A 50-something woman with atypical chest pain

This was provided by Mustafa Alwan, an internist from Jordan, on Facebook EKG Club   

A 50-something female presented with atypical chest pain described as stabbing, with no radiation 
PMHx : DM poorly controlled 
VITAL signs stable 

Here is the initial ECG with the question "should the cath lab be activated?"
This is suspicious for ischemia because of the T-wave inversion in aVL.
However, this is very nonspecific and one would not activate the cath lab!


Another ECG was recorded 20 minutes later:
This has more obvious T-waves and T-wave inversion in aVL
Here is my response:
"This 2nd one is an extraordinarily subtle but real change!!" (i.e., this is diagnostic of MI).  "These often resolve with nitro, so I would try that first. It depends on your resources: if activating at night tires out your team for the next day, you try to avoid if possible.
But this pain and ECG may not resolve, in which case you must activate."

In other words, this is diagnostic of inferior MI, but not of STEMI, and may not need emergent cath lab activation.

If the pain and ECG findings resolved with nitroglycerine, it will need at least maximal medical therapy and continuous 12-lead ST segment monitoring

See these cases for the importance of ST segment monitoring:
http://hqmeded-ecg.blogspot.com/search/label/ST%20Segment%20Monitoring

A third ECG was recorded at 45 minutes:
Now it is unequivocally diagnostic of inferior MI, even though it does not meet millimeter criteria for inferior STEMI.
The cath lab must be activated.

Here are all 3 ECGs, one after another, so you can see the changes:




The cath lab was not activated, but a 4th ECG was recorded at one hour:
Now it meets STEMI criteria.
Cath lab was activated
What else do you notice?









There is also new ST elevation in V1.  So this is a right ventricular MI also

Echo: Basal inferior wall hypokinetic, pseudonormal LV filling pattern

Initial Troponin T: less than 0.01 ng/mL initial
Troponin T after 2 hours: 0.49 ng/mL


Troponin T after 4 hours: 1.6 ng/mL (this is a large MI)

Cath showed a 100% proximal RCA occlusion.


Learning Points:

1. T-wave inversion in aVL may be the first sign of inferior MI
2. Pay attention to slightly enlarged T-waves
3. When you see these subtle, nonspecific abnormalities, make certain you get serial ECGs!
4. Any patient with ongoing potentially ischemic chest pain should get serial ECGs!




What is this? A Perplexing ECG.

A 46 year old woman had syncope.  

Before seeing the patient or reading the chart, the physician viewed the ECG and was perplexed:
What is going on??


















Then he found out she had a heart transplant.  Now can you tell what is going on?





It turns out that both the native heart and the transplanted heart are beating.  The native heart is paced by the transplanted heart.  The sequence is given in the legend of the annotated version below.

How does this work mechanically??


Both left ventricles pump blood into their respective aortas, then these two aortas converge immediately after their origins.  Thus, the hearts work in parallel, but the native heart beating slightly later than the transplanted one, and synchronized by the pacemaker. 

In this case, the patient had pulmonary hypertension.  If she had had a normal orthotopic transplant, the new right ventricle would not have been able to pump against the high pulmonary resistance.  Therefore, the native right ventricle pumps into the pulmonary artery, while the atria are connected (right with right and left with left).

The transplanted heart is over the native heart, with the apex directed rightward and upward (lead I, II and III are indeed negative). 

Annotated ECG:

Here I have drawn vertical lines at the beginning of each QRS:

The start of the native QRS is the first line
The start of the transplanted, paced QRS is the second line.

1. Transplanted heart P-wave 
2. Transplanted heart (abnormal) QRS (axis negative because heart is upside down!)
3. Native heart atrial spike (having sensed on the transplanted ventricle); no clear P-wave. 
4. Native heart ventricular spike followed by 
5. Native heart QRS. 



A Patient with Syncope

A young man had sudden syncope without a prodrome, after which he was aysmptomatic.  He presented to an ED and had this ECG recorded:
What do you see?

















There is an abnormal rSr' in V1, with the r'-wave not falling quickly back to baseline.  The T-wave is inverted, but this is also a normal finding in V1.  The whole morphology is suggestive of Brugada morphology, but by no means "diagnostic" because the r'-wave is not 2 mm.

Here are the criteria for ECG Brugada morphology.  This comes from the paper entitled (with full text link): Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report

Criteria for Type 1 Morphology:
1. R'-wave at least 2 mm in V1 or V2
2. But no distinct R'-wave because the ST segment takes off at an angle from the peak
3. The ST segment is convex upward ("coved"). [They use terminology of "concave downward"]
4. The peak at the high takeoff does not correspond with the J-point.  It is BEFORE the J-point, as measured in other leads (such as lead II across the bottom).
5. Gradual downsloping of ST segment such that at 40 ms after the takeoff, the decrease in amplitude is less than 4 mm.  In normal RBBB, the decrease in amplitude is much greater (see this example).
6. ST is followed by a symmetrically negative T-wave
7. "The duration of QRS is longer than in RBBB," and "there is a mismatch between V1 and V6." This criterion is perplexing and not well explained.
8. The downsloping should be such that the Corrado index is greater than 1.0.
This is the ratio: [ST elevation at the J-point] divided by [ST elevation at 80 ms after the J-point]. 



Diagnosis of Brugada Syndrome requires both:

1. Brugada pattern ECG (either Brugada Type 1, or the newly defined Brugada Type 2)
Findings may be dynamic and are sometimes concealed; findings may be observed only in certain circumstances such as fever, intoxication, electrolyte imbalance, presence of sodium channel medications/drugs, or vagal stimulation.
2. At least one of the following:
(a) survivor of cardiac arrest,
(b) witnessed/recorded polymorphic ventricular tachycardia (VT),
(c) history of nonvagal syncope,
(d) familial antecedents of sudden death in patients younger than 45 years without acute coronary
syndrome
(e) Type 1 Brugada pattern in relatives.


Criteria for Type 2 Brugada morphology:
First, there must be:
a) An RSr' with a typical saddleback pattern in V1 and/or V2. 
b) V1 may have either an upright, flat, or inverted T-wave (in our case above it is inverted).
c) T-wave in V2 is usually but not always positive.
d) Minimum ST segment ascent of 0.5 mm.  There could be no saddle without an ascent.
Once these are fulfilled, there should be, in lead V2:
1.  High take-off of the descending limb of the r' at least 2 mm above the isoelectric line (in our case, it is less than 2 mm, so this does not meet criteria for Type 2 Brugada).   The r'-wave is thus not distinct, as it is in benign causes of rSr'
2.  Mismatch between QRS duration in leads V1 and V6 (longer in lead V1).  This helps to distinguish from RBBB, in which the QRS duration is equal in V1 and V6.
3. As with Type 1, the peak of the r'-wave does not correspond to the J-point in other leads.
4. A large Beta angle.  Go to this post to learn about the beta angle.




So this ECG cannot be said to fulfill the criteria for either type 1 or type 2 Brugada, but it is suggestive, and the patient had non-vagal syncope.

Case continued: 
The patient presented with syncope and fever 3 years later.  Here is the ECG:
Now the ECG, in the presence of fever, is diagnostic of Brugada morphology



The patient underwent an EP study and had a ICD implanted.

Learning Point:

The patient and doctor dodged a bullet here.  He could have died in the intervening 3 years.  This sort of cardiac syncope is death that terminates with awakening.

The first ECG is nonspecific but suggestive of Brugada, and in the context of non-vagal syncope the patient should at least get early referral to a cardiologist, preferably an electrophysiologist, for EP testing or for challenge with a sodium channel blocker.

Read more about Type 1 and Type 2 Brugada syndrome here:

Is this Type 2 Brugada syndrome/ECG pattern?


Here are many articles on Fever unmasking Brugada syndrome:

https://scholar.google.com/scholar?hl=en&q=brugada+fever&btnG=&as_sdt=1%2C24&as_sdtp=



Proportionality and Serial ECGs Make the Diagnosis

This case comes from Jason Winter, of The Facebook Clinical Electrocardiology ECG Page.

A 60-something woman called EMS for chest pain.

Here is her first prehospital ECG:
What do you think?
















There is very low voltage in the precordial leads, with a total QRS amplitude of only 3.5 mm in V2 and 4 mm in V3.  

In spite of this low voltage, there is ST elevation (as measured at the J-point and relative to the PQ junction, and as measured by the computer and shown on the right), of 0.54 mm in V2 and 0.65 mm in V3.   

The ST/QRS ratios in V2 and V3 are, respectively, 0.154 and 0.162.  These are a high ST/QRS ratios.  
In our study of subtle LAD occlusion vs. early repolarization, the mean ratio of ST/QRS was:

-- 0.215 and 0.195 for V2 and V3 in LAD occlusion vs. 
-- 0.077 and 0.081 for V2 and V3 in early repolarization.

The specificity of a value in V2 greater than or equal to 0.154 was 90% (90 of 100 cases).
The specificity of a value in V3 greater than or equal to 0.162  was 84% (79 of 94 cases).

However, we did not include cases with less than 1 mm of ST elevation, so strictly speaking, one should be circumspect about applying such ratios.  Nevertheless, these high ratios certainly suggest that there is abnormal ST elevation in the leads of the LAD territory.

How about if we apply the LAD occlusion/early repol formula?  
STE60V3 = 1
QTc = 397
RAV4 = 0.5 
This produces a value of 24.46 (greater than 23.4 is nearly diagnostic of LAD occlusion).  However, again, the formula was developed only in ECGs with at lead 1 mm of STE in V2 and V3, so does it apply?

Here is the same ECG stretched vertically so that the QRS amplitude is closer to normal:
Now one can appreciate the ST elevation a bit better.


Clinical Course

I don't know if the medics noticed these ECG findings or not, but if not, they recognized the value of serial ECGs in a patient with chest pain.

Here are these serial ECGs, starting with the first one again:

#1: Time zero:
STE in V2 and V3 = 0.54 and 0.65

 #2: 27 seconds later:
STE in V2 and V3 = 0.70 and 0.79

#3: 74 seconds after #2
STE in V2 and V3 = 1.11 and 1.21

#4: 56 seconds after #3:                 [157 seconds (2 min 37 sec) after the first]:
STE in V2 and V3 = 1.57 and 1.73




The medics administered aspirin (no Nitroglycerine), and the pain resolved.




#5: 18 minutes after #4:
STE is resolved

#6: 4 minutes after #5:
And remains resolved

Case Outcome

Because of ST resolution, the patient was not taken that night to the cath lab.  She was treated for NonSTEMI with antiplatelet and antithrombotic agents and went to cath the next day, where an where multiple LAD thrombi were found and the lesion will be stented.

Waiting to cath a transient STEMI can be hazardous.  See this case in which I made that mistake.


Learning Points:

1.  Repolarization (ST-T) is proportional to depolarization.  All ST elevation (and T-wave size) should be assessed relative the QRS amplitude.

2.  Serial ECGs improve the sensitivity of ST elevation on the ECG for MI.  In the only ED study of its kind, sensitivity increased from 46% to 62%.

Where is the lesion in this STEMI?

A middle aged male presented with chest pain.  EMS was called and an ECG was recorded which is virtually identical to the first ED ECG.

The cath lab was activated by the medics.

Here is that first ED ECG:
There is obvious inferior ST elevation, with reciprocal ST Depression in aVL (inferior STEMI).

There is also ST Depression in lead I.  This is good evidence that the inferior STEMI is caused by an RCA occlusion.

There is ST depression maximal in lead V2.  Thus, there is a posterior STEMI.

There is also ST depression in V5 and V6.

Where else is there evidence of STEMI?? (see below)?























There is absence of ST depression in lead V1.  Given the profound ST depression (of posterior MI) in lead V2, there should also be ST depression in lead V1, but there is not.  This suggests that something is "pulling up" the ST segment in lead V1.  In other words, there is relative ST elevation in lead V1.  As V1 sits directly over the right ventricle (RV), this suggests STEMI of the RV, which is caused by a proximal RCA occlusion, proximal to the RV marginal branch.

This patient did not have any of the hemodynamic characteristics of RVMI (hypotension, nitroglycerine sensitivity).

However, when I saw this I suspected RV MI and suggested to the treating physician that a right-sided ECG be recorded.

Here it is:
V1 should be labelled V1R, which is the same lead as V2
V2 should be labelled V2R, which is the same lead as V1
V3 is V3R
V4 is V4R
V5 is V5R
V6 is V6R
There is huge ST elevation across the right sided leads, diagnostic of RV STEMI.



Does this matter?  Won't the interventionalist just find the lesion and fix it?

Here is a case (in video form) in which the ST elevation in V1 was not noticed, a right-sided ECG was not recorded, and the angiogram showed occlusion of the mid-RCA, which was fixed.  When I called the interventionalist to ask about the proximal RCA due to STE in V1, he went back to look at the angiogram: what he had not noticed was that this occlusion was an embolus from the ulcerated plaque in the Proximal RCA.  He was thus able to go back and stent the actual culprit lesion.

Furthermore, it is good to know that the RV is involved in order to anticipate right sided heart failure with hypotension and nitroglycerine sensitivity.

How sensitive and specific is STE in V1 in the setting of RV MI, in cases with and without concomitant ST depression in lead V2?

We are just finishing a manuscript on this and cannot reveal our results.  Suffice it to say that STE in V1 is pretty specific but not sensitive.  Furthermore, that ST depression in lead I, though it does predict RCA occlusion, does not give any further information about whether that RCA occlusion is proximal (RVMI) or not.

In other words, all patients with inferior STEMI should have a right sided ECG recorded.