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.

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