Monday, June 4, 2018

Left Bundle Branch Block, Severe Chest pain, Previous Normal Angio. What is going on?

A middle-aged woman with idiopathic cardiomyopathy and biventricular failure, with previous EF of 15%, presented with sudden onset severe substernal chest pain.  

She had LBBB with a wide QRS, and therefore was a candidate for biventricular pacer for cardiac resynchronization, but when they had inserted her pacemaker, they could not get the LV lead into place (technical difficulties).  Therefore, she had a typical RV pacer.

She had a recent near perfect angiogram, described below.  

Here is her initial ED ECG:
1.  Is it paced?
2. What do you notice compared to the previous, below?
3. Is there any evidence of ischemia here?

Normal LBBB with normal proportional discordance of ST-T's.
Left axis deviation, which is common in LBBB

1.  It is not paced.  It is simply left bundle branch block (LBBB)

2.  The initial ECG has an inferior axis.  This suggests the limb leads are reversed because, whereas the previous has a large monophasic R-wave in aVL, with a negative QRS in III, the initial ECG has the opposite.

3. This initial ECG has no evidence of ischemia.

Previous normal angiogram, done to assess reason for cardiomyopathy:

Minimal coronary artery disease

Impression and recommendations:
No epicardial coronary artery disease noted to explain advancing systolic
heart failure or abnormal TTE

Suspect non-ischemic cause of cardiomyopathy

The LMCA is relatively a small caliber vessel.
No significant coronary artery disease noted.

The LAD extends to the apex.
The LAD is a medium caliber vessel.
There is a medium caliber, branching first diagonal branch with tubular 20% stenosis
stenosis in the ostial-proximal vessel segment.
There is mild plaque in the mid LAD beyond D1.
D2 is absent.
D3 is a small caliber vessel.

Large caliber vessel.
OM1 is absent (due to presence of Ramus)
OM2 is a large caliber branching vessel that supplies a majority of the
inferior and inferolateral wall to the apex.
There is a small caliber OM3.
No significant coronary artery disease noted.

Large caliber vessel.
RCA has Normal take off.
The rPDA is a medium caliber vessel (with slightly early take off) that
reaches the cardiac apex.
The RPAV is a medium caliber vessel that supplies two small rPLA branches.
No significant coronary artery disease noted.

There is a medium caliber Ramus intermediate with mild ostial plaque.

With a previous angiogram that is so nearly normal, new ACS is very unlikely.  See this post from last week about completely normal angiograms:

Chest pain, Ventricular Paced Rhythm, and a Completely Normal Angiogram 3 Months Prior.

Case continued:

The pain continued, severe, and a 2nd ECG was recorded at 24 minutes:
What do you see now?

The upright R-wave in aVL is restored.  Leads have been changed.

There is now a significant ST change in III and aVL, with new ST elevation in III that meets the modified Sgarbossa criteria: there is 2 mm of discordant ST elevation in lead III, which is 33% of the preceding S-wave, measured at 6 mm.  This exceeds the 20-25% criterion and even in just one lead is diagnostic of acute coronary occlusion.  This is especially true in that there is a change.

Comment: Patients with previous severe systolic failure are at extreme risk when they have a new coronary occlusion.  They should get the benefit of the doubt, if there is any doubt, and go to the cath lab.  It is incumbent upon the providers to prove absence of coronary occlusion.  A previous normal angiogram should not be depended upon.

The occlusion was diagnosed by the resident, who wanted to activate the cath lab, but the faculty was not convinced.

Another ECG was recorded at 46 minutes:
Now the axis is reversed, again!
And now there is excessively discordant ST elevation in aVL, with excessively discordant ST depression in lead III.
So is this an inferior MI?  Or high lateral MI?
It doesn't matter!  Activate the cath lab!

Cardiology was consulted but alas, for whatever reason, the cath lab was not activated (perhaps because of the previously near normal angiogram), and another ECG was recorded at 92 minutes:
Increasing disproportionate ST deviation

105 minutes

122 minutes
Axis changed again
Ischemia not changed

The cath lab was finally activated.


Acute Lateral ST elevation MI with LBBB.
Culprit is 100% occlusion of the LCX OM2
Lesion reduced to 0%
Very suspicious for extracoronary source of thrombus in OM2: Paroxysmal atrial fib vs. LV
thrombus.  AICD interrogation will be helpful incase of P Afib!

No significant CAD in LAD or RCA.

Coronary angiogram with OM2 occlusion treated with PTCA - clot displaced to distal vessel. Imaging suggests possible embolic etiology rather than plaque rupture. 

Post cath:
ST deviation is resolved.

Troponin I peaked at 88 ng/mL
Echo showed EF now less than 10%
Probable new regional wall motion abnormality of inferolateral wall.

Pt did not have much improvement in her symptoms after cath.  


Absence of atherosclerosis on angiogram raised concern about embolic etiology but no AF on device interrogation and TTE without e/o LV thrombus. Would like to obtain TEE to better evaluate for presence of thrombus.

A transesophageal echo (TEE) was done and a thrombus was found in left atrial appendage.  This is the apparent source of embolism and occlusion!

Learning Points:

1. The Smith Modified Sgarbossa criteria are perhaps 75-80% sensitive (similar to STEMI criteria in normal conduction).

2. However, they are 99% specific.

3.  There are reasons other than atherosclerosis for acute coronary occlusion.

4.  Thus, do not let a previous normal angiogram become an obstacle to ECG interpretation.

5. Lead placement may confuse the location of the MI, but it should not prevent you from making the diagnosis and activating the cath lab.

Comments by KEN GRAUER, MD (6/5/2018):
Superb blog post by Dr. Smith with numerous teaching points! I’ll aim my Comments on augmenting several key concepts that were addressed.
  • Among the reasons for delay in optimal treatment of this patient was failure to recognize lead misplacement. Most experienced clinicians are comfortable recognizing the most common form of lead misplacement — which is mix-up of the LA-RA electrodes. This technical mishap is often obvious due to global negativity of the P, QRS and T wave in lead I (which should otherwise never happen) — and global positivity in lead aVR. Other types of lead misplacement may be far subtler. This is the case here!
  • The 1st ECG done in the ED manifests LA-LLead Reversal. The BEST summary I have seen on recognition of the various types of lead reversal is found in Life-In-The-Fast-Lane. It is comforting that no crib sheets of key findings are needed — because all you need do is Google, “LITFL Lead Reversal” — and a link to this invaluable post immediately comes up!
As per LITFL — the findings of LA-LL Lead Reversal are:
  • Lead III becomes inverted (from its previous appearance).
  • Leads I and II switch places.
  • Leads aVL and aVF switch places.
  • Lead aVR remains unchanged.
  • PEARL: The KEY to rapid recognition of probable LA-LL Lead Reversal — is that the P wave is unexpectedly larger in lead I than it is in lead II (whereas it is usually the other way around).
For clarity — I’ve put the first 3 ECGs shown in this blog into a single figure (Figure-1). Sinus rhythm with LBBB morphology in the chest leads is present in all 3 tracings. As per Dr. Smith — there is a dramatic change in the limb lead QRS axis between the Initial ECG done in the ED (Top tracing in Figure-1) — compared to the Prior (Baseline) ECG (Middle tracing).
  • What is unusual about the relative size of the P waves in leads I and II in the Initial ED ECG?
Figure-1: A simultaneous look at the first 3 tracings in this case.
ANSWER: The P wave in lead I is much larger than the P wave in lead II in this Initial ECG (Top tracing in Figure-1). In contrast — the P wave in lead II is larger (as it should be) in the Prior (Baseline) ECG. Other findings consistent with LA-LL Lead Reversal are seen when comparing the Initial ED ECG with the Baseline ECG:
  • The appearance of leads I and II is essentially switched.
  • The appearance of leads aVL and aVF is essentially switched.
  • Polarity of the P wave, QRS complex, and ST segment in lead III is inverted.
  • Lead aVR is unchanged.
The 3rd (Bottom) tracing in Figure-1 was the 2nd ECG obtained in the ED, 24 minutes after the Initial ECG.
  • Comparing this 2nd ECG in the ED with the Baseline ECG — suggests there is subtle-but-real qualitative change in the ST-T waves in each of the inferior leads. These ST-T waves now look hyperacute. The magic “mirror-image” opposite picture is seen for the ST-T waves in leads III and aVL. In a patient with new chest pain — these changes are highly suggestive of acute coronary occlusion.
Return to the Initial ECG (Top tracing in Figure-1). Considering that we now know there was LA-LL Lead Reversal in this Initial ECG — I think the same hyperacute changes we noted in the 2nd ECG done in the ED were probably already present in this Initial ECG.
  • If you “invert” the P wave, QRS complex and ST-T wave in lead III of the Initial ECG … — Isn’t the picture you get very similar to what we see in lead III in the 2nd ED ECG?
  • If we consider that aVL in the Initial ECG was actually lead aVF — Don’t we see some of the subtle ST elevation that we now see in aVF of the 2nd ECG?
  • And, if we consider that aVF in the Initial ECG was actually lead aVL — Wouldn’t we have that magic “mirror-image” opposite picture for inverted lead III and lead aVL?
BOTTOM LINE: Great case by Dr. Smith, with numerous important teaching points on all aspects of this case. Add to those the PEARL of remembering that marked axis change with unexpected large size of the P wave in lead I (compared to lead II) may be a “tip-off” to LA-LL Lead Reversal.

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