Left Bundle Branch Block and Left Anterior Descending Artery occlusion: Serial ECGs then T-wave inversion after reperfusion

A 50 yo male presented with chest pain.  This ECG was recorded at 0415.

There is sinus tachycardia.  There is left bundle branch block (LBBB).  All ST-T complexes are discordant.  However, the ST-T in V1-V4 is excessively discordant: with 6 mm ST elevation, V3 meets criterion 3 of Sgarbossa's criteria (giving 2 points, not enough for a diagnosis of "MI").  By the Smith modification of Sgarbossa's criteria, the ratio of the ST elevation at the J-point (6 mm) to the S-wave (24 mm) is 0.25.  Since this is greater than the cutoff of 0.20, it would be diagnostic not just of MI, but of LAD occlusion.

The occlusion was not appreciated by the treating physicians, and another ECG was recorded at 0457:

Now the R-wave in V3 is gone (QS-wave), the S-wave is "fragmented" (an indication of infarction analogous to Q-waves), and the ST elevation remains at 6mm, with an S-wave of only 12 mm, for a ratio of 0.50.  The injury is worsening.

The notching in V3 is also known as "Cabrera's sign" (prominent notching of at least 40 msec in the ascending limb of the S-wave in any of leads V3-V5).

The patient was taken to the cath lab and a 100% LAD occlusion was opened.

Here is the ECG after reperfusion:

There is less tachycardia, as the stroke volume is now higher with improved myocardial function.  The ST elevation has mostly resolved.  There are now concordent T-waves diffusely, especially in the LAD territory.

Such T-wave inversion is a frequent sign of reperfusion even in LBBB, and when seen alone (without the preceding ECGs diagnostic of STEMI) is a common sign of NSTEMI.  T-wave concordance can be normal, so it is not a very specific nor sensitive sign of ischemia.  But it should raise your suspicion.  In the context of this case and the preceding ECGs, it is diagnostic of reperfusion and is definitely the result of ACS.

Should we activate the cath lab if the STEMI is spontaneously reperfused?

Will be on vacation until August.  Last post until then!

I received a question yesterday: "If spontaneous reperfusion (or aspirin/nitro assisted reperfusion) occurs, why is it so important to rush for reperfusion therapy?"  This is a very good question.  To my knowledge, there is no randomized trial of immediate PCI vs. delayed PCI for transient STEMI.  There is a study that randomized patients with NSTEMI to early vs. delayed PCI. It showed that patients at high risk, as measured by a GRACE score of 140 or greater (corresponding to an in-hospital mortality of 3%), had better outcomes if they underwent immediate angiogram and PCI.
[Mehta SR et al.  NEJM May 21, 2009; 360(21):2165.]

I do let the following anecdote affect my practice: 

This was a 52 year-old male I saw a few years back.  He was playing cards with his friends when his left hand became numb.  He had no CP or SOB, no arm or jaw or other pain.  His friends thought he was having a stroke and called 911.  The medics wisely recorded the following ECG prehospital.

He arrived in the ED still without any chest pain, and the medics showed me this ECG:

There is marked ST elevation in anterior precordial leads, and reciprocal ST depression in inferior leads.  This is diagnostic of proximal LAD occlusion.

I activated the cath lab at 2129 in spite of the fact that the patient was asymptomatic.

We then recorded this ECG:

There is some ST depression in V2 and V3 and hyperacute T-waves.  

Hyperacute T-waves can occur "on the way up" or "on the way down" as I like to say; this means they can be present shortly after occlusion before ST elevation, or shortly after reperfusion, after ST segments have resolved.  I considered this to be diagnostic of reperfusion.


So I de-activated the cath lab at 2135.

Then the patient became hypotensive.  We recorded this ECG:

Obvious anterior STEMI

I re-activated the cath lab at 2145.  The total delay, then, was 16 minutes.

Shortly after the LAD angiogram, which showed 100% occlusion, the patient arrested and could not be resuscitated.

If I had let the cath lab be activated in spite of reperfusion, he would be alive.

This was a big mistake of mine.

Any STEMI is very high risk, even if reperfused.  I don't believe you'll ever be criticized for activating the cath lab if you have just one ECG that is diagnostic of STEMI.

Wait until after the ECG to give Nitroglycerine

Here is the ED ECG of a 58 yo male whose chest pain is resolved:


There is sinus rhythm with a PAC (which has aberrant conduction -- RBBB).  There is nondiagostic ST depression in V3 and nondiagnostic ST-T abnormalities in precordial leads.

Without any ECG from earlier when the patient had chest pain, this is nondiagnostic.  With a negative troponin, the patient would be admitted for observation.



Let's go back to the beginning:

A 58 yo male with a h/o CABG developed on and off chest pain which became constant while playing golf.

911 was called.  Here is his initial prehospital ECG at 1129:

There is sinus rhythm and clear posterolateral STEMI, with ST elevation in I and aVL and reciprocal ST depression in III and aVF.  There is ST depression in right precordial leads diagnostic of posterior STEMI.

The computer read ***Acute MI***.  The cath lab was activated prehospital.  

He received aspirin and Nitroglycerin, had relief of chest pain, and had this ECG recorded at 1136:

There is now minimal ST elevation in aVL with minimal reciprocal ST depression.  Clearly the artery is reperfused.

Did NTG cause this reperfusion?  That can't be known.  But had this second ECG been the first one recorded, there would be no indication for immediate reperfusion.
He arrived in the ED and had this ECG recorded at 1153:

This is the ECG shown first, above, with the PAC with aberrant RBBB conduction and non-diagnostic ST-T findings.

Imagine if you did not have the prehospital ECGs.  It would be tough to diagnose ACS, in spite of a very high risk situation.

He did develop chest pain again, and had this ECG recorded at 1206:

Sinus rhythm with 2 aberrantly conducted (RBBB) PACs.  Now there is again ST elevation in aVL with reciprocal depression in lead III

The initial troponin was normal.  He was taken for immediate angiography, where a 99% 2nd diagonal (2nd major lateral branch off the LAD) lesion was found and opened.

The next AM he had a completely normal echocardiogram with EF of 65%.  Peak troponin was 0.85 ng/ml.  Here is his ECG the next AM.

Notice the reperfusion T-waves in I and aVL.

Thus, the next day, the ECG was more sensitive than echo for MI.   This is not unusual, but sometimes, due to a negative echo, cardiologists can be convinced (in spite of contrary evidence), that no MI occurred.  I have heard expressions of high faith in the sensitivity of echo for ACS.

Learning points:
1. NTG may cause reperfusion
2. Record an ECG before NTG
3. Always look at prehospital ECGs
4. Even after STEMI (if reperfused, with small amount of myocardium infarcted), and even when the ECG is diagnostic of ACS (as it was the next day), the simultaneous echocardiogram may be normal.

Here is an interesting abstract regarding NTG after the EKG:

Mahoney BD, Hildebrandt DA, Allegra P. Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy. Prehospital Emergency Care 2008;15:105, Abstract 24.

 Hypothesis. The decision to take a patient for emergent reperfusion therapy is largely determined by an ECG diagnostic for ST Elevation Myocardial Infarction (STEMI). Hildebrandt et al have proven that  prehospital 12 Lead ECGs followed by an immediate call for reperfusion team mobilization reduce door to balloon times.We hypothesize that prehospital ECGs will normalize in some STEMI patients after  nitroglycerin (NTG)therapy or due to spontaneous reperfusion.  NTG therapy before an ECG, or the absence of a prehospital ECG capacity in some services may lead to missing the early diagnosis of STEMI thus delaying reperfusion therapy. Methods. A prospective analysis of consecutive adult patients  presenting to an urban/suburban two paramedic ambulance service fromJuly 15, 2006, to August 15, 2007, who have diagnostic ECGs for STEMI.  Paramedics managing a possible myocardial infarction patient were instructed to obtain rapidly an ECG prior to treatment with NTG. If the initial ECG was diagnostic for STEMI the paramedic called to mobilize the reperfusion team. A second ECG was done prior to arrival at the ED. The ECGs were later reviewed by emergency physicians and cardiologists who confirmed the presence of a diagnostic prehospital ECG and STEMI.  Results. During the 13 month interval, 87 patients had an initial ECG that was diagnostic for STEMI. These patients received no NTG from the paramedics prior to obtaining the first ECG. An average of 16 minutes 42 seconds later, 3 patients had an ECG that was no longer diagnostic for STEMI and 3 had a partial normalization in their ECG that made diagnosis of STEMI more difficult. Conclusions. Prehospital ECGs diagnostic for STEMI can normalize or become nondiagnostic after NTG administration or due to spontaneous reperfusion or evolution. In the absence of a prehospital ECG, it is possible that 6 of 87 (7%) of STEMI patients in this study would have had reperfusion delayed due to a rapid change in their ECG. Limitations includenocontrol groupreceiving NTG prior to the first ECG.

Missed STEMI, spontaneously reperfused

Click here for other very instructive cases of missed STEMI.

This is a 48 yo female with no risk factors for CAD had sudden onset of arm numbness radiating to bilateral arms, followed by substernal chest heaviness that radiated to both sides of chest.  She had some associated SOB.  In previous weeks she had been having SOB when climbing 2 flights of stairs.  She called 911.  Medics arrived and recorded the following ECG at 1756:

There is sinus rhythm and a wandering baseline.  There is no ST elevation nor hyperacute T-waves, nor ST depression anywhere.   The ST segments are upwardly concave.  R-wave progression is normal.  It is a normal ECG.

The medics gave her sublingual NTG with some decrease in symptoms. They gave her an aspirin.



She presented to the ED at 1832 is some distress; the nurse's note mentions "grunting, mottled." 

This is the patient's first ED ECG, recorded at 1845:

There is now 1 mm of ST elevation in V2 and minimal STE in V3.  The ST segments are straight.  There is poor R-wave progression.  The T-waves are larger.  This description makes it sound like MI, but really, at a glance, it is not terribly remarkable on its own -- until you compare it with the previous.

The physicians caring for the patient were unaware of the prehospital ECG, and did not go look for it.  The patient remained in some discomfort, but no serial ECGs were obtained.  The first troponin was negative.  At 2016 the patient had no more grunting respirations.

With the ECG read as normal, a negative troponin, and a low risk patient, the providers did not have a high suspicion for ACS, so admitted her to observation with no further antiplatelet or antithrombotic therapy.  By the time of admission to observation, she had no more chest pain.  No more ECGs had been done.

Troponins

First trop at 1932 "normal" (negative)


Drawn at 2335: 34.8 (this returned at 0100, prompting the following ECG at 0111, 6.5 hours after the last one)

There are now Wellens' T-waves in V1-V5 and poor R-wave progression.

What happened?

One needs to view the prehospital ECG and the ED ECG side by side:

ED ECG is on the right.  Notice the T-waves are taller and fatter, the ST segments straight, and the R-waves have less voltage.  This is almost certainly a developing anterior STEMI.

Had this side by side comparison been done, the index of suspicion would have been much higher.  Perhaps a second, or third, ED ECG would have been recorded.  It almost certainly would have revealed more ST elevation and had indication for immediate reperfusion.

That her pain eventually spontaneously subsided indicates probable spontaneous reperfusion.

Subsequent troponins
0250: 41.7
0455: 35.6

An echocardiogram the next day showed an EF 55% and a regional wall motion abnormality in the distal septum, anterior and apex.

An angiogram later that day showed the culprit lesion at a 60% LAD stenosis (the patient did indeed have spontaneous reperfusion, but not before losing a significant amount of myocardium).

Learning points
1.  This is labelled a NonSTEMI, and shows one of the many ways in which a damaging coronary occlusion is called a NonSTEMI rather than a STEMI: the fewer ECGs you record, the less chance your STEMI is called a STEMI.
2. Always do serial ECGs in patients with ongoing unexplained substernal chest pain.
3. Always compare the ED ECG with the prehospital ECG
4. Beware of straight ST segments, and any ST elevation that is not accompanied by well-formed R-waves.  Early repolarization always has well formed R-waves.  This is the main reason why my early repol vs. MI equation works (although, in the study, I excluded any patients with straight ST segments).