Only the ECG Diagnoses Acute Coronary Occlusion. Do not be Fooled by a Negative High Sensitivity Troponin.

This case was sent by Peter Hammarlund, 2nd year Internal Medicine/Cardiology resident (and self-proclaimed ECG nerd) at Helsingborg Hospital, Sweden.  

Peter frequently sends me great cases like this, but I never post them because the Swedish standard, explained below, is very difficult to interpret.

This time I could not resist.

Especially interesting is the troponin data and the manipulated images seen below.

Case

Hi Steve,

I was involved in this highly interesting case just the other week.

A previously healthy young man (in his 20s), who smokes two cigarettes a day and has a family history of MI (his father had his first MI in his early 50s), was brought to our ED by ambulance with severe central chest pain without radiation for one hour. The pain was not relieved by Nitroglycerine and only slightly relieved by morphine. 

Smith comment: do NOT use morphine until you are either: 

1) committed to the cath lab (or other definitive diagnostic modality, such as CT for dissection or PE)

or 

2) CERTAIN that the pain is not due to serious pathology. 

Case continued

He was tachycardic, but his vitals were otherwise initially normal. 

The initial high sensitivity troponin T was 5 ng/L.

(99% reference is 14 ng/L, or less than 15 ng/L; Level of detection is 5 ng/L).

I was working in our CCU when the cardiology consultant (who was sitting right next to me) got a phone call from the ED doctor taking care of the patient. While he presented the case to the consultant we looked at the prehospital ECG (attached as EKG1, time 7.53 am) and the ED ECG (attached as EKG2, time 8.10 am). 

At the moment (time 10.45 am) the patient was in the radiology department performing a CT aorta, but right after the CT he developed shortness of breath and only had a saturation of 88% with 15 L/min of O2.

I was immediately very worried about the patient when I saw the ECGs.

What do you say? My answer is below.

Note on technique: These are recorded at the Swedish standard of 50 mm/second.  So all intervals appear twice as wide as you are accustomed to!  Furthermore, there is only one average complex per lead.

What do you think?

Here is my answer, after a quick glance:

Peter,

Hyperacute T-waves are developing over 17 minutes in V2-V4.  LAD occlusion or at least dynamic thrombus.

Steve

As an afterthought just this minute before posting, I compressed the ECGs to 25mm/sec.  The difference becomes much more obvious to me:

Peter's Detailed Comment on the ECG interpretation:

The ECG at t = 0 (prehospital ECG) shows sinus rhythm with a minimal ST depression in V3-V4 as well as minimal ST depression in the lateral leads. No significant ST depression is seen in the inferior leads although there is a TWI in lead III that could be non-specific. However, the T wave in V2 looks abnormally large with a hyperacute appearance. Young people might indeed have large T waves in the anterior leads, but the T wave is in fact as large as the whole QRS complex. The positive T wave in V1 could indicate an early sign of anterior ischemia. Although many of these findings may be considered non-specific the appearance is highly unusual in a previously healthy 28 yo man. With a complaint of ongoing chest pain, this is worrisome.

The ECG at t = 17 min (1^st ECG in the ED) shows no significant change in V2, but the T wave in V3 is now also hyperacute and the T wave in V4 is also a bit taller. Since the QRS complexes don’t look exactly the same, some of the ST-T changes may be due to different lead placement, but the dynamic change in V3 is too abnormal to ignore. The ST depression in the lateral leads are now gone – could this be pseudonormalisation? There might even be a tiny bit of ST elevation in aVL, and development of slightly downsloping ST segment in the inferior leads (at least aVF and III). Although neither of these ECGs are clearly diagnostic of MI alone, the dynamic changes in combination with a presentation consistent with ACS is highly worrisome.

Smith comment: The ST depression is due to early, and possibly incomplete, LAD occlusion, which is often called "de Winter's T-waves" a type of hyperacute T-wave.  17 minutes later the artery is completely occluded and the ST depression has become ST elevation.  

There should NEVER be ANY ST depression in the precordial leads of a young man.

Peter's response:

You are of course spot on. Me and my colleague saw this immediately, and since these ECGs were recorded 2½ hours before the consultant got the phone call we were very worried about the patient. 

EKG3 (not shown) was recorded 2.5 hours later (Smith comment: treatment was very delayed!) during the consultation and the diagnosis was now obvious with a huge anterolateral STEMI.  The providers had not noticed the ST depression nor the diagnostic T-waves.

Echo hadn't been performed initially, but showed EF 40% and akinesis of the anterior wall. CT of the aorta was of course normal. CT of the lungs showed bilateral infiltrates with gravitational distribution, that initially were interpreted by the radiologist as infectious, but in retrospect were considered to be flash pulmonary edema. 

The patient went for coronary angiography that showed an almost complete occlusion in the distal part of LM with a stenosis extending into the proximal part of the LAD. 

During PCI the patient needed CPAP and small doses of norepinephrine. He was fully revascularized and was initially admitted to the ICU, but could be moved to the coronary care unit the next day. A formal echo a couple of days later showed EF 50%. The hospitalization was prolonged, due to the development of fever and a small pericardial effusion (postinfarction syndrome?), but otherwise the patient did OK. 

This case was up for discussion the next day in our clinic, and I pointed out the subtle, but real dynamic changes, that might have been picked up, not delaying the diagnosis for another 2½ hours.

Many of my colleagues still considered the initial ECGs to be practically normal, although I pointed out that these findings might be considered non-specific if the patient was presenting with e.g. cellulitis in the leg, but highly worrisome in this particular case, since the patient was having ongoing chest pain. 

Another thing that made the case a bit more complicated was that the initial hs-Troponin T was only 5 ng/L (positive at < 15 ng/L, level of detection at 5) i.e. not positive, but just above the level of detection. This was when the chest pain had been going on for a little more than one hour. 

I think that the ED physician might have been fooled by this. The next troponin measurement in the ICU (6 hours after the onset of chest pain) showed a level of >9998 ng/L. 

In retrospect this was indeed a tricky case, but as I pointed out to my colleagues we should learn from it rather than just call it tricky and convince ourselves that it was unavoidable. 

Regarding the use of your formula: I believe if you use it on the 2nd ECG it comes out positive with a value of 23.678 (if I measured correctly using 2.5 mm of STE at 60 ms, QTc of 428 and RV4 of 14 mm) clearly indicating subtle STEMI.  (A value greater than 23.4 is nearly diagnostic of LAD occlusion in the right circumstances)

Here I have superimposed the ECGs so that you can see the evolution more clearly.  The darker lines are the second ECG at time = 17 minutes after the first:

Notice the significant increase in T-wave amplitude in V3 and V4.
Notice also the new but subtle ST Elevation in I and aVL, with reciprocal ST depression in lead III.

The formula is negative in the 1st ECG due to minimal STE at 60 ms after the J-point in lead V3.
(Remember that 60 ms in this recording format is 3 little boxes, not 1.5)
The formula is positive in the 2nd ECG.
Referring to: Formula for differentiating normal STE from STE due to LAD occlusion

Here it is compressed:

Take home points: 

1) Young people do have MI.

2) Beware hyperacute T-waves

3) Beware any ST depression in precordial leads

4) Do not mask your diagnosis with Morphine (or other opiates)

Serial ECGs would probably have made the difference in this case. 

5) Echo is very helpful in these situations.

4) Don't rely on the first troponin, even if high sensitivity (if there is a short time from the onset of chest pain to the blood testing) 

//Peter

Comment on the formatting:

In Sweden the different leads usually are presented in the so called Cabrera sequence, which basically means that lead aVR is replaced by -aVR (i.e. aVR with switched polarity, which gives the lead an “up-side-down” appearance) and that the limb leads are presented in a anatomically contiguous order (aVL = -30°; I = 0°; -aVR = 30°; II = 60°; aVF = 90° and III = 120°). This means that the inferior leads are presented next to each other (vertically) and that the high lateral leads (aVL and I) are placed next to each other with -aVR in between. This makes it easier to spot ST-T-changes localized to a specific anatomic area of the heart (at least if you are used to the formatting).

In this case the recordings also have another feature. The tracings that are recorded with a paper speed of 50 mm/s are so called signal-averaged ECGs. There is only one complex presented in each lead, which is an artificially created “mean value” of several ECG complexes. The point of this is to eliminate artifacts. 

On the right side (not shown here) we display short rhythm strips at a paper speed of 12,5 mm/s (thereby looking twice as fast as usual if you’re accustomed to a paper speed of 25 mm/s).  

Persistent Chest Pain, an Elevated Troponin, and a Normal ECG. At midnight.

A middle aged male presented at midnight after 14 hours of constant, severe substernal chest pain, radiating to his throat and to bilateral jaws, and associated with diaphoresis.  It was not relieved by anything.  The pain was not positional, pleuritic, or reproducible.  He had no previous medical history.  The blood pressure was 110/60.  Physical exam was normal and there was no murmur.

I delved into his reasons for arriving so late after onset, thinking that perhaps the pain had only recently increased, or that it had been intermittent until now, but he confirmed that it was 14 hours of constant pain and it was his significant other who insisted that he go to the ED.

Here was his ED ECG:

I read this as normal
--One might say there is ST depression in II, III, and aVF, but this is merely an atrial repolarization wave.  
--You can see the PR segment sagging down, such that the PQ junction is also depressed.  Thus, there is no elevation of the J-point relative to the PQ junction.
--ST segment deviation is measured at the J-point, relative to the PQ junction
--("Inferior" ST depression would have told us that there is unseen ST elevation in aVL and be a strong clue to high lateral MI)
Click here for a couple posts on Atrial Repolarization

He was given an aspirin and a troponin was drawn.  If this is MI, then after 14 hours, the troponin should be elevated.

The troponin I returned at 4.1 ng/mL (ULN = 0.030 ng/mL), diagnostic of myocardial injury.




We recorded a posterior ECG:

V4-V6 are moved around to the back and are really V7-V9.
The "criteria" for posterior STEMI are 0.5 mm STE in one lead.
There is zero ST Elevation.
There are tall R-waves in V2, which could be a sign of old or well developed posterior MI
However, the ECG shows no evidence of acute MI whatsoever.

We gave ticagrelor and heparin and sublingual nitro, with plans to start a nitro drip, but the BP dropped to 80/50 before the drip was started.

The pain was unrelieved.


What do you want to do?







The elevated troponin is diagnostic of myocardial injury. Is it acute or chronic?

There was a normal creatinine and no evidence of heart failure and no other reason for chronic injury, so it must be acute.

Acute myocardial injury: 

Is it myocardial infarction, or perhaps myocarditis?
If it is MI, is it type 1 or type 2?
Is it STEMI or NonSTEMI?  
Is it acute persistent occlusion?

The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis.

The patient had been on a long drive, suggesting possible pulmonary embolism (this was unlikely given absence of tachyardia, hypoxia, or any other feature of PE), so we sent a d dimer.  [We also looked at his aortic root by both parasternal and suprasternal views, and the aorta was normal.]  The d dimer returned below the level of detection, ruling out PE and making dissection very unlikely.

So this was not a type 2 MI.  And was not a PE or dissection.

A bedside echo showed good LV function but was inadequate to assess wall motion.  We attempted Speckle Tracking Strain Echocardiography but could not get clear enough images without contrast.

We could not rule out acute epicardial coronary (large artery) occlusion.

What do you want to do now, considering you will need to awaken the hospital's only catheterization team, which must be alert for the next long day in the cath lab?


















I called the cardiologist on call and we agreed that we needed to activated the cath lab.

The patient was found to have an acute 100% occlusion of the circumflex proximal to 2 obtuse marginal branches.  It was opened and stented with a door to balloon time of about 120 minutes (this is long for STEMI, but very short for a high risk Non STEMI).

A post cath ECG is shown:

No significant change

The third troponin, drawn before the artery was open, returned at 6.2 ng/mL.
The 4th, after the opening of the artery and release of troponin from the cardiac circulation, was 99.9 ng/mL

So this was a very large MI!!

The formal contrast echo the next morning was difficult technically but showed an inferior wall motion abnormality.  It is unclear if this is "inferobasal" which is the new echo term for Posterior.



Learning Point

Acute coronary occlusion may occur with no ECG findings whatsoever.  Some NonSTEMI require emergent cath lab activation to save viable myocardium at risk.  A patient who has a high clinical suspicion of MI should go to the cath lab.  This is not just my opinion, but the opinion of the American College of Cardiology and American Heart Association.

This is from the 2014 ACC/AHA guidelines.  Earlier versions are more specific. "A subgroup of patients with refractory ischemic symptoms or hemodynamic or rhythm instability are candidates for urgent coronary angiography and revascularization."

Here are the European Guidelines:
Timing of invasive strategy:  Immediate invasive strategy (less than 2 h) in Very-high-risk NSTE-ACS patients (i.e. with at least one very-high-risk criterion according to Table 13 (pasted below) 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.

This includes:

1. Patients with ACS and hemodynamic instability
2. Patients with ACS and acute pulmonary edema
3. Patients with ACS and electrical instability
4. Patients with ACS and refractory chest pain or refractory ischemic ECG findings, usually ST depression

A patient who presents with chest pain and an otherwise unexplained elevated troponin has acute MI.  If the pain is refractory to medical management, no matter what the ECG shows, the patient should go emergently to the cath lab.

Acute Chest Pain: Computer reads "Nonspecific ST-T abnormalities"

A male in his 60's had a history of previously stented infero-posterior-lateral STEMI due to an occluded dominant circumflex, which had been opened and stented.

He called 911 for acute chest pain.

Here is the first prehospital ECG at time zero.  The computer read "Nonspecific ST-T abnormalities."

Time zero:

The computerized QTc was 431 ms.
The computer read "nonspecific ST-T abnormalities"
What do you think?

There is minimal ST elevation in V2 and V3.
T-waves are large in V2 and V3.
There are minimal down-up T-waves in III and aVF.

This is LAD occlusion until proven otherwise.  One must explain the minimal ST elevation in V2 and V3.  It is not due to LVH, LV aneurysm, or pericarditis.

Thus, it must be either normal variant ST elevation (loosely called "early repolarization") or acute LAD occlusion.  To me it is clearly LAD occlusion.

One can use the LAD occlusion/early repol formula to differentiate.  There is an iPhone app for it which really helps to be certain you are applying the formula correctly.

It is critical to use this formula only when the differential is subtle LAD occlusion vs. early repol (normal variant ST elevation). There must be ST Elevation of at least 1 mm. 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), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI.

If you use these values:
Computerized QTc = 431 ms
ST elevation at 60 ms after the J-point in lead V3 (STE60V3) = 1.5 mm
R-wave amplitude in V4 (RAV4) = 6.5 mm

The resulting value = 25.1.  Any value greater than 23.4 is very likely to be LAD occlusion.

Case continued

This was recorded 22 minutes later: Again, nonspecific ST-T abnormalities

What do you see here?
The computer still reads "nonspecific ST-T abnormalities"
Note the computer reads the ST segment:
For V2, it is 1.03 mm
For V3, it is 1.58 mm
"Normal" for a male over age 40 is up to 2.0 mm in V2 and V3.

Now there is straightening of the ST segment in V2.  A straight ST segment is very rare in normal variant ST elevation, and the change makes it diagnostic of LAD occlusion.  Inferior ST segments have also evolved.  aVL has suspicious coving; it is probably a proximal LAD occlusion.

The ST elevation "criteria" are incorrect.

The patient arrived in the ED and had this ECG recorded at 25 minutes after the 2nd ECG (t = 47 minutes)

So this is the first ED ECG:

The computer interpretation: "Possible old inferior myocardial infarction."
Very similar, but now with more ST depression in inferior leads and subtle ST elevation in aVL.
Again, diagnostic of LAD occlusion, with evolution of findings.

The cath lab was activated.

This ECG was recorded 26 minutes later, just before the patient was transported to the cath lab:

Very interesting:
1. The ST depression in the inferior leads is gone, as is the STE in aVL, suggestive of reperfusion of the high lateral wall.
2. There is T-wave inversion in aVL, also suggestive of reperfusion.
3. V3 has developed terminal QRS distortion (loss of S-wave), suggestive of evolution of injury to the anterior wall.
4. There are the beginnings of Q-waves in V2-V4
Thus, it appears as if there has been worsening of the anterior wall and reperfusion of the high lateral wall.

My interpretation when I saw this was that the LAD thrombosis was at the ostium of the first diagonal (D1) and that it had partly reperfused, leaving D1 open and the LAD still occluded.


A 100% proximal LAD occlusion was found, with left-to-left collaterals (from the circumflex) perfusing the 1st diagonal.  This explains the reperfusion of the high lateral wall.

Here is the next day ECG:

Reperfusion T-waves in I and aVL, and V2.  Some persistent, minimal, ST elevation.

Peak Troponin I: 99 ng/mL (very high)

Echo:

The estimated left ventricular ejection fraction is 50%

The estimated pulmonary artery systolic pressure is 39 mmHg + RA pressure.

Regional wall motion abnormality-distal septum anterior and apex akinetic

.

Regional wall motion abnormality-inferolateral (from previous STEMI).

Normal estimated left ventricular ejection fraction lower limits of normal.

Note there is no lateral wall motion abnormality because of the reperfusion, through collaterals, of that wall

Syncope Several Times, Complete Heart Block, And a Surprise ECG in the ED!

This was sent by one of our graduates who will remain anonymous.

A 55 year old male with a history of DM and HTN had 2 syncopal episodes, then a third while in the presence of EMS.  There was no drug use.

ECG 1. He was put on the monitor and it showed this:

There is a slow, wide complex.  There are P-waves that are regular but completely dissociated from the QRS.  In fact, they don't ever conduct.
So it is third degree heart block with a ventricular escape.

ECG 2. Within minutes, his heart rate normalized:

Normal sinus rhythm, diffuse non-specific T-wave inversion

ECG 3. He had no complaints on arrival to the ED. This ECG was recorded at 0209:

No obvious abnormalities

ECG 4. At 0416 (2 hours later) he developed "chest burning."  Here is his ECG:

Obvious Inferior Posterior STEMI

ECG 5. His burning quickly resolved, and this ECG was recorded 20 seconds later:

Resolving ST Elevation (That was fast!!)

The patient was "rattled" by this experience, felt as if something very bad had just happened.


ECG 6. 7 minutes later, the burning returned.  Here was the ECG at 0424:

This was the doctor's (my ex-resident's) response:
"He now has ST elevations in a different distribution.  Was inferior before, now lateral What the heck?  I had been considering coronary vasospasm, but the changing distribution seems to make that less likely."

He thought it might be vasospasm of two different coronary arteries.



ECG 7. At 0428 the burning persisted and this was recorded:

Now they are inferior again!!

7 minutes later the burning was gone and this ECG was recorded at 0435:

All STE has resolved again.

The Cath Lab was activated.  Here is the last ECG before he left for the cath lab at 0449:

There are now inferior reperfusion T-waves (inferior Wellens' waves!)
This supports some degree of infarction.
The troponin will be elevated, but not by much as these occlusions were brief.

Outcome

The cath did not show an occlusion or a definite culprit, but some diffuse non-occlusive disease.  No PCI was performed.

I do not have the subsequent troponin.

Subsequent Echo was showed LVH and evidence of hypertrophic cardiomyopathy, without a wall motion abnormality.  EF was 65%.

The caregivers (emergency physician and cardiologists) were perplexed about what happened.

What happened?

Why the change in location of ST Elevation??? (There are two explanations below)













Look closely at ECGs 4, 6, and 7:

This was my explanation, which Haim Katalan shows was incorrect (his is below mine)

In 4. and 7., which have inferior  ST elevation, the QRS is positive in II, III, and aVF, but negative in aVL (5. also has this QRS axis)

In 6. which has lateral ST elevation, the QRS is negative in lead III, isoelectric in aVF and positive in aVL.

Thus, the limb lead placement was inadvertantly reversed between ECG 5. and 6.  And it was inadvertantly reversed back for ECG 7.

So this was a transient inferior STEMI.

Haim Katalan explanation

I looked carefully at ECG 6-7 and the first ECG with inferior STE. I don't think limb leads was misplaced. i) the chest leads looks different in ECG 6 from 7.  That can not be accounted for by limb lead swap. ii) Also in ECG 6 the STE in I & aVL have an action potential shape completely different from the STD in ECG 7 . iii) also no P wave axis change as would expected in lead swap. 

So my impression is that it was multi vessel spasm.

Transient STEMI is usually due to brief thrombotic occlusion that then lyses.  This occlusion happened several times.  The first time it did not result in chest pain but did result in complete heart block.  In Acute Coronary Syndrome, a thrombotic event, a culprit is not always found.  And the coronary disease may be mild in such cases: the thrombosis just happens at a minimally stenotic, but vulnerable lesion.  It is even possible to have thrombosis with a completely normal angiogram, though in less than 1% of cases.  In such cases, all the the atherosclerosis is outside the lumen, in the wall of the vessel. So you cannot see it on an angiogram, which is a "lumenogram."  You can see this with intravascular ultrasound, which very well images the thickness of the vessel wall.

Of course vasospasm is usually blamed for these transient ST elevation events, but unseen thrombosis is more common.

The good news is that transient STEMI has a better prognosis than non-transient STEMI, AND ACS with a non-obstructive angiogram has a better prognosis than those with tight stenoses or large thrombus burden.

Learning Points:

1.  Always check lead placement when things do not seem right!
2.  Beware of Transient STEMI
3.  Beware that ACS may have minimal findings on angiogram.

Right Precordial T-wave Inversion

This was posted on Facebook EKG club by Massimo Bolognesi, from Italy.  He is a highly respected Sports Medicine Cardiologist.
https://www.facebook.com/Maxb1953?fref=ts
http://www.dottorbolognesi.it/

He graciously allowed me to re-post it here.

"This ECG was recorded on an asymptomatic 50 year old marathon runner who presented for pre-participation screening."

(This ECG could easily be seen in an ED chest pain patient, and I have seen many)

What do you think?

Description
Sinus bradycardia.
There is high voltage.
There is ST elevation in V2 and V3
There are inverted T-waves in V2 and V3
There are prominent U-waves in V2 and V3

Many responders were worried about ischemia or hypertrophic cardiomyopathy.

Here was Massimo's response:

"I'm very sure of Early Repolarization (ERP) diagnosis in this case. 
First because I have a good eye on ECGs of endurance athletes
Second because I see a lot of these tracings
Third because the stress test determines the disappearance of ECG abnormalities found at rest
Fourth because the echocardiogram is normal
Fifth and last, the clinical presentation speaks clearly."  

Comment

I (Smith) have seen many similar ECGs in ED chest pain patients.  I have always believed them to be benign for the reasons described below.  But I have never had any data to support my beliefs, so I've never posted them.

Notice also that the QTc is very short. First, one must realize that the last wave is a U-wave, which is common in ERP.  So the QT must not be measured in V2 or V3.  The QT as measured in other leads is about 420 ms, with a preceding RR of 1500ms, resulting in a Bazett corrected QT interval of 345 ms. This short QT at least makes ischemia all but impossible.  ERP is, of course, associated with an increased long term risk of sudden death, but only marginally and only if in inferior or lateral locations: 

http://www.nejm.org/doi/full/10.1056/NEJMoa0907589#t=article

http://www.nejm.org/doi/full/10.1056/NEJMoa071968#t=abstract

In addition, many readers of this Facebook post were worried about ischemia, including Wellen's syndrome ("What if this patient had presented with chest pain?"): 
Even in the setting of ischemia, the ischemia would not be represented by this ECG. This is a classic pattern and the QT is so short as to make ischemia very unlikely.  This is a normal variant.  I have seen this innumerable times in chest pain patients in the Emergency Department. At first glance, it may appear to be similar to ischemic T-waves, but it is not. The large upright U-wave, this high voltage, and the short QT interval differentiate it from ischemia.  

It is important to remember that even a patient with a normal variant could have a myocardial infarction, just as patients with completely normal ECGs may have MI.  

It is only to say that the ischemia is not represented on this ECG.

See this post on Benign T-wave Inversion.

Here is a relevant post on the inverted T-waves of Persistent Juvenile T-wave Pattern with many other the normal variants of T-wave inversion.

ST Elevation in aVL. Reciprocal ST depression in III. Is it MI?

I was reading this ECG in the queue, with no clinical info.

What do you think?

My interpretation was LVH, no evidence of MI.   There was no previous ECG or echo for comparison.

My ECG diagnosis may surprise you, as I have long discussed "ST elevation in aVL with reciprocal ST depression in lead III" as due to high lateral MI.

This is different because:
1) There is saddleback morphology in aVL, and
2) There is also high voltage.

I have previously talked about ST elevation with saddleback morphology in lead V2 as rarely being due to anterior STEMI.  See this post (the only case I've seen in which it was STEMI): 

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

Voltage on this ECG does meet Estes criteria for LVH: 
1) At least one R- or S-wave greater than 20 mm (lead II) = 3 points.
2) ST-T abnormalities in the absence of digoxin = 3 points
Total = 6 points
5 points is definite
4 points is probable
This scoring system comes from this original article.

However, meeting LVH criteria is not critical, as they are not sensitive.  Many cases of LVH show themselves only by the typical repolarization abnormalities.  In this case, we see somewhat typical repolarization abnormalities in leads III and aVF.

Estes criteria are only 34% sensitive for LVH as diagnosed by echo.   

In this paper that used other criteria, the sensitivity for LVH by echo was less than 10%!
At least one of, with or without ST-T abnormalities:
1) R-wave 11 mm in aVL
2) R-wave at least 25 mm in left precordial leads
3) S-wave at least 25 mm in right precordial leads
4) Sum of precordial SV1 or SV2 plus RV5 or RV6 at least 35 mm
5) Sum of lead I plus lead II at least 25 mm.

In both studies, specificity of the criteria was nearly perfect.

Case Continued

This 30-something presented with headache and chest pain.  He had a history of hypertension, apparently completely untreated.  His chest pain had lasted 40 minutes and was now gone.

Blood pressure was 170/105.

Another ECG was recorded several hours later:

No significant change

The history of HTN, the elevated BP, the high voltage, and the saddelback make it very unlikely that this ST elevation is due to STEMI.

The patient ruled out for MI by negative delta troponins.

Here is a post on True Positive ST elevation in aVL vs. False Positive ST elevation in aVL
However, I do not discuss saddleback in aVL in this post.

A Young Man with Recurrent Chest Pain and Dyspnea with Exertion

Case

This is a young man who has had chest pain and dyspnea with exertion for years.  He presented to the ED with these symptoms again.  On this occasion, the CP was associated with stress and accompanied by some SOB, 7/10 at it's worse and made worse with activity, with radiation up into the left side of his neck and face.

No h/o hypertension.

Here is the ECG:

Probable Diagnosis?
I was shown this ECG and gave my opinion, as below.

Here is an ED bedside echo, parasternal long axis:

Look at the small the end-systolic LV chamber size

Parasternal short axis:

Again, look at the end-systolic chamber size!

What is the Diagnosis?

The ECG shows profound LVH with secondary ST/T abnormalities.  There is deep ST depression and T-wave inversions that are discordant to (in the opposite direction of) large voltage R-waves.  These ST-T abnormalities do not represent ischemia, although they could certainly hide ischemia.  Instead, these repolarization (ST-T) abnormalities are entirely secondary to depolarization abnormalities (huge voltage).

The echo shows profound LVH.  Whether it is definitely concentric or assymetric (which is seen in HOCM with assymetric septal hypertrohy) is hard to tell for certain with these bedside echos.

Comment: In a young man with no history of hypertension, and with these typical symptoms of hypertrophic cardiomyopathy (HOCM), this is HOCM until proven otherwise.

Case continued

He refused hospital admission.  He was discharged with followup for a formal contrast ultrasound and cardiology clinic.

Comment: In someone like this who refuses to be admitted, it is wise to start a beta blocker.

Case continued

He returned about a week later with similar symptoms: Central CP and SOB that can last minutes or hours, but this time it lasted for less than an hour and was again worse with activity.  There was no nausea or diaphoresis.

Here is his ECG on this visit:

Slower sinus rate, but otherwise the same.

His serial troponin I (Abbott Architect contemporary troponin, 99% = 0.030 ng/mL):
0 hour: 0.034 ng/mL
3 hour: 0.024 ng/mL
6 hour: 0.011 ng/mL

Thus, he had symptoms compatible with myocardial infarction and a diagnostic fall of troponin with one level (the first) above the 99% cutoff.  This meets the definition of MI, but only if the troponin elevation is also thought to be due to ischemia.


A Formal stress echo was done:

Dynamic intraventricular gradient 15 mmHg at rest and increased to 26 mmHg post stress.
Normal estimated left ventricular ejection fraction at rest.
Normal estimated left ventricular ejection fraction improved with stress.
No wall motion abnormality at rest.
No wall motion abnormality with stress.
Left ventricular hypertrophy concentric .
Dynamic intraventricular gradient .
Hypertrophic cardiomyopathy .
Left ventricular hypertrophy concentric obstruction.

Comment: So he has HOCM and it is likely that stress induces some ischemia in this hypertrophic myocardium. Therefore, one would call this a type 2 myocardial infarction due to outflow obstruction in HOCM.

Case continued

He was started on metoprolol and discharged.

Comment: Explanation of outflow obstruction and use of beta blockade:  In obstructive HOCM, the end-systolic volume is very small due to the hypertrophic myocardium, and it thus obstructs aortic outflow at end systole.  This the source of the "gradient."  It is similar to mild aortic stenosis, but only at end systole.  Beta blockers: 1) diminish the contractility and thus result in a larger end-systolic volume and less outflow obstruction and 2) slow the heart rate, allowing for more time to fill, resulting in larger end-diastolic volume which also results in higher end-systolic volume.


Here are some other cases of HOCM:
Exertional Chest pain and Near Syncope in a Young Adolescent
In this case, the more typical large septal R-wave is present in V1, indicative of hypertrophy of the septum.

Here is a fascinating case in which dehydration leads to low end-systolic volume and shock in an HOCM patient.  Esmolol works to manage the patient:

History of Hypertrophic Cardiomyopathy (HOCM), with Tachycardia and High Lactate

What are these wide complexes?

A middle-age male arrived by private car with chest pain.  He immediately became unresponsive, before an ECG could be recorded.

He was resuscitated from ventricular fibrillation and this 12-lead was recorded:

What are the wide complexes in the precordial leads?

Same ECG with annotation:

One may perceive these as wide complexes, but they are deceptive.
The arrows in V5 and V6 point to narrow complex QRS's.  What appears to be a very wide complex tachycardia is really narrow complex with massive ST elevation and huge hyperacute T-waves.

The rate is about 160.

The rhythm strip across the bottom (lead II) shows that these relatively normal duration QRS complexes are regular, but with intervening premature ventricular beats (PVC's, one of which is highlighted by the arrow, complexes 5, 6, 11, 12, 19, 22).
Thus, it is a supraventricular rhythm with PVC's.

Although no P-waves are visible in this, I suspect that it is sinus with PVC's.  PSVT should be converted by a PVC.

The cath lab was activated and the patient was intubated and received ticagrelor and heparin.  There was no treatment of the rhythm, but it gradually slowed down (as one would expect from supportive care in sinus tachycardia).


This ECG was recorded just before transportation to the cath lab:

Sinus tachycardia at a rate of about 100.
Massive ST elevation continues.

A mid LAD 100% thrombotic occlusion was opened and stented.  Door to balloon time was less than 60 minutes.  Echo next day showed 57% EF.  Peak troponin I was 250 ng/mL.  

Diffuse Subendocardial Ischemia on the ECG. Left main? 3-vessel disease? No!

This was contributed by some folks at Wake Forest:
Jason Stopyra, Shannon Mumma, Sean O'Rourke, and Brian Hiestand.
It was edited by Smith

CASE:

A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chest pain, weakness and nausea. The paramedic’s initial impression of the patient was that he was critically ill. The patient’s mental status was altered and his skin was pale and dusky. The initial blood pressure was 80/palp with a heart rate of 104, respirations 20, oxygen saturations of 94% and a finger stick blood glucose of 268. Exam was otherwise notable for audible wheezes, sluggish cap refill, confusion, and difficulty following commands and answering questions.

An immediate 12-lead EKG was obtained:

There is ST elevation in leads aVR and V1, with marked ST depression in I, II, III, aVF, V3-V6.
What should be done?  
Should the cath lab be activated?

Smith comment:
This patient did not have a bedside ultrasound.    Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip):

This is recorded with the LV on the right.

Look at the aortic outflow tract.  What do you see?  Answer below in the still shot.









Clinical Course

The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. En route, EMS administered aspirin 325mg by mouth, but withheld nitroglycerin due to initial hypotension. In addition, the patient received 750 mL of fluid resuscitation with transient improvement of blood pressure.

The patient was brought directly to the cardiac catheterization lab for PCI, bypassing the ED. In the cath lab, the patient’s blood pressure remained low. The diagnostic coronary angiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Aortic angiogram did not reveal aortic dissection. During the procedure, the patient had an increasing oxygen requirement and was intubated for airway protection and oxygenation. A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis, severe LVH, and a small LV cavity. The patient was transported to the CCU for further medical optimization where a pulmonary artery catheter was placed.

Here is the still shot of the ultrasound above:
This still shot shows the area of interest:

There is a hyperechoic area at the aortic valve
This is aortic sclerosis and is highly associated with aortic stenosis.
If you see this, you should Doppler the valve.
The aortic valve in this example also had critical stenosis by Doppler

The patient continued to be hemodynamically unstable with poor cardiac output and very high LV filling pressures. Despite the use of multiple high dose vasopressors, he continued to be hypotensive. The following day, the patient underwent balloon aortic valvuloplasty for severe symptomatic aortic stenosis with hypotension and NYHA class IV symptoms. Post-valvuloplasty, the patient’s pressure gradient improved, but was still substantial. Patient was continued on maximal pressors, but remained hypotensive. Approximately seven hours after he returned from valvuloplasty he went into asystolic arrest.

DISCUSSION:

The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.  Although this is considered a "STEMI equivalent" and the ACC/AHA guidelines even approve of thrombolytics for ACS with this ECG, the usual criteria used to alert the cath lab team of an inbound Code STEMI are not met by this ECG.

Smith comment:
Remember, ST depression does not localize to the area of ischemia, so "infero-lateral" does not tell you where the ischemia is - in fact, it is diffuse subendocardial ischemia.  ST elevation in lead aVR is reciprocal to this ST depression of diffuse subendocardial ischemia; the ST depression vector is towards II and V5 and thus the ST elevation vector is towards aVR.

Author continued:
STE in aVR is often due to left main coronary artery obstruction (OR 4.72), and is associated with in-hospital cardiovascular mortality (OR 5.58).¹ ST elevation of 1 millimeter or greater has been shown to be 80% sensitive and 90% specific for severe left main coronary artery and/or 3-vessel disease that may require coronary artery bypass grafting, in some series.² The astute paramedic recognized this possibility and announced a CODE STEMI.

Smith comment:
I would change the above statement to: "In the setting of ACS, STE in aVR is often due to left main or 3-vessel obstruction...."  The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.  Diffuse subendocardial ischemia is more often due to supply/demand mismatch in the absence of ACS than it is due to ACS.  Common etiologies of supply/demand mismatch are hypoxia, tachydysrhythmias,  hypotension (from whatever cause), anemia, coronary artery stenosis without ACS, or (intraventricular) hypertension.

--Oxygen supply is determined by: 1) oxygen carrying capacity, 2) O2 saturation, and 3) Coronary flow.   Thus, in the absence of athero-thrombotic mechanism (ACS), myocardial ischemia can be brought on by:
1) Hypotension (diastolic hypotension, as all coronary flow happens during diastole because intramyocardial pressure during systole stops blood flow).  Hypotension may of course be a result of a brady- or tachydysrhythmia.
2) Hypoxia, including poisons of oxidative phosphorylation such as HS, CO, CN.
3) Anemia, or poisons of hemoglobin such as methemoglobin or CO
4) Fixed coronary stenosis that limits flow.

--Oxygen demand is determined by:
1)  Afterload (high resistance to LV outflow), which is increased by elevated blood pressure or by aortic stenosis
2)  Heart rate: sinus tachycardia

--This patient has both decreased supply (hypotension) and increased demand from 1) high afterload (LV pressures are very high because of the aortic stenosis outflow resistance) and 2) high heart rate.

--This demonstrates that there may be some value to heart auscultation, to listen for an aortic murmur.  In fact, bedside ultrasound might even find severe aortic stenosis.  If you can use Doppler, then you can diagnose it.


Authors' commentary: Cardiogenic shock in the setting of severe aortic stenosis.

As I met the paramedics and cath team in the lab, I was ready to see severe coronary disease (CAD), but the vessels were non-obstructive. This patient’s severe aortic stenosis (AS) and associated severe cardiogenic shock likely created the ECG pattern, resulting in a very difficult challenge for our inpatient team.

Fundamentally, cardiogenic shock is an issue of decreased cardiac output. This may be secondary to multiple factors, including decreased cardiac contractility (ie. myocardial infarction), arrhythmias, valvular pathology, shunts, or outflow obstructions.

As with other cases of shock, initial fluid resuscitation may be considered. In cardiogenic shock, fluid may worsen the pulmonary edema associated with acute heart failure, but may still be required to support the hemodynamic status of the patient.

Guidelines from the American Heart Association have been unchanged for decades with recommendations for positive inotropes, such as dobutamine and dopamine, in cases of cardiogenic shock.³ There is evidence to show that using sub-maximal doses of both dobutamine and dopamine in conjunction, rather than using a single agent, provides benefit for the patient. Benefits include improvement in the patient’s MAP and cardiac output, while minimizing the amount of myocardial oxygen used with the increased cardiac output (CO).⁴ This is crucial, as these patients may have already had some degree of cardiac ischemia. This was particularly important for the patient presented above, given the baseline increase in oxygen consumption seen in AS due to the outflow obstruction.

Smith comment: 
In a large randomized trial of dopamine vs. norepinephrine (11) for shock which was published after the above-mentioned recommendations, dopamine had more adverse events (especially severe dysrhythmias, and especially atrial fibrillation).  In the subgroup of patients with cardiogenic shock, dopamine had a 33% statistically significant elevated mortality over norepinephrine.   Thus, norepinephrine is a better choice in cardiogenic shock (as in this patient) than dopamine or dobutamine.  Dobutamine may be preferred in patients without severe hypotension who have high vascular resistance.
--De Backer D et al.  Comparison of Dopamine and Norepinephrine in the Treatment of Shock.  NEJM 362(9):779; March 4, 2009. 


Author continued: 
Another positive inotrope to consider would be milrinone as it decreases SVR and increases cardiac output; however, one must proceed with caution as the pharmacological mechanism of milrinone can cause vasodilation and worsen hypotension.

When pressors are not able to sustain blood pressure, balloon valvuloplasty may be considered. This is a procedure whereby a catheter is introduced through the femoral artery, and advanced to the have the tip distal to the left subclavian artery. A balloon is then threaded over the catheter, and is inflated and deflated with diastole and systole, respectively. It has been recommended as a bridge to surgery in those that are not candidates for surgery.⁵ Unfortunately, availability is generally limited to major medical centers.^6,7 Surgical repair of AS, by either TAVR or SAVR, is the definitive treatment for this condition. It should be noted, though, that emergent surgical intervention in unstable AS patients is associated with significant mortality, with rates between 30-50%.⁸

Vasodilator therapy for critical AS

Although not applicable to the case above given the patient’s hypotension, nitroprusside may be appropriate for patients with pulmonary edema in the setting of acute heart failure secondary to AS. Though long thought to be contraindicated in AS due to the condition’s preload-dependent state, there has been some evidence to indicate nitroprusside is beneficial to these patients. In one important uncontrolled study, nitroprusside used in patients with critical AS and heart failure with reduced ejection fraction (mean EF of 21%, mean MAP of 81 mm Hg) had significant improvement of cardiac index, without any episodes of hypotension, ischemic EKG changes, arrhythmias, or dyspnea.⁹  The only criterion for exclusion from this study was hypotension, defined as either the need for intravenous inotropic or pressor agents (dobutamine, dopamine, epinephrine, milrinone, norepinephrine, or phenylephrine) or a mean systemic arterial pressure below 60 mm Hg. The mean MAP for these patients was 81 +/- 13.

Furthermore, a study compared patients with AS to patients without AS in acute pulmonary edema who received nitrates. There was no significant difference between the percentage of patients in each group who developed hypotension after starting therapy. However, there was note that once these patients did develop hypotension, patients with moderate and severe AS were more likely to have sustained hypotension despite interventions.¹⁰

The 2014 ACC/AHA guidelines for the Management of Patients with Valvular Heart Disease, referencing this article, gives this recommendation:

"CLASS IIb 1. Vasodilator therapy may be reasonable if used with invasive hemodynamic monitoring in the acute management of patients with severe decompensated AS (stage D) with NYHA class IV HF symptoms. (Level of Evidence: C) In patients who present with severe AS and NYHA class IV HF, afterload reduction may be used in an effort to stabilize the patient before urgent AVR. Invasive monitoring of LV filling pressures, cardiac output, and systemic vascular resistance is essential because of the tenuous hemodynamic status of these patients, in whom a sudden decline in systemic vascular resistance might result in an acute decline in cardiac output across the obstructed aortic valve. However, some patients do benefit with an increase in cardiac output as systemic vascular resistance is slowly adjusted downward due to the reduction in total LV afterload. AVR should be performed as soon as feasible in these patients."

CONCLUSION:

The variables that interplay in cases of severe aortic stenosis are what cause these patients to be so difficult to manage, and specific therapies targeted to fix one issue often worsen the effects of another issue. If someone is in respiratory distress, their airway and breathing needs to be secured, either through non-invasive or invasive means. Next, the patient’s blood pressure needs to be stabilized. Oftentimes the most appropriate agent will be a positive inotrope, with consideration of a vasoactive agent in persistent hypotension. Once a patient is stabilized, determining the extent of damage to their myocardium and a plan for definitive management can then be determined.

Smith comment:

Supportive care is often overlooked in the management of cardiogenic shock.  The work of breathing demands significant cardiac output and thus puts demands on the heart.  Mechanical ventilation with paralysis removes up to 50% oxygen demand and can put the heart to rest.  I would immediately intubate a patient who is this ill.

As for other invasive therapies, intra-aortic balloon counterpulsation (12, 13) appears to work well in non-randomized studies, and this would also make sense: the balloon in the aorta inflates in diastole, increasing diastolic pressure and thus coronary flow. It also deflates during systole, which normally would reduce afterload; however, in the setting of aortic stenosis, the afterload is determined mostly by the valve, not by post-valve resistance.

Smith Final Comment:It is uncertain what initiated this patient's instability.  Any alteration in physiology can change "compensated" AS to "decompensated" AS.  For instance: sepsis, bleeding, dehydration, hypoxia, and mild ACS.  This patient had a small LV cavity which is unusual for someone with AS, poor LV function, and high filling pressures, but is probably due to severe LVH.  As LV filling pressures were found to be high, this small LV cavity would not be a result of volume depletion.  In any case, once AS becomes decompensated, for whatever reason, it is extremely difficult to manage because of the low coronary perfusion pressure and high oxygen demand.

REFERENCES:

1.   Taglieri N, Marzocchi A, Saia F, et al. Short- and long-term prognostic significance of ST-segment elevation in lead aVR in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol 2011;108:21-8.

2.   Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol 2011;107:495-500.

3.      Overgaard, Christopher; Dzavik, Vladimir. Contemporary Reviews in Cardiovascular Medicine. Inotropes and Vasopressors: Review of Physiology and Clinical Use in Cardiovascular Medicine. Circulation. 2008;118:1047-1056.

4.      Richard, C; et al. Combined Hemodynamic Effects of Dopamine and Dobutamine in Cardiogenic Shock. Circulation 67, No. 3, 1983.

5.      Safian RD, Berman AD, Diver DJ, et al. Balloon aortic valvuloplasty in 170 consecutive patients. N Engl J Med 1988;319:125-30

6.      Rahimtoola SH. Catheter balloon valvuloplasty for severe calcific aortic stenosis: a limited role. J Am Coll Cardiol 1994;23:1076-1078

7.      Moreno PR, Jang IK, Newell JB, Block PC, Palacios IF. The role of percutaneous aortic balloon valvuloplasty in patients with cardiogenic shock and critical aortic stenosis. J Am Coll Cardiol 1994;23:1071-1075

8.      Hutter AM Jr, De Sanctis RW, Nathan MJ, et al. Aortic valve surgery as an emergency procedure. Circulation 1970;41:623-627

9.      Umesh N. Khot, MD; et al. Nitroprusside in Critically Ill Patients with Left Ventricular Dysfunction and Aortic Stenosis. N Engl J Med 2003; 348:1756-1763, 5/1/2013.

10.  Claveau, D; et al. Complications Associated with Nitrate Use in Patients Presenting with Acute Pulmonary Edema and Concomitant Moderate or Severe Aortic Stenosis. Annals of Emergency Medicine. 2015 Oct; 66(4):355-362.
11.  De Backer D et al.  Comparison of Dopamine and Norepinephrine in the Treatment of Shock.  NEJM 362(9):779; March 4, 2009. 

12.  Folland ED, et al.  Intraaortic Balloon Counterpulsation as a temporary support measure in decompensated critical aortic stenosis.  J Am Coll Cardiol. 1985;5(3):711-716. 

http://content.onlinejacc.org/article.aspx?articleid=1111078
13.  Olcay A. et al.  Cardiogenic shock in the setting of severe aortic stenosis: role of intra-aortic balloon pump support.  Heart 2011;97:838-843
http://heart.bmj.com/content/97/10/838.short
14.  Nishimura RA and Otto CM, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease.  Journal of the American College of Cardiology 63(22):e57-e185; June 10, 2014.