showed concentric LVH and there
was also a subtle abnormality which the echocardiographer thought suspicious for LAD
distribution ischemia. So he underwent a coronary angiogram which was completely normal.
This is not Wellens'. Why?

1. LVH frequently causes T-wave inversion which mimics Wellens'

2. In Wellens', the chest pain is nearly always resolved by the time of the ECG. It is reperfusion
that results in the T-wave inversion and the pain is thus resolved by this time.

3. Wellens' is defined by chest pain and ECG abnormalities. Though Acute MI can present as
epigastric pain, it is not at all common and T-wave inversion in the setting of epigastric pain is
not high risk for ACS.

4. T-wave inversion in Wellens' is primarily V2-V4. When T-wave inversion is V3-V6, one
should think more about LVH or Benign T-wave Inversion
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.
The development of an inferior-posterior STEMI, from prehospital to hospital

Case

A 65 yo woman called 911 for pain in her upper back (between the shoulder blades) and in the
left shoulder and left biceps, and some "mild chest pressure" elicited by the medics. Exam was
normal. All but the back pain resolved with nitroglycerine

Medics recorded 6 prehospital ECGs. Below are 3 of them:

There are hyperacute T-waves in II, III, and aVF. Note T-wave inversion in aVL, which is the
earliest finding in acute inferior STEMI, as well as in V2, suggesting posterior wall involvement

No significant change
Now there is clear ST elevation in inferior leads. T-wave inversions in aVL and V2 have
evolved to ST depression.

They arrived in the ED at 1503. BP was 116/70. CXR and cardiac and aortic ultrasound were
done to look for any evidence of aortic dissection. All were normal except for a possible inferior
wall motion abnormality.

In the ED, the following ECGs were recorded.

ST segments have almost normalized. Hyperacute Ts are less prominent, as is T inversion.

There is probably some spontaneous reperfusion of the infarct-related artery. The computer
noticed only some "minimal" ST depression.
Inferior ST elevation is more obvious, with 1 mm in II and III, but T-waves have normalized.
ST depression in V2 is clearly abnormal. Computer did not read MI.

Now the most obvious findings are ST depression in aVL and V2

Cardiology was consulted. Again, a cardiology fellow opined that this was not a STEMI, and
went to talk with the interventionalist.

A posterior ECG was recorded:

Only aVL was of great concern. There is no posterior ST elevation.

The interventionalist was very concerned and activated the cath lab. The patient was taken to the
cath lab. The proximal RCA was 100% occluded. It was stented. Door to balloon time was 62
minutes. Peak troponin I was 5.15 ng/ml.

Post PCI ECG

T-waves and ST segments are back to normal

Looking at this, I'm not sure that the "posterior ECG" really was posterior, as the QRS looks
exactly the same as the previous. However, to answer your question in more general terms: the
posterior leads must record electrical activiity through a lot of lung tissue (air), which is a good
insulator. This diminishes the voltage. Freqently, posterior lead give a false sense of security. So
I always recomment that, if you diagnose posterior MI on the regular 12-lead, do NOT change
your mind based on absence of STE in posterior leads. And remember that the "criteria" for
posterior leads is 0.5 mm, not 1 mm, and to especially evaluate in the context of proportionality
to the QRS.
Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the
Diagnosis?

A male in his 60's with med h/o only significant for HTN and hyperlipidemia presented for CP
and SOB. On the day prior, he became very SOB and felt like he was going to pass out when he
tried to stand up from bed. This was accompanied by chest heaviness and followed by left
chest pain and a stiff sensation in his neck. The pain progressed but he went to bed but awoke in
the AM with a heavy and "throbbing" chest. VS were: 122/92, pulse 82, RR 18, O2sat (room
air) = 95% Here is his initial ED ECG:

What is the Diagnosis?

The first troponin returned at 0.092 ng/ml (99% reference 0.034).

Does the elevated troponin confirm ACS?

There are both precordial T-wave inversions AND T-wave inversion in lead III. this is highly
suggestive of pulmonary embolism. There is also S1Q3T3 (this post helps to explain its
significance).

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also
inverted in lead III and V1, then pulmonary embolism is far more likely than ACS. In this study,
(quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS
compared with 88% of patients with APE (p less than 0.001). The sensitivity, specificity,
positive predictive value, and negative predictive value of this finding for the diagnosis of PE
were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in
both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients
with negative T waves in the precordial leads."

The patient was treated for NonSTEMI, including ACS dosing of heparin and including
nitroglycerin, which could be hazardous in pulmonary embolism. He was admitted to cardiology
where he immediately underwent an echocardiogram, which showed RV strain, alerting the
clinicians to PE. A CT pulmonary angiogram confirmed multiple pulmonary emboli.

Strangely, there is no tachycardia and the patient was not on beta blockers.

Lessons:

1. Chest pain with a positive troponin may be due to many causes, not just ACS. Always
consider these.

2. Precordial T-wave inversion, along with a negative T-wave in lead III, should alert you to the
strong possibility of pulmonary embolism.