A 50-something woman with chest pain, BP 230/120, and LBBB with 7 mm ST Elevation

A 50-something woman with history of CHF of unknown etiology, and of HTN, presented for evaluation of chest pressure.

Her BP was 223/125, Sp02 98% on RA. HR 106, RR 18. 

Here was her ED ECG:

There is sinus rhythm with Left Bundle Branch Block (LBBB)
There is a large amount of ST Elevation in V2 and V3 (more than 5 mm)
Thus, this meets the unweighted Sgarbossa Criteria of 5 mm of discordant ST Elevation
But it does NOT meet the Smith Modified Sgarbossa Criteria, which depend on the ST/S ratio.

This ratio is critical because LBBB with very large depolarization voltage (QRS) also has very large repolarization voltage (ST/T).

Here the highest ratio is 6-7/60, which is 10-11%, which is normal

There is no concordant STE or concordant STD in V1-V3

The patient was given NTG with improvement of pain.

This was recorded 3.5 hours later.

There is no evolution 

A bedside echo showed good function, concentric LVH, and no wall motion abnormality could be seen.

Her first troponin was elevated at 0.217 ng/mL, but this does not absolutely differentiate between acute and chronic myocardial injury.

Patients with heart failure and cardiomyopathy frequently have elevated troponins from chronic injury, but not usually this high.

Acute MI is a subcategory of acute injury (Injury caused by ischemia).

Type I MI is acute MI caused by plaque rupture, whereas Type II MI is caused by supply/demand mismatch or endothelial dysfunction and a few other entities.

By far most likely this will be acute MI, but it is very uncertain whether it is Type I or Type II.  Severe hypertension with LVH causes increased demand (pumping against high pressure) and decreased supply (massive LVH constricting blood flow in arteries that perforate into the myocardium).

Here is the troponin profile:

Earliest on top

Now we can see a rise and fall of Troponin.  A rise and/or fall is necessary to diagnose acute myocardial injury (vs. chronic myocardial injury, which has relatively stable troponins

A Nitro Drip was started, as was heparin (in case this might be a type I MI).

Cardiology did not think it was type I.

They did a Sestamibi stress test:

1. Normal perfusion study with a high degree of certainty.
2. There was no evidence of relative ischemia during regadenason-induced 
hyperemia.
3. Left ventricular size was normal with pharmacologic stress while the 
ejection fraction was 56%.
4. There were no regional wall motion abnormalities.
6. The patient did not experience anginal symptoms. 
7. Stress EKG was uninterpretable for ischemia due to baseline left 
bundle-branch block.
8. No prior studies available for comparison.

The echocardiogram showed:

Normal left ventricular size, moderate to severe concentric left ventricular hypertrophy and normal systolic function.

The estimated left ventricular ejection fraction is 61 %.

There is no left ventricular wall motion abnormality identified.

2 days later:

No change, proving that this is the baseline ECG.

Learning Points:

1. This is a baseline ECG with LBBB and huge but proportional discordant ST Elevation.
2. Myocardial infarction may be present without plaque rupture.  This is called type II (or type 2) MI and may be due to severe hypertension or other causes of poor supply (anemia, hypotension, thick ventricle) or excessive demand (tachycardia, hypertension).

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Comment by KEN GRAUER, MD (9/25/2019):

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Providers sometimes overlook the concept of proportionality when assessing the amount of ST segment elevation. As emphasized by Dr. Smith above — the Smith-Modified-Sgarbossa Criteria for assessing ST elevation in the presence of LBBB tells us that despite 7mm of ST elevation in the initial ECG of this case — this is not abnormal given dramatic depth of anterior S waves.

I focus My Comment on 3 additional Take-Home Points regarding the initial ECG in this case.

• For clarity — I’ve put this initial ECG from the ED ( = ECG #1) — together with the 3rd ECG, done 2 days later ( = ECG #3) in Figure-1.

Figure-1: The initial ED ECG in this case, and ECG #3 done 2 days later (See text).

POINT #1 — Don’t forget about half-standardization.

• Although obvious that anterior S waves in ECG #1 are HUGE — it is exceedingly difficult to accurately measure S wave amplitude. This is because of marked overlap of QRS complexes in leads V1, V2, V3, and in that portion of the long lead II rhythm strip that lies directly below these 3 anterior leads. Immediately repeating the recording of this ECG at half-standardization could simplify measurement — allowing instant clarification of the relative amount of J-point ST elevation with respect to S wave depth, as is needed for application of Smith-Modified Sgarbossa Criteria.

POINT #2 — Despite the presence of complete LBBB — we can call LVH on these ECG tracings! Echocardiography is clearly superior to ECG for assessment of ventricular wall thickening and chamber enlargement. That said, a major focus of this ECG Blog — is to optimize clinical ECG interpretation. Because complete LBBB changes the sequence of ventricular depolarization — the usual voltage criteria for ECG determination of LVH are altered in the presence of this conduction defect. However — there are other ECG criteria that have high correlation for LVH when there is LBBB.

• IF S waves in one or more of the anterior leads (ie, leads V1, V2 V3) are very deep (ie, >25-30mm) in a patient with LBBB — this greatly increases the likelihood of LVH. All 3 of the anterior leads in ECG #1 easily surpass this threshold!
• The QRS complex in ECG #1 is extremely wide (I measure ≥0.16 second in some leads). Although I’m not aware of data directly correlating QRS width on ECG to degree of LVH — excessive QRS widening as seen here in this patient with such dramatic anterior S wave amplitude clearly suggests more significant underlying structural abnormality.
• Finally — is the matter of statistics. Unlike complete RBBB — complete LBBB virtually never occurs in the absence of underlying heart disease — and, most patients with complete LBBB will also have LVH. Considering this patient’s age, her history of HF (Heart Failure) and longstanding hypertension — and her presenting BP = 223/125 — it would seem almost certain that this patient must have LVH even before you saw her ECG. Now when we add in the excessive anterior S wave depth described above — all doubt should be removed.

POINT #3 — There is RAA (Right Atrial Abnormality) — and — the size of these enlarged P waves decreases as this patient’s clinical condition improves!

• Atrial abnormality is diagnosed independent of QRS amplitude. The finding of tall, peaked and pointed P waves in the “pulmonary leads” (ie, inferior leads) that look “uncomfortable to sit on” and, which achieve a P wave amplitude of ≥2.5 mm satisfy criteria for RAA. The 4 mm P wave amplitude that we see in lead II of ECG #1 is huge!
• NOTE: For those wanting a user-friendly review on ECG Diagnosis of Right & Left Atrial Abnormality — CLICK HERE.
• Finally — It has been my observation over the years that P wave amplitude sometimes varies from one day-to-the-next due to fluctuations in intravascular volume and/or intracardiac pressures. I found it especially interesting in this case to see progressive decrease in P wave size in lead II as this patient’s clinical condition improved (See P wave size in lead II of ECG #3).

Our THANKS again to Dr. Smith for this interesting case!