2 Cases of Acute Ischemic Stroke -- What is the Etiology?

Case 1.

An elderly patient had sudden onset of severe hemiplegia.  He had no chest symptoms.  Head CT was negative.  tPA (alteplase) was started and an ECG was subsequently recorded:

There are well formed QS-waves in V2 and V3, suggestive of old MI with LV aneurysm.
Is the ST elevation due to LV aneurysm?
Unlikely: there is too much ST elevation.
V3 especially has a high T/QRS ratio, with 4 mm of T-wave divided by 7.5 mm of QRS, for a ratio of 0.55.  A value in any of leads V1-V4  greater than 0.36 makes acute STEMI far more likely than LV aneurysm.
However, there is also T-wave inversion, suggesting an open artery or prolonged (subacute) MI.

So this is either:
1.  Subacute STEMI (~24 hours old), or
2.  Old anterior STEMI (with probable aneurysm) with superimposed acute and reperfused STEMI (with inverted reperfusion T-waves).
3.  Recent (within a week or two) anterior STEMI with "no-reflow" resulting in marked persistent ST elevation.

An initial troponin I returned at 0.788 ng/mL.

If this were a subacute STEMI, already having formed well developed QS-waves, the initial troponin would be substantially higher.

Therefore, this is either #2 or #3.

When someone has a stroke and has old QS-wave MI, or especially a recent QS-wave STEMI on the ECG, one should be looking for LV thrombus.  LV aneurysm results in an akinetic (immobile) LV wall, which results in blood stasis which is thrombogenic.  Subacute STEMI adds inflammation to the endocardium, which enhances thrombogenicity.

Formal echo was therefore done:

1. Regional wall motion abnormality-distal septum anterior and apex akinetic
2. LV thrombus

The patient was treated medically for the MI.  (I now can't remember if the patient went for stent retrieval and, if so, the outcome.)

Subsequent troponins trended down and hit a plateau at a slightly lower level of 0.660 ng/mL.

This suggests the MI was recent (within many days to a week or so), not subacute.

This model fits best with the presentation, as a recent transmural STEMI in the LAD territory would result in a thrombogenic endocardium and LV thrombus, which is then at risk to embolize and result in stroke.

In the era before reperfusion therapy (early 1980's), all anterior STEMI were routinely put on heparin drips to prevent the occurrence of LV thrombus with its attendant stroke risk.

Diagnosis: Recent completed anterior wall STEMI with subsequent akinetic anterior wall, thrombus formation, and subsequent embolism with large middle cerebral artery ischemic stroke.  And that entire diagnosis could be gleaned from the clinical presentation and the ECG.

Case 2

This elderly patient had sudden onset of left-sided hemiplegia.  He had this ECG recorded before going for a head CT:

ECG:

There are wide, well-formed Q-waves in inferior leads, diagnostic of subacute or old inferior MI.
Not all LV aneurysms have persistent ST elevation, especially in the inferior location.
Additionally, inferior aneurysms usually do NOT have QS-waves (as they do with anterior MI); rather, they have QR-waves, as here.
So absence of QS-wave does not rule out inferior LV aneurysm.   

He also had this ED bedside echo done prior to head CT.  Here is the parasternal short axis:


What do you see in addition to a dense inferior wall motion abnormality?  (Answer is below)

Clinical course:

The head CT showed no bleed and tPA was given.

Here is one image from the head CT.  What do you see?

What do you see?

There is a hyperdense MCA sign in the left Middle Cerebral Artery [radiodenseity (white) in upper right part of brain].  Hyperdense MCA sign is seen more commonly in cerebral embolism (though most embolism is from atrial fibrillation) than in carotic artery thrombosis, as the thrombus is mature and more radiodense at the time of stroke onset.  So this is further evidence that there is a cardio-embolic source.  Since the patient is not in atrial fibrillation, that embolic source is likely to be a mural thrombus.  Since the patient has a dense inferior wall motion abnormality to go along with the large Q-waves, this is the likely source.


Bedside Ultrasound Legend:

Here is a still shot at the 1 second mark of the above ultrasound, where the ultrasound is pointed closer to the apex than the base:

Here I have circled the finding of the ultrasound:

There is a myocardial rupture with pseudoaneurysm of the inferior wall, with thrombus filling the pseudoaneurysm.

Clinical course:

CT angiogram stroke protocol revealed thrombus in the right internal carotid artery and middle cerebral artery.  The patient received tPA (alteplase) very quickly, then went for a stent retrieval. Unfortunately, the clot could not passed with the stent retrieval system, consistent with a mature thrombus.  It could not be retrieved.  The patient was started on long term anticoagulation.

Here the interpretation of the subsequent formal ultrasound (this formal US is not shown):

Regional wall motion abnormality, inferoposterior, akinetic with rupture and thrombus filled left ventricular pseudoaneurysm.

Clinical course:

The tPA did not cause catastrophic bleeding in this patient with a myocardial rupture, as the thrombus in the pseudoaneurysm was quite mature.  The stroke completed, as this mature thrombus is resistant to thrombolysis and could not be retrieved.

Learning Points

LV aneurysm can be diagnosed by ECG.  In the context of stroke, it strongly suggests cardioembolic source.

An Unusual Tachycardia

This Case was sent by Atif Farooqi and Scott Weingart, from Stony Brook.

This is a 70-something with history of CABG who presented with 30 minutes of SOB and palpitations.

Here is his ECG:

What is it?

Atif wrote this:
"My first thought was perhaps a bidirectional V Tach, though the pt is not on digoxin and otherwise has no discernable reason to be in BVT.  Scott was considering maybe an intermittent aberrant conduction, though we thought it odd for it to be strictly alternating beats.

Here is my answer:
Atif,

Interesting EKG!

I think it is SVT with every-other-beat-aberrancy. 
--Every QRS comes right on time, perfectly regular, so it can't be Bigeminy. 

--Every other beat is RBBB, which is the most common type of aberrancy because the right bundle has a longer refractory period than the left.

--The inbetween beats are of normal duration (100 ms).  The axis does not alternate.  There is no alternating RBBB and LBBB.  So it can't be bidirectional tachycardia (neither bidirectional VT nor bidirectional SVT).
--There are no P-waves.

So this is AVNRT with alternating aberrancy (Scott was right!).

Additionally, both the aberrant and the normally conducted beats have significant ST depression.

Bidirectional Tachycardia implies alternating frontal plane axis, from -60 to +120, or alternating LBBB and RBBB.

Bidirectional tachycardia can be Bidirectional Ventricular Tachycardia, as with Digoxin toxicity.  The etiology may be:
1. alternating location of origin of the VT ectopic focus, or
2. alternating routes of depolarization from a single ectopic focus

Bidirectional VT may also result from aconite toxicity, as in this case I reported, which has alternating RBBB and LBBB.

Bidirectional Tachycardia can alternatively be due to SVT with Bidirectional Aberrancy:  the aberrancy may be due to:
1. RBBB with alternating LAFB (left axis) and LPFB (right axis), or
2. Alternating RBBB and LBBB.

Here is the ECG from this case of Aconite Toxicity:

Alternating RBBB and LBBB.  Intervals are regular.

This case presented here today does NOT have alternating frontal plane axis, nor does it have alternating RBBB and LBBB, so is not bidirectional tachycardia.


Case continued:

The attending gave IV Metoprolol, (the patient was supposed to be taking oral metoprolol as an outpatient), and the rhythm changed to the following: 

This appears to be sinus, though the P-waves are not obvious.
This subsequent ECG proves that the first was SVT with aberrancy: the complexes are identical to the non-RBBB beats of the first ECG.
There is also persistent ST depression.  Hopefully now that there is no longer tachycardia, this ischemia will resolve.
It is typical for metoprolol to convert an AVNRT. 
I would have tried adenosine.

A 25 year old with Epigastric Discomfort, Worse Supine, Better Sitting Up.

This is another case provided by Mustafa Alwan, an internist from Jordan, on Facebook EKG Club  

This is a 25 year old male diabetic who presented with epigastric heaviness for 12 hours.  The discomfort was intermittent and associated with sweating and dizziness; it was increased increased by lying flat and relieved when sitting up.

Here is his initial ECG, with pain and diaphoresis:

It is really quite normal.
When I first saw it, I did not know the patient still had pain, and I responded on FB:
"This is normal.  However, the sharp downturn of the T-wave in V4-V5 suggests possible development of Wellens' waves, but is nonspecific. The T-wave flattening in limb leads is non specific."
However, with ongoing pain, these are unlikely to be vestigial Wellens' waves.

He was given NTG and Morphine and pain was improved.

An interventionalist was consulted.  
He performed an echocardiogram which showed no wall motion abnormality.  

The first Troponin T returned at 0.017 ng/mL, slightly elevated but indeterminate.  

The interventionalist diagnosed pericarditis and prescribed an NSAID.

[This ECG shows no evidence of either pericarditis or of STEMI.  The diagnosis must have been based on the positional nature of the pain.]

Dr. Alwan smartly recorded more ECGs.   Here is the second one recorded 4 hours later:

No significant change

6 hours after the first ECG, and 2 hours after the 2nd, a third ECG was recorded:

Now there is new ST elevation, the change being diagnostic of LAD occlusion.
This is not an ECG one would see with pericarditis, which manifest inferolateral ST elevation.

Even if this were the first and only ECG, the differential diagnosis would be early repol vs. LAD occlusion, and the formula could be used:

STE60V3 = 2.5 mm
 computerized QTc = 437
(notice how it lengthened from the earlier values of 372 and 402 ms!)
R-wave amplitude V4 = 9 mm
formula = 25.839 (greater than 23.4 is all but diagnostic of LAD occlusion)

The patient was taken for angiogram.  Here is the report:

Here is the post reperfusion ECG

Typical reperfusion T-waves, identical to Wellen's waves (Wellens' waves represent reperfusion!)

Learning Points:

1.  Young People can have myocardial infarction
2.  Though positional pain lowers the likelihood that chest pain is MI, it does not eliminate it!
3.  Always get serial ECGs.
4.  Pay attention to even slightly elevated troponin levels.  This could have been myocarditis, but that is a diagnosis of exclusion, after a negative angiogram.

Lecture: Acute Coronary Syndromes, Part (Overview and Non-STE-ACS) and Part 2 (STEMI)

Here is a pdf of all the slides (parts I and 2).
This contains some extra slides which were "hidden" in the presentation.


Part 1: Overview and Non-ST Elevation ACS







Part 2: ST Elevation Myocardial Infarction

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=

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.