Wednesday, March 14, 2018

Syncope, History of Coronary Disease, and ST Elevation: Should Medics Activate the Cath Lab?

A 60-something male had a syncopal episode.  911 was called.   The patient had no complaint of chest pain or shortness of breath. A prehospital ECG was recorded:

Limb leads
Precordial Leads
There is ST Elevation in V1-V3, and in aVL, with reciprocal ST depression in II, III, and aVF.
There is also some ST depression in V5 and V6, and ST elevation in aVR.
What do you think?

The medics interpreted the ST elevation, with reciprocal ST depression, as STEMI, and activated the cath lab.

Note that you cannot see the entire QRS on the prehospital ECG.  The R-waves in leads II and III are cut off.  The S-waves in V1-V3 are cut off.  There is likely to be very high voltage that is cut off.

It is important to remember that not all ST elevation with reciprocal ST depression is a manifestation of STEMI.   LVH, LBBB, and WPW can all have ST Elevation with reciprocal ST depression. Especially LVH.

On arrival, I looked at the ECG and immediately knew it was a false positive due to LVH.

An ECG was recorded in the ED:
This confirms high voltage. QRS is 118 ms.
There is no evidence of STEMI.
All ST deviation is a result of LVH with secondary repolarization abnormalities
These are secondary to abnormal depolarization due to LVH, with high voltage.
These are expected ST-T abnormalities given the high voltage abnormal QRS.
They are not "primary" ST-T abnormalities of ischemia.

This ECG has similarities to Left Bundle Branch Block (LBBB), but it is NOT LBBB because the QRS is not long enough and there is not enough delay from onset of the QRS to peak of R-wave in lateral leads.  Q-waves in V5 and V6, and absence of monophasic R-wave in aVL also argue against LBBB.  See more on LBBB and LVH at the bottom of the post.

The cath lab was de-activated.

There was further history:

The patient had not anything to eat or drink all day long and felt subjectively dehydrated. He had been walking much of the day, then went to the bathroom and after urinating became light headed and fell w/ brief loss of consciousness.

There was never any chest pain or dyspnea.

He had a history of CABG and ischemic cardiomyopathy.

A repeat ECG 3 hours later was not different.


The troponins were slightly positive, peaking at 0.52 ng/mL (not consistent with STEMI).  Cr. was elevated, consistent with dehydration.

Echo showed:

Decreased left ventricular systolic performance, moderately-severe, EF about 35%, with LV enlargement.
Asynchronous interventricular septal motion consistent with left bundle branch block (although the ECG did not show LBBB).
Regional wall motion abnormality-distal septum and apex.
Evidence for dilated left ventricle with regional dysfunction in the LAD distribution. 
Markedly dysynchronous septal motion consistent with LBBB.

Thus, there is echo evidence of myocardial infarction (new or old), thought to be old.  Syncope could have been vasovagal (neurocardiogenic, triggered by dehydration), but with poor LV function, it could also have been due to ventricular tachycardia.  Acute type I MI is much less likely.  Troponin elevation is probably due to type II MI: underperfusion in the setting of chronic coronary disease.

The patient refused further investigations and was discharged.

Learning Points:

1. Syncope alone is an uncommon presentation of STEMI.  Any ECG finding with ST elevation should be approached with skepticism if there is no chest pain or chest discomfort.

Corollary: It should be very unusual for medics to activate the cath lab for syncope alone, without chest pain, as any associated ST Elevation is likely to be a false positive.

2. LVH is a common cause of false positive ST elevation, and often has reciprocal ST depression.

LBBB has recently been re-defined:

Strauss DG, Selvester RH, Wagner GS. Defining left bundle branch block in the era of cardiac resynchronization therapy. Am J Cardiol. 2011;107(6):927–34.

Here is a quote from the abstract: 

"Three key studies over the past 65 years have suggested that 1/3 of patients diagnosed with LBBB by conventional electrocardiographic criteria may not have true complete LBBB, but likely have a combination of left ventricular hypertrophy and left anterior fascicular block. On the basis of additional insights from computer simulations, the investigators propose stricter criteria for complete LBBB that include a QRS duration ≥140 ms for men and ≥130 ms for women, along with mid-QRS notching or slurring in ≥2 contiguous leads. Further studies are needed to reinvestigate the electrocardiographic criteria for complete LBBB and the implications of these criteria for selecting patients for CRT." 

One more very short article with full text: 

Int Cardiovasc Res J. 7(2):39-40.LBBB: State of the Art Criteria.


  1. Admittedly I thought this was LBBB at first, although I did not think it looked like occlusion.
    I had wondered also if perhaps hypokalemia was a possibility based on the T waves in the inferior leads which are somewhat reminiscent of that wavy appearance.
    In LVH, there is often inverted hockey stick-like TWI in the lateral leads as well, whereas they are upright in I and aVL here, which also led me to think LBBB.
    The QRS in I and upward concavity in V4 also steer away from coronary occlusion, no? Or are those findings clinically insignificant in LVH?
    Thanks for sharing your insight, fascinating case and especially the new info about LBBB criteria!

  2. Of note in this case — there is significant change in QRS morphology between the pre-hospital ECG (multi-fragmented and essentially isoelectric lead I — with QRS duration of >0.12 second) vs the slightly less wide ED tracing (RED background = ECG #2) which shows an all positive QRS complex in lead I. Neither tracing looks like a stemi, given QRS widening and markedly increased QRS amplitudes. Marriott questioned the terminology used to define “complete LBBB” several decades ago … I remember him showing us tracings with typical LBBB morphology and sufficient QRS widening (say 0.13 second) to define “complete LBBB” — only to then show us follow-up tracings on a given patient over the next few years evolve into QRS widening of ~ 0.14 then 0.16, 0.17 second … and then rhetorically ask us the question that if earlier ECGs were called “complete” LBBB — Did that mean that these later tracings with even more QRS widening were “More Complete” LBBB? It is known that both hemiblock & LVH may produce QRS widening (typically of ~0.1-0.2 second each — though perhaps even more than that in this case, given how markedly increased QRS amplitude is in ECG #2). I’d propose calling ECG #1 in this case an atypical IVCD in a patient with LVH and significant underlying heart disease. Given the change in Axis and QRS morphology in lead I between these 2 tracings — perhaps the conduction defect seen in ECG #1 is intermittent … Persistence of septal Q waves in leads V5,V6 in ECG #2 tell us this is not LBBB (which when complete, should result in complete loss of all septal Q waves). Thus — GREAT points made by Dr. Smith in this post re: i) Syncope alone (without chest pain) is an uncommon presentation of stemi; and ii) QRS widening (with or without LVH) may be associated with ST-T wave abnormalities that are longstanding and not reflective of acute coronary disease. Such tracings are usually false positives when there is no chest pain. Final THOUGHT: The wider the QRS in LBBB patients — the better the chance for benefit from CRT. Whether QRS duration criteria for LBBB should be “redefined” along the way to selecting candidates for CRT would seem not to be needed, if one carefully tracks QRS duration with LBBB when contemplating CRT candidates. I suspect ( = my opinion) that LBBB would not be misdiagnosed (overdiagnosed) as much if more attention was paid to QRS morphology before bestowing this diagnosis. THANKS again to Dr. Smith for stimulating commentary!


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