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)


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.

Prehospital Inferior STEMI: Bedside Echo in ED is normal

A woman in her 60's complained of chest pain.  911 was called.  She had this prehospital ECG:
Obvious Infero-posterior and lateral STEMI

The cath lab was activated.

While waiting for the cath team to be ready, I recorded this bedside echo:

This shows excellent wall motion everywhere.  I was amazed and realized that she must have had spontaneous reperfusion.  (I cannot say for certain that a high quality echo with contrast would have been normal)

So I recorded an ED ECG:
This is near normal, except for the abnormal T-waves (down up in aVL, and note the abnormal T-wave in V2).

Here is an enlargement of V1-V3:

Note the morphology of V2, because this is a one of the typical morphologies seen early after reperfusion of the posterior wall. As time goes on, the T-wave will become fully upright and taller then normal, unless there is re-occlusion


So this patient had spontaneous reperfusion.  She went to the cath lab and by the time she arrived, the RCA was again 100% occluded.  There was ruptured plaque and thrombus.  It was opened rapidly.

Peak troponin I was 0.60 ng/ml.  Formal echo was normal except for a probable anterior wall motion abnormality, only seen on one view, and possibly pre-existing.  EF 66%.

Here was the post cath ECG:
Note the tall T-wave in V3.  This is tall because the an opposite view of an inverted posterior T-wave (which is positive) is superimposed on a normal upright anterior wall T-wave.  I call this "posterior reperfusion T-waves."  There is a Q-wave in V2 which would correlate with the echo finding.

 Lessons:

1. Spontaneous reperfusion normalizes BOTH the ECG and the echocardiogram.  Only if there is persistent myocardial stunning from ischemia (which usually is present with prolonged severe ischemia) is wall motion persistently affected.  If we had done an echo during the ST elevation, there would have been a wall motion abnormality, but it disappeared with reperfusion.
2.  Learn this reperfusion morphology in lead V2 from reperfused posterior STEMI. It is important in recognizing ACS if you do not have a recording during pain.
3. Down-up T-waves (e.g., aVL here) is almost always a reperfusion morphology (alternatively, it can be a U-wave masquerading as a T-wave)

A Very Unstable Angina. No STEMI present, but needs the cath lab now.

An elderly woman with h/o diabetes and hypertension but no prior cardiac history had been having exertional chest pain for months, though with a normal stress test.  She had onset at rest of severe substernal chest pressure radiating to the neck.   There was associated SOB and diaphoresis. EMS came and recorded this ECG:

What is it?  See annotated ECG below.











I have put arrows where I think the P-waves are.  They march out regularly, but are non-conducting.  This is complete, 3rd degree, AV block.  The escape is regular at a rate of about 36 and looks like a right bundle branch block and left anterior fascicular block, which means that the escape originates from the posterior fascicle.  (Another possibility would be junctional escape with RBBB/LAFB, but this should be faster).  There are no clear ischemic ST segments or T-waves, though the expected discordant ST depression in V2 is not there, and there is a hint of upwardly sloping ST elevation in V1.

She received nitroglycerin and aspirin and her pain very much improved. She arrived in the ED with a pulse of 81 and very elevated BP at 200/90.

This ECG was recorded:
Now there is sinus rhythm with LBBB.  The only hint of ischemia are concordant T-waves in V5 and V6 (these were quite specific for MI - but not STEMI - in Sgarbossa's study).  This ECG also confirms that the previous escape was NOT junctional because nodal escape would also have associated LBBB.



The transcutaneous pacer was placed, she was given clopidogrel and heparin, and the cath lab was activated.  Electrolytes and CBC were normal.  A formal echo was done which showed an anterior and apical wall motion abnormality consistent with LAD ischemia.  The EF was about 40%.



She became bradycardic again and this was recorded:
The first half of the ECG has second degree block Mobitz II (by ECG alone, this could be Mobitz I; but in this clinical context, with previous complete AV block, it must be Mobitz II), then changing to normal rhythm with every P-wave conducted.  All conducted beats have LBBB morphology and there is no clear evidence of ischemia.


Here is a third ED ECG:
There is 2:1 AVblock for 3 beats, with every 2nd P-wave conducting to LBBB.  Then there are 3 P-waves that do not conduct, followed by an RBBB escape (just like on the prehospital ECG).  Then 2:1 block resumes.


The patient went to cath and had severe 3 vessel disease.  She ruled out for MI!!  Maximum troponin I was 0.016 ng/mL (99% reference = 0.030 ng/mL.

She had a pacer placed and went for CABG, successful.  Here is her paced ECG after surgery:
Paced rhythm with no evidence of ischemia



Later, she was in sinus rhythm:
Sinus with LBBB, again, no ischemia.




Lessons:

1. Ischemia can be severe enough to result in low EF, wall motion abnormality, and heart block, but with negative troponins.
2. There are other indications for the cath lab than ST segment or T-wave abnormalities.  These include hemodynamic instability, heart failure, dysrhythmias, heart block, and ischemic chest pain that cannot be controlled by medical means.


A Non STEMI that needs the cath lab now.

A male in his 60's called 911 for chest pain.  He had some cardiac risk factors including hypertension, on meds, but no previous coronary disease.   His pain was intermittent and he was vague about when it was present and when it was resolved.  Here is his prehospital ECG:

Diagnosis? 

He had an immediate ED ECG:
There is artifact, but the findings appear to be largely gone now





















The diagnosis is acute MI, but not STEMI.  There is slight ST elevation in lead III with reciprocal ST depression in aVL.  The T-wave is inverted in III, indicating reperfusion (what I like to call "inferior Wellens' syndrome).  There is no Q-wave, so this is unlikely to be old MI, and more likely to be acute NonSTEMI of the inferior wall.

I saw these ECGs, and since there was no immediate urgency, allowed the resident to manage it without any comment.  However, he did not see the abnormality on the prehospital ECG, so I finally said something like: "What are you going to do about the MI patient?".    When I pointed out the findings, we recorded another ECG:
Now there is increased ischemia, but where is it? My interpretation was that this is an inferior MI with posterior extension, as the ST depression in the precordial leads was maximal in V3 (opposite the posterior wall). There is about  1 mm of STE in aVR  I considered but rejected subendocardial ischemia.  

The ST elevation vector is posterior, inferior, and right, to the right of lead III and also posterior.  Is it subendocardial ischemia, or inferior MI?  See this post on the (Five primary patterns of ischemic ST depression, without ST elevation)

Because of the dynamic ACS, we activated the cath lab in the middle of the night.  Aspririn, Plavix (in spite of STE in aVR, because I thought this was inferior MI), Heparin were given.  The BP was elevated, so we gave metoprolol 5 mg IV x3 + 50 mg po.

His pain resolved and another ECG (but with precordial leads on the right) was recorded:
ST Depression is Resolved in V2 (=V1 R).  No evidence of RV MI.


Then the patient complained of increasing pain again:
There is now profound ST depression and STE in aVR, and the ST depression extends deeply in V5 and V6.  There is little ST elevation in inferior leads.

This time, the ST vector is more rightward, toward aVR and also posterior.

Now I regretted giving Plavix, as the probability of 3 vessel disease or left main insufficiency (not occlusion!) was much higher.  Thus, the chance of needing CABG was higher and Plavix can cause much operative bleeding.

Amazingly, the bedside echo showed very good LV function.

A nitro drip and sublingual nitro was given, the drip rapidly titrated to 80 mcg/min.  The BP came under better control and the patient was moved to the cath lab.

Outcome:

Was it RCA or LCX with inferior MI?  Or was it 3 vessel disease/left main insufficiency?

Both!

The active culprit was an RCA thrombus with 99% occlusion, but there was severe LAD and circumflex disease as well (severe 3 vessel disease).

The RCA was opened with POBA ("plain old balloon angioplasty") and eptifibatide was started.  The patient was referred for CABG and did well.


New ACC poster: many STEMI patients present with subtle ST elevation.

New ACC poster: many STEMI patients present with subtle ST elevation. Their prognosis is similar to those who meet STEMI "criteria". They need early reperfusion.

However, this study could have missed many occlusions because they only studied patients who did get immediate primary PCI.  They did not study the NonSTEMI patients who were later found to have limited coronary flow and might have benefited from immediate reperfusion.