Chest pain in a middle-aged male

A middle-aged male presented with acute onset of typical ischemic type chest pain.

Here is his initial ECG:
What do you see?










He had a previous ECG from 10 years prior:
This shows either subaute anterior MI (Q-waves, ST Elevation, T-wave inversion) or acute MI superimposed on previous MI.  LV aneurysm is possible but unlikely (no QS-waves, significant T-wave amplitude, even though largely negative).


So we know he has LAD disease and previous MI.

The acute ECG (first one at top) clearly shows the previous MI (Q-waves).  The T-waves are upright.  Is this pseudonormalization?  No.  Over weeks to months and certainly years, inverted T-waves of MI normalize as part of the natural history of the ECG in MI (Although, in LV aneurysm, they often remain with shallow invertion).  So before this acute event the T-waves were likely upright.

But these previous T-waves were not upright and hyperacute, as they are here in the top ECG: the T-waves in that first ECG are suspiciously large, and there is some hint of reciprocal ST depression in inferior leads.  These findings need aggressive investigation with frequent serial ECGs or immediate echocardiography.  They could represent LAD occlusion.


The pain continued and another ECG was recorded 1 hour later:
What is the diagnosis?















These are now subtle de Winter's hyperacute T-waves; see the subtle ST depression in V3.

These were not seen or appreciated.  The initial troponin returned at less than 0.04 ng/mL.  The patient was admitted to the hospital without angiography in spite of continued chest pain.  

A second troponin at 6 hours returned at 0.7 ng/mL (elevated).  He was diagnosed with NonSTEMI.  The pain continued.


A third ECG was recorded at 7 hours:
Now the T-waves are less acute, but there are deepening Q-waves and loss of R-wave height



The troponin I was 16 ng/mL at hour 13.  

Here is the 13 hour ECG:
T-waves are smaller yet, especially in V4




He went for cath and it showed 100% ostial LAD occlusion.  There was no mention of collateral circulation.

Echo: Anterior wall motion abnormality with EF of 35-40%, although it is unknown what the EF was before this event.  There was no myocardial wall thinning to suggest that this WMA was due to old MI, though the previous ECG is fairly conclusive about that.


Here is a post cath ECG at 26 hours:
Now there is also some inferior ST elevation with reciprocal ST depression in aVL.  This is highly suggestive of inferior MI.  The RCA was anomolous, arising from the left coronary cusp, and it is possible (though not mentioned) that it was affected during the procedure.  There is no more information on this.




Diagnosis: LAD occlusion in the context of previous MI, and manifesting subtle de Winter's T-waves. 




Here are some more examples of the wide variety of de Winter's T-waves from LAD occlusion:


















Anterior STEMI?

The patient presents to the emergency Department with complaints of substernal left-sided chest pain present for 4 days but worse in the last 24 hours.

Here is his ED ECG:

ED ECG
The computerized QTc is 451.  What do you think?  The previous ECG, with interpretation, is below.














Here is the Previous ECG.
My reading was printed on the ECG as "probable benign T-wave inversion."    I had discharged the patient at his previous visit.  His presentation had not been concerning for ACS and his ECG was, to me, a benign variant.




The physicians were appropriately worried about the previous ECG and used the formula (see sidebar Excel applet) and came out with a value above 23.4  (I cannot remember what the value was, but they did use 3 mm for the STE variable).

When I apply the formula, even if I use 3 mm as the ST elevation as 60 ms after the J-point, and use R amplitude in V4 at 22 mm, I get 23.03 (which is less than 23.4 and thus indicates early repol).  Furthermore, the morphology of V4 is nearly diagnostic of "Benign T-wave inversion."

In general, if there is T-wave inversion, I do not recommend using the formula. Patients whose ECGs had T-wave inversion in V2-V5 were excluded from the study because T-wave inversion, as a general rule, should imply MI.  However, if you are familiar with the morphology of Benign T-wave Inversion (BTWI), then you would see that these ECGs manifest probable BTWI and be less worried about the ST Elevation.

As for the formula, when you get a value that is close to 23.4, it is wise to not rely on it too heavily.  The sensitivity and specificity of 23.4 was close to 90%, but I the closer the value is to 23.4, the less sensitive and specific it is.

Appropriately, they ordered a 2nd ED ECG about 20 minutes later:
QTc is 445



They thought there might be more STE in lead V3.  I do not see any significant change.

They were still worried, but instead of activating the cath lab, they appropriately consulted the cardiologist and together decided on an immediate formal echocardiogram.

The echo showed:

--Normal left ventricular size, mild concentric left ventricular hypertrophy and hyperdynamic systolic function.
--The estimated left ventricular ejection fraction is 75 %.
--No left ventricular wall motion abnormality identified.
--Normal right ventricular size and function.

The patient was admitted and ruled out for MI.


Benign T-wave Inversion (this link takes you to many examples)

There are many etiologies of T-wave inversion.  We are most worried about ischemic T-wave inversion.  Wellens' syndrome is particularly dangerous, as it signifies an unstable critical LAD stenosis.  I have several posts on this; here is one that shows the entire evolution.

Another etiology is "Benign T-wave Inversion", which has long been recognized. I first saw it described in Chou's textbook.  It is a normal variant associated with early repolarization.  K. Wang recently studied it.  He reviewed ECGs from all 11,424 patients who had at least one recorded during 2007 at Hennepin County Medical Center (where I work) and set aside the 101 cases of benign T-wave inversion.  97 were black.  3.7% of black men and  1% of black women had this finding.  1 of 5099 white patients had it.  Aside from an 8.8% incidence (9 of 109) black males aged 17-19, it was evenly distributed by age group.

I have reviewed these 101 ECGs, and what strikes me is:

1. There is a relatively short QT interval (QTc < 425ms)  (this case would be an exception!)
2. The leads with T-wave inversion often have very distinct J-waves.
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves).
5. The leads with T-wave inversion (left precordial) usually have some ST elevation
6. Right precordial leads often have ST elevation typical of classic early repolarization
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
9. II, III, and aVF also frequently have T-wave inversion. 

Anterior STEMI?

The patient presents to the emergency Department with complaints of substernal left-sided chest pain present for 4 days but worse in the last 24 hours.

Here is his ED ECG:

ED ECG
The computerized QTc is 451.  What do you think?  The previous ECG, with interpretation, is below.














Here is the Previous ECG.
My reading was printed on the ECG as "probable benign T-wave inversion."    I had discharged the patient at his previous visit.  His presentation had not been concerning for ACS and his ECG was, to me, a benign variant.




The physicians were appropriately worried about the previous ECG and used the formula (see sidebar Excel applet) and came out with a value above 23.4  (I cannot remember what the value was, but they did use 3 mm for the STE variable).

When I apply the formula, even if I use 3 mm as the ST elevation as 60 ms after the J-point, and use R amplitude in V4 at 22 mm, I get 23.03 (which is less than 23.4 and thus indicates early repol).  Furthermore, the morphology of V4 is nearly diagnostic of "Benign T-wave inversion."

In general, if there is T-wave inversion, I do not recommend using the formula. Patients whose ECGs had T-wave inversion in V2-V5 were excluded from the study because T-wave inversion, as a general rule, should imply MI.  However, if you are familiar with the morphology of Benign T-wave Inversion (BTWI), then you would see that these ECGs manifest probable BTWI and be less worried about the ST Elevation.

As for the formula, when you get a value that is close to 23.4, it is wise to not rely on it too heavily.  The sensitivity and specificity of 23.4 was close to 90%, but I the closer the value is to 23.4, the less sensitive and specific it is.

Appropriately, they ordered a 2nd ED ECG about 20 minutes later:
QTc is 445



They thought there might be more STE in lead V3.  I do not see any significant change.

They were still worried, but instead of activating the cath lab, they appropriately consulted the cardiologist and together decided on an immediate formal echocardiogram.

The echo showed:

--Normal left ventricular size, mild concentric left ventricular hypertrophy and hyperdynamic systolic function.
--The estimated left ventricular ejection fraction is 75 %.
--No left ventricular wall motion abnormality identified.
--Normal right ventricular size and function.

The patient was admitted and ruled out for MI.


Benign T-wave Inversion (this link takes you to many examples)

There are many etiologies of T-wave inversion.  We are most worried about ischemic T-wave inversion.  Wellens' syndrome is particularly dangerous, as it signifies an unstable critical LAD stenosis.  I have several posts on this; here is one that shows the entire evolution.

Another etiology is "Benign T-wave Inversion", which has long been recognized. I first saw it described in Chou's textbook.  It is a normal variant associated with early repolarization.  K. Wang recently studied it.  He reviewed ECGs from all 11,424 patients who had at least one recorded during 2007 at Hennepin County Medical Center (where I work) and set aside the 101 cases of benign T-wave inversion.  97 were black.  3.7% of black men and  1% of black women had this finding.  1 of 5099 white patients had it.  Aside from an 8.8% incidence (9 of 109) black males aged 17-19, it was evenly distributed by age group.

I have reviewed these 101 ECGs, and what strikes me is:

1. There is a relatively short QT interval (QTc < 425ms)  (this case would be an exception!)
2. The leads with T-wave inversion often have very distinct J-waves.
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves).
5. The leads with T-wave inversion (left precordial) usually have some ST elevation
6. Right precordial leads often have ST elevation typical of classic early repolarization
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
9. II, III, and aVF also frequently have T-wave inversion. 

Unstable Angina: Dr. Braunwald asks if it is time for a Requiem

In a recent commentary, Dr. Eugene Braunwald asked if it is time for a Requiem for Unstable Angina (ACS without a positive troponin, as defined by a rise and/or fall with at least one level above the 99% reference value).

http://circ.ahajournals.org.ezp2.lib.umn.edu/content/127/24/2452.full.pdf+html

Here is a quote:

"Indeed, in its 2008–2009 report, the World Health Organization revision of the definition of MI stated: 'Many patients who in the past would have been diagnosed as having unstable angina will now be diagnosed as having had an MI.'  In the next few years, there will likely be much wider use of higher-sensitivity assays for cTn and acceptance of the universal definition of MI.  As a consequence, UA is likely to be further marginalized, its definition will become highly dependent on the particular assay for cTn used, and the term will become ever more ambiguous and cause confusion because it will mean different things to different people. Indeed, it is not clear that ACS events can occur without some increase in circulating cTn when measured by a high sensitivity assay."

This article prompted some recent Tweets about whether Unstable Angina (UA) still exists in the age of sensitive biomarkers. Don't all ACS rule in by serial trops now?

UA certainly does still exist, at least for now, because in the U.S. we do not yet have FDA approval for high sensitivity troponin (hscTnI).  And we do not yet know for certain whether hscTnI will abolish UA, or just diminish the number of patients with troponin (-) ACS.

Perhaps when we get hs troponin in the U.S. (not yet), it will be exceedingly uncommon, but with the use of contemporary troponin assays, it is an important phenomenon still.

Below are some old examples, and one new one:

Here are several previously posted cases.  

Here is another that was just posted on April 4.

Now I have yet another to post:

A patient with DM and, it seems, heavy alcohol use had also been recently admitted for chest pain: she ruled out for MI (sorry, I do not have the ECGs from that presentation), then had a positive stress test, which led to an LAD stent (thus, she had unstable angina, but that is only the first of two episodes for her).

She presented to the ED some time after the stent, complaining of fatigue and chest pain.  She had stopped taking her Clopidogrel.  She had also stopped her propranolol.  She was dehydrated and ketotic.  BP was normal and she was tachycardic.  There was a systolic murmur.

Here is her ED ECG:
There is sinus tach, perhaps due to both dehydration and possibly also to some propranolol withdrawal.  It is abnormal, but there is nothing specific for ischemia.  It certainly could represent ischemia, but no definite active ongoing ischemia.  The QT appears to be about 380 ms and thus QTc = 570ms (see leads II and III).  This QT is very long and suggests that the "T" waves in II, and III are really U-waves.  I strongly suspect hypokalemia, but (oddly) no K was measured until over 24 hours later.  


She had a stat formal echo which showed hyperdynamic heart and anterior wall motion abnormality but with EF of 85%.  There was no serious valvular disorder.

Her pain resolved.  She ruled out for MI with contemporary high sensitivity troponins.

The next morning she had a VT arrest and was resuscitated.  Here is her post resus ECG:
Large ST elevation.  It has a very odd morphology, even mimicking Brugada and Hyperkalemia, but it must be assumed to be LAD occlusion

She was taken for cath and had a 100% LAD occlusion that was stented.

She did well.

Lesson:

Unstable Angina still exists.  It is dangerous.  It may be missed by both ECG and (by definition) troponin.  It happened twice in this patient.  It is too early for a Requiem.

Chest pain in a patient with previous inferior STEMI. Scrutinize both the ECG and the history!

I was looking through a stack of ECGs (I can't help myself) and saw this one, which caught my eye:
What do you think?  Computerized QRS duration is 120 ms.











My thought was that it looked like there was likely very subtle anterior injury.  In spite of the slightly prolonged conduction, I applied the anterior STEMI calculator (see sidebar excel applet, or "subtleSTEMI" iphone app), using:

1. ST elevation at 60 ms after the J-point in lead V3: 2 mm (it is probably really 2.5 mm, but I wanted to be conservative)
2. computerized QTc = 413 ms
3. R-wave amplitude in V4 = 9 mm

Result = 23.83 (greater than 23.4 and thus indicating likely LAD occlusion)

One reader thought this was LBBB and that the modified Sgarbossa rule should apply instead.
My answer: It is not a true LBBB.  The intrinsicoid inflection in V5 and V6 is only about 30 ms and must be 50 ms to be LBBB.  That is to say, it must take a long time for the left ventricle to depolarize.  Furthermore, it just doesn't "look" like LBBB.  It is simply a slightly wide QRS.


He did come in by EMS and the prehospital ECG was identical.

Here is his previous ECG:
Note the inferior ST elevation that was present even after opening the infarct artery causing the inferior STMEI.  But also look at V1 and V2.  The ST segments and T-waves are different from the ED ECG.  Thus there is new ST elevation, suggesting anteroseptal STEMI and greatly increasing the suspicion for LAD occlusion.



So I went to look at the chart:

He was a male in his 60s who complained of chest pain.  He had h/o inferior STEMI which was stented.

As I suspected, these ST and T-wave changes were not seen.  Most physicians do not see such abnormalities, even if they are changes, as in this case.  They are extremely subtle.  That is why I recommend scrutinizing them, comparing carefully with the previous ECG, and using the formula to see if your suspicions are worth pursuing.

A positive result with such scrutiny does NOT mandate cath lab activation, but does require further intense scrutiny.

One area of further scrutiny is to look at the previous cath findings:  was there LAD or left main disease?  Is LAD ischemia a real possibility?  If they had looked, they would have found that the left main had a 50% lesion and the LAD had a 90% distal stenosis.  The distal stenosis does not fit with this ECG which looks like septal STEMI, but the left main does.

This patient was treated for unstable angina medically.  His initial troponin was negative.

However, he did not get evaluated for possible acute LAD occlusion.

Outcome:

Later, his next troponin 3 hours later was 1.3 ng/mL.  At this time, he underwent another ECG, five hours after the first:
The ST elevation is resolved.  This again strongly supports that the first one had acute ischemia causing ST elevation



The next day he went for an angiogram and was found to have severe 3 vessel disease involving the left main and the LAD.  The LAD had a new, open, 80% ostial lesion.  The left main had a new 60-70% stenosis.  I am not sure which (or both?) was the culprit, but either could have resulted in death.

It is all but certain that one of them was occluded, or nearly so, when the patient was having chest pain and ST elevation.

Fortunately for all involved, this LAD (or left main) reperfused spontaneously, with the aid of aspirin, plavix, and heparin.  Had it not done so, it could have been disastrous for the patient.

He went for CABG.

Lesson:

Scrutinize the ECG
Scrutinize the History

These findings are discoverable: I found them by just glancing at the ECG in a random stack, without any other information.  They are there on the ECG.  You just have to get good at looking for them, use the formula, compare with the previous, and look at the previous angiogram results.  If suspicion persists, pursue even further scrutiny.

Waxing and Waning Chest Pain

A male in his 50s presented with Chest pain on and off during the day.  At the time of presentation, he had only some jaw pain.  An ECG was recorded:
What do you think?










There are inferior and lateral T-wave inversions (reperfusion T-waves, analogous to Wellens' waves which were described in the LAD distribution, V2-V4, but this also applies also to other coronary distributions).  There is also ST depression in V2 and V3: this is of course really ST elevation of the posterior wall, as recorded from the anterior wall.  

T-waves are upright in V2 and V3 because, just like the inferior and lateral walls, the posterior wall is also reperfused.  If we had posterior leads, it would show posterior T-wave inversion.  Instead, we have anterior lead recordings, which superimpose a positive anterior T-wave with the opposite (because recorded from the opposing anterior chest) of a negative posterior T-wave (reperfusion of the posterior wall).  Thus, we have the oppositve of a negative, which is positive; this positive is added to the anterior positive, which is two positives, and so the T-wave is upright with some added voltage.

This had me very worried, so even though the patient had no new symptoms, within 15 minutes I recorded another ECG to be certain that the artery was not re-occluding.  Here it is:
What do you think?














Now the T-waves are upright in inferior and lateral leads (pseudonormalization), indicating re-occlusion of the infarct-related artery.   There is new minimal ST elevation in II, III, aVF and reciprocal ST depression in aVL.  This is diagnostic of inferior MI (though technically not a "STEMI" because it does not meet the artibrary "criteria" for STEMI which we know are useless numerical cutoffs.

This is another NonSTEMI that needs the cath lab now, as the ECG shows signs of coronary occlusion even without 1 mm of ST elevation.

The T-waves in V2 and V3 are still upright. The predominant forces are still from the anterior wall, which is closest to the overlying leads, so any small amount of posterior positivity (which would result in a negative T-wave as recorded anteriorly) is overwhelmed by the anterior wall positive T-waves.

I activated the cath lab immediately.

Shortly thereafter, the patient reported no pain at all, including absence of neck pain.  We recorded this ECG:
Now the T-waves are inverted again, the ST segments have all but normalized, and the precordial T-waves are much larger becuase of the addition of anterior wall positive T-waves to the negative of posterior negative T-waves (see explanation above).

   

On arrival in the cath lab he was pain free.  The angiogram showed an ulcerated thrombotic plaque in the distal RCA with good flow, plus a very tight lesion in a right posterolateral branch to the posterior and lateral walls.

Diagnosis: Infero-postero-lateral MI due to dynamic ACS of the RCA.

Peak troponin I was 1 ng/mL.  

Standard management in these cases is to admit the patient on medical management for ACS: aspirin, heparin or LMWH, P2Y12 inhibitor.  If the patient rules in, then he/she goes to the cath lab the next day.  But this is not adequate for a significant percentage of NonSTEMI patients; namely, those who have evidence of coronary occlusion or an artery that is opening and closing.  There are no randomized trials of this management strategy, but there are several studies showing that when NonSTEMI patients do get their next day cath after a rule in by troponins, the infarct related artery is closed about 25-30% of the time.  These patients have higher biomarkers, worse LV function, and higher mortaility than patients whose artery is open.

1. Wang T et al.  Am Heart J 2009;157(4):716-23.
2. From AM, et al. Am J Cardiol 2010;106(8):1081-5.
3. Pride YB et al.  JACC: Cardiovasc Interventions 2010; 3(8):806-11.

Lessons:

1. Wellens' syndrome has analogous findings in the inferior and/or lateral walls.
2. T-wave changes of the posterior wall record in the opposite direction from the anterior wall.
3. Reperfusion T-waves indicate a very unstable plaque that can instantly re-occlude at any moment. The re-occlusion is signaled by a "pseudonormalization" of T-waves.  
4. Many coronary occlusions do not have 1 mm of ST segment elevation
5. Many NonSTEMIs need the cath lab now.