Saturday, January 24, 2015

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

A male in his 50's called 911 for constant 8/10 midsternal chest pressure.  Here was his prehospital ECG:
Computerized QTc is 423 ms.  The ST elevation at the J-point was measured by the computer (see right side), and is less than the "criteria" for anterior STEMI (2 mm in males over age 40).  There is also almost a saddleback morphology in V2.  I say "almost" because the R' wave is not tall enough to be a typical saddleback.
By the subtle LAD occlusion vs. Early Repol formula, this is clearly LAD occlusion: STE60V3 = 2, RAV4 = about 7, value = 25.07 (greater than 23.4 indicates probable LAD occlusion)

Here is a typical saddleback morphology, which is rarely due to STEMI:
This saddleback ST elevation prompted a false positive cath lab activation.  It was due to LVH.  Notice how tall the R' wave is.  Such saddleback ST elevation is rarely due to STEMI (I have never seen one that was!).

This nearly meets ECG criteria for type 2 Brugada morphology (I will post on that difficult topic soon).  Full text link:  Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report

Case continued:

He was given 2 sublingual NTG, with improvement of pain to 4/10.  Here was the second prehospital ECG:
Computerized QTc is 421 ms.  There is no significant change.

He arrived in the ED and had this ECG recorded:
QTc is 435 ms.  There is still less than 2 mm STE at the J-point, so it does not meet STEMI criteria.  The formula, using 1.5, 435, and 11 gives a value of 23.8, which, greater than 23.4 is unequivocally positive.  LAD occlusion must be assumed until proven otherwise.

The ECG was read as normal by both the computer and the physician.

Comment: Readers of this blog may be critical of this, but that is because you have been sensitized to this diagnosis.  This is the normal assessment throughout the world!  To do better than this is the exception, not the norm.

That is why in study after study, 20-30% of angiograms done for "rule-in MI" by troponins find an 100% occluded artery at next day angiogram.

Don't be critical of this assessment; rather, pass the word and help your fellow emergency physicians and cardiologists to see these findings.

The initial contemporary, sensitive troponin (but not high sensitivity troponin -- these are not yet available in the U.S.) was less than 0.10 ng/mL (undetectable).

The first troponin is negative in 50% of acute STEMI.

A repeat ECG was done 140 minutes later:
QTc is 444 ms.  There is no more STE than before.  T-waves are slightly different, but not larger.
Q-waves are beginning to form in V2 and V3.  This proves it is an acute anterior MI.

A troponin drawn almost 4 hours after the first one was 0.18 ng/mL.  It doesn't sound very high, does it?  The Q-waves were not noticed.

Case continued

At 4.5 hours, another ECG was recorded:

At this point, the Q-waves were noticed and the cath lab was activated.

A 100% LAD occlusion was stented.

No further followup is available.

Learning point

I repeat this theme over and over: Acute coronary occlusion may be very subtle.  It is frequently missed.  Readers of this blog probably would not miss this.  The person who sent it to me does read the blog, and he was doing QA when he noticed this and immediately recognized that it was a missed subtle occlusion.  It would be classified as a NonSTEMI.  He states that it is difficult to convey to his colleagues how to recognize these.

Thursday, January 22, 2015

Subtle Anterior STEMI Superimposed on Anterior LV Aneurysm Morphology

A male in his early 30s was playing soccer when the ball hit him in the chest.  At some point after this, he began having chest pain.  The pain radiated into the L arm, and was 8/10 in severity. The pain was similar to pain he had with a previous STEMI, for which he received a bare metal stent in the LAD a couple years prior.  He was on no medications.  
BP was 160/100. 

Here was his first ED ECG with 8/10 pain:
There is sinus rhythm.  There is minimal ST Elevation in anterior leads.  There is a QS-wave in V2, due to the old anterior MI.  The T-wave is taller than expected for old MI.  In V4, the T-wave size is far out of proportion to the QRS.  There is minimal STE in aVL with reciprocal ST depression in lead III.

Here is the last ECG from 3 years prior:
There are QS-waves in V2 and V3.  The terminal part of the T-wave in V3 is inverted, and the T-wave in V2 is not tall.
This is typical of LV aneurysm morphology (persistent ST elevation after previous MI)

We have derived and validated a rule to differentiate "LV aneurysm" ST elevation from STEMI (just finishing validation manuscript).  The rule depends on the principle that acute STEMI has a tall T-wave and LV aneurysm does not.  There are two versions:

In the first rule, if there is any single T/QRS ratio in V1-V4 that is greater than 0.36, it is likely STEMI:  for the ECG from 3 years prior, that would be lead V2.  At 5mm/21mm, the ratio is less than 0.36 and would indicate LV aneurysm.  But for the first acute ECG above, lead V2 is 8.5/15 which is 0.56 and would NOT indicate LV aneurysm.

In the second rule, one takes the sum of T-wave amplitudes in V1-V4 and divides by the sum of the QRS amplitude in V1-V4.  A value less than 22 indicates LV aneurysm.  In the second ECG from 3 years ago, that comes to 10/47 = 0.215, consistent with LVA.


Records showed that his STEMI was anterior and resulted in an EF of 40%, an anterior wall motion abnormality, and peak troponin I of over 100 ng/mL.

He was given sublingual NTG with some pain relief.  Here is the second ECG 13 minutes after the first, with 6/10 pain:
There is decreasing T-wave amplitude, consistent with some reperfusion.  

The cath lab was activated.  The interventionalist did not think the ECGs were different from before, but he was glad to take the patient for an angiogram.

In the meantime, the patient was given aspirin, clopidogrel, and a heparin bolus.  While waiting for cath, a NTG drip was started.

At 27 minutes after the first ECG, the patient had 5/10 pain on a Nitroglycerine drip at 200 mcg/min, with a BP of 130/80, and had this ECG recorded:
The T-waves are beginning to invert.  This is consistent with some reperfusion.


There was an in-stent thrombosis in the mid LAD with with 90% thrombotic occlusion and an embolism to the distal LAD.  Plain old balloon angioplasty (POBA) was performed, and the patient was put on aggressive antiplatelet and antithrombotic therapy.

Here is the post cath ECG:
T-waves are fully inverted now.

The troponin peaked at 12 ng/mL (not very high).  The formal echo showed dense anterior, septal, and apical wall motion abnormality, with an EF of only 29%.  This probably indicates "stunning," and there will probably be recovery of wall motion and EF, as reperfusion was quick.

Stunning may take up to 6 weeks to recover.

Learning Points

1. T-wave height correlates with acute infarction.
2. Absence of tall or large upright T-waves in the presence of QS-waves correlates with large old infarction, or LV Aneurysm morphology.
3. Acute STEMI can be superimposed on LV aneurysm morphology.  When it is, the T-wave turns upright with higher amplitude.  

Wednesday, January 21, 2015

Dyspnea on Exertion in a Middle Aged Woman.

A middle-aged woman presented to the ED with increasing dyspnea on exertion.  She had a normal physical exam except for a heart rate slightly over 100.  No other history or vitals are provided.  This ECG was recorded:
What do you see?  Answer below.

The patient was admitted to the hospital for rule out MI.  A later cardiology read of the ECG identified electrical alternans and the patient was re-examined and found to be hypotensive.  An echo confirmed tamponade.   Pericardiocentesis was performed and the patient improved.

No more details are available.

Notice that not only does the voltage alternate, but the QRS morphology also alternates, with slight changes in QRS axis, especially in precordial leads (see lead V3).

Electrical Alternans (EA):

Here is a great old review (full text pdf):

EA is relatively rare, and only about 1/3 of EA is associated with pericardial effusion.  Total electrical alternans (involvement of both atrial and ventricular components) is diagnostic of tamponade, but only a fraction of tamponade manifests this (low sensitivity, high specificity).

In patients in sinus rhythm, EA is almost never found in simple pericardial effusion (without tamponade: thus, EA in sinus rhythm is almost always due to tamponade).

Patients with PSVT frequently have EA without any effusion or tamponade, so this rule only applies to patients in sinus rhythm.

Bottom line: do an echo whenever you see EA.

Monday, January 19, 2015

Massive Osborn Waves of Severe Hypothermia (23.6 C), with Cardiac Echo

This patient was found down in the Minnesota Winter.  He felt cold and was unresponsive.  He had palpable pulses at a rate of 30, and his BP was 65/45.  A core temperature was 23.6 degrees Celsius.   Here is his first ECG.
Regular rate of about 30 beats per minute.  It appears to be atrial fibrillation, though it is possible that P-waves are hidden.  If atrial fibrillation, there is AV block and a junctional escape.  
There are MASSIVE Osborn Waves

Here is the bedside echo (this is not slowed down!):

There are very slow contractions with bradycardia, but the ejection fraction is good enough.

Although the patient is hypotensive and has a very low cardiac output, little cardiac output is required in a hypothermic patient with very slow metabolism.  The Postassium was not elevated.

Internal Rewarming was started with an intravascular catheter.  One hour later, the temp was 25.2 and this was the ECG:
The first complex is sinus with a narrow QRS and an Osborn wave.  The subsequent beats appear to be wide ventricular escape beats.  Beats 3, 4, and 5 appear to occur immediately after a P-wave; they appear to have escaped before the P-wave had a chance to conduct.   

Another 1/2 hour after that, the temp was 26.4
Sinus rhythm with 2:1 AV block, with Osborn waves

3 hours later, the temp was 29.0:
Sinus rhythm with 2:1 AV Block.  The heart rate is increasing.

The patient completely rewarmed and did well.

Sunday, January 18, 2015

You Must Read the ECG in Clinical Context....

An elderly male presented with cough and dyspnea, progressive for several days.  He had no chest pain.  Among his many tests, the ECG was done first, and was handed to me before I ever saw the patient:
There is minimal ST elevation in inferior leads, with reciprocal ST depression in aVL and marked ST depression in V2-V5.

This is consistent with inferior and posterior MI (posterior STEMI), but also with subendocardial ischemia.  The clinical context is critical.  Although a patient with acute chest pain and this ECG is likely to have a posterior MI, a complex medical patient may have reasons for supply/demand cardiac ischemia that are not related to ACS.

Such "demand ischemia" is usually diffuse and subendocardial, but it may be focal, especially if there is a coronary stenosis in a particular territory.  In such a case, it may present with ST elevation.

Subendocardial demand ischemia may have ST depression that mimics posterior STEMI.  But the minimal ST elevation in lead III suggests that this really is transmural ischemia generating ST elevation of inferior and posterior walls.

On exam, the patient was slightly hypoxic and very pale; he appeared to be anemic. His hemoglobin was 4.8 g/dL and so he was transfused.  He had heme + stools but no melena or gross blood.  He also had pneumonia, and a core temperature was 38.5.

I knew this was not a typical ACS and so I activated our "Pathway B", which is a compromise between activating the cath lab ("Pathway A") and not activating.  It is for emergent cardiologic evaluation for patients who might need emergent angiogram and PCI, but are complicated by an equivocal ECG or complicated medical problems.

The cardiologist came immediately.  An emergency formal echo showed an inferolateral wall motion abnormality.  In the record, an old angiogram reported a chronically occluded obtuse marginal (OM).  The previous echo was normal, but a stress echo had shown induced inferolateral hypokinesis.  Thus, there was prior proof that this area was vulnerable to stress; the territory of this artery was reliant on collateral circulation for oxygen delivery.

The first troponin I returned at 3.9 ng/mL.

The etiology of these ECG findings was not ACS, but rather transmural ischemia (with resulting ST elevation) in the territory of the chronically occluded OM due to poor oxygen delivery in this vulnerable area.

After resuscitation, especially with blood products, the hemoglobin was 8.8 and the ST depression was resolved.  The troponin I peaked at 12 ng/mL and then fell.  Here is the next day ECG:
Still abnormal but no severe ischemia remains

The patient did not undergo an angiogram.  He did well.

Learning Points:

Type 1 MI (due to ACS) vs. Type 2 MI (due to poor oxygen delivery and/or high oxygen demand)

1. Don't automatically activate the cath lab for ischemic ST elevation on the ECG (in this case is was posterior ST elevation).  Think first about why there is ischemia.

2. Don't forget Type 2 MI as the etiology of ischemia (ECG or troponin elevation).  In our studies at HCMC, 65-75% of all MI are type 2 MI.

3.  Most ischemia from type 2 supply demand mismatch is subendocardial.  It will usually have more diffuse ST depression.

4.  The echo is likely to have no new wall motion abnormality when there is subendocardial ischemia.

5.  Even MI with ST elevation may be Type 2 MI.

6.  From 2-5% of Type 2 MI have ischemic ST Elevation.  We believe it should not be called STEMI.  See this article by Sandoval, Smith and Apple.

7.  Here is the most recent review of Type II MI, by Sandoval, Smith, Thordsen, and Apple.

Here are 3 more examples of type II MI with ST elevation.

Wednesday, January 14, 2015

Cardiac arrest, severe acidosis, and a bizarre ECG

A middle aged male had an unwitnessed PEA arrest associated with cocaine use.  Whether there was a shockable rhythm prior to PEA is unknown, but he was never defibrillated.  He received chest compressions with LUCAS and 3 doses of epinephrine, and was intubated by prehospital providers.  He had intermittent pulses.  Here is his initial ECG, with a pH of 6.50:
The rhythm is uncertain: probably an accelerated junctional rhythm with RBBB and PVCs, but it could be an accelerated rhythm initiated in the left bundle, mimicking RBBB.  It is important to ascertain the end of the QRS, which I attempt to do below.
Also present are 6 PVCs: complexes 3, 6, 7, 9, 10 (second PVC morphology), and 13  

With this wide complex, hyperkalemia should be high on the differential diagnosis

Here I try to find the end of the QRS:
Try to find the end of the QRS in any lead.  If you use lead II, it appears as if the blue line is at the end of the QRS. But it is uncertain.  The black line may represent the end of the QRS in leads V5 and V6, but I don't think so.
If the QRS end is represented by the blue line, then there is quite a bit of ST elevation (V1-V4) and ST depression (V5 and V6).

I was very suspicious of hyperkalemia, so we gave 3 g of calcium gluconate.  But the K returned at 4.5 mEq/L.

So is this STEMI?

Some clinical context is important:

1. It was not ventricular fibrillation, but PEA.  This suggests another mechanism other than ischemia.
2. We found that the pH was 6.50 (pCO2 100, HCO3 8).  Severe acidosis can result in very deranged ECGs.
3. Cocaine complicates the clinical picture.  As he had zero neurologic function after resuscitation, we were suspicious of possible cocaine associated head bleed followed by resp arrest then PEA arrest.

I did not think this was STEMI, but rather the consequences of cocaine, acidosis, and cardiac arrest.

The patient was ventilated and another ECG was recorded at 15 minutes, at a pH of 6.70 (pCO2 50, HCO3 5):
 I believe it is easier to find the end of the QRS in this one.  See below.
Also, it now it resembles Brugada Type 1 pattern ECG, which can be induced by cocaine, a sodium channel blocker (like all ***caines, including lidocaine).

Here I draw lines again:
The end of the QRS is indicated by the blue lines.  There still appears to be some ST elevation and depression, but it is less.  There is a Brugada Type 1 morphology in V1-V3.

The patient was in cardiogenic shock, partly due to bradycardia and partly due to presumed low SVR, as the ejection fraction by bedside ultrasound was excellent.  He was put on an epinephrine drip to increase heart rate and Systemic Vascular Resistance.  75 minutes later, the pH was 7.00 and this was the ECG:
Still bizarre, and Brugada-like, but normalizing.

Further information:
It turns out he had had a bradycardia arrest 7 weeks prior, also associated with cocaine, and with apparent status epilepticus.  In that case, there probably was never a shockable rhythm.  This was his first ECG at that time (pH 6.68)
Again, it is a bizarre RBBB pattern with Brugada type 1 morphology.  There is ST elevation but it does not look like the ST elevation of STEMI as it is downsloping with a negative T-wave.

7 minutes later, this ECG was recorded:
It is narrowing a bit but still bizarre with RBBB morphology and downsloping STE.

And yet another had been recorded at 24 minutes after the 1st (17 after the 2nd)

At that visit, he had been cooled. Angiogram had shown no Coronary disease.  He had awoken and been discharged.  His cardiac arrest had been attributed to status epilepticus and polysubstance abuse.

Further Events on this Presentation:

Pupils were still fixed and dilated. Even with the ambient lights off, there was no response to light.  Since PEA arrest with severe neurologic deficits may be due to intracranial bleed, including subarachnoid hemorrhage (and SAH may be caused by cocaine), we obtained a head CT before initiating cooling.  It was negative.

He was cooled and admitted to the ICU.

The next day he was moving all extremities, had a peak troponin of 0.50 ng/mL, and had a normal echocardiogram.

Here was the next day ECG at a temp of 33 degrees:
I am uncertain, but I suspect that he is shivering.  All the bizarre findings are gone.

He awoke fully and neurologically intact (so much for GCS 3 with fixed and dilated pupils!).

We consulted the electrophysiologist, who plans to do a workup for occult Brugada syndrome.  The workup may include family history, provocative testing with Na channel blocking agents, and ECGs of family members.

1. Cocaine-induced myocardial infarction in patients with normal coronary arteries probably involves adrenergically mediated increases in myocardial oxygen consumption, vasoconstriction of large epicardial arteries or small coronary resistance vessels, and coronary thrombosis.  Such ischemia may cause cardiac arrest.

2. But cocaine can also cause cardiac arrest from its sodium channel (local anesthetic) properties. There need not be an underlying sodium channel defect (e.g., Brugada) for cocaine to result in arrhythmic cardiac arrest.

3. Furthermore, these same Na channel blocking effects can unmask underlying Brugada syndrome, just like any Na channel blocker.  Electrophysiologists perform provocative testing with Na channel blockers to help diagnose Brugada syndrome.

Literature on Cocaine and Brugada Pattern ECG is limited to case reports:

1. Here is one case report in which the ECG looks like hyperkalemia, but the author assures me the K was only 4.5 mEq/L: Cardiac arrest from cocaine with Brugada pattern (full text)

2. Here is another full text case: Brugada Pattern ECG and cardiac arrest in cocaine toxicity: reading between the white lines.

3. Aborted Sudden Death, Transient Brugada Pattern, and Wide QRS Dysrrhythmias After Massive Cocaine Ingestion

4Hyperkalemia and cocaine induced dynamic Brugada-type electrocardiogram


Severe Acidosis may also affect the ECG, but this pattern was quite specific and unlikely to be due to acidosis alone.

Saturday, January 10, 2015

Wellens' waves are NOT equivalent to Wellens' syndrome: Pseudo-Wellens' due to LVH and HTN

A 20 year old male with end stage renal disease (ESRD) and hypertension presented with 1 hour of chest pain ("cramps").

He was hypertensive at 170/100.  Here is his initial ECG:
There is high voltage of LVH and biphasic T-waves, reminiscent of Wellens' waves.
The clinicians were concerned for Wellens' syndrome.
He had been admitted 24 hours prior with fluid overload.  Here was his ECG from that visit:
There were no T-wave inversions at this time. Voltage is somewhat high, but not diagnostic of LVH.
During that visit, his BP had been as high as 220/110.  He had been dialyzed and discharged.

Back to this visit

Is this Wellens' syndrome?

NO.  Wellens' syndrome is a PAIN-FREE syndrome.  It is also not associated with LVH or hypertension, which may result in Wellens' mimics.  It depends to a high degree on pretest probability, which is very low (but not zero!) in a 20 year old.

He underwent a bedside cardiac echo (there was no previous echo for comparison).  Here is the parasternal short axis view:

This shows concentric LVH and no anterior wall motion abnormality.

If this were Wellens' syndrome, and the patient were pain free, then it would be common to have no wall motion abnormality, as Wellens' syndrome represents a state of reperfusion, when there is no persistent transmural ischemia and the wall motion may have recovered.  Normal wall motion after reperfusion (after resolution of chest pain) should not be reassuring, but normal wall motion during pain should be reassuring.

An immediate formal echo was also normal:

Enlarged left ventricular size, marked concentric left ventricular hypertrophy and lower limits of normal systolic function. The estimated left ventricular ejection fraction is 55%  There is no left ventricular wall motion abnormality identified.

He ruled out for MI by serial contemporary (not high sensitivity) troponins (troponin I, all undetectable).  He was supposed to get a stress echo to evaluate for coronary disease but he signed out against medical advice.

Case continued

7 weeks later he presented to the ED with dyspnea again and had this ECG.  BP was 170/100.:
T-wave inversion is less deep, still biphasic.  
He was discharged.

He returned one week later with chest pain and pulmonary edema.  His BP was 193/120.  Here is his ECG:
Shallow terminal T-wave inversion

I saw him at this time and treated with Noninvasive ventilation and high dose IV nitroglycerine (250 mcg/min).  Pulmonary edema resolved and he was admitted.  I did not think he was having ACS.

And 8 hours later, this was his ECG:
These are typical of Wellens' Pattern B (deep symmetric) T-waves and are diagnostic of ischemia.  They are NOT diagnostic of ACS or Wellens' syndrome. 

His troponin I was elevated, and rose slowly to 0.394 ng/mL, and then slowly dropped.  This is diagnostic of MI, but troponin does not differentiate between supply/demand ischemia (Type II MI) and ACS (type I MI).

These EKG and troponin findings are not at all unusual for a patient with LVH and severe hypertension and pulmonary edema with hypoxia.

The patient underwent an angiogram.  It was normal.

Learning Points

1. Wellens' syndrome is a syndrome, not merely an ECG finding.
2.  The syndrome does not include LVH, elevated BP, or pulmonary edema, and these findings will cause false positive ECGs.
3. "Anterior" T-wave inversions that look like Wellens' waves have many mimics; they are only fairly specific in the appropriate clinical syndrome.
4. The diagnosis here is type II MI due to demand ischemia from hypertension and hypoxia.

Wednesday, January 7, 2015

Persistent Juvenile T-wave Pattern

This article is written by Brooks Walsh, MD, an emergency physician, as well as Steve Smith, and with help from Ken Grauer, who is quite an ECG whiz.  

Brooks tackles the difficult issue of Persistent Juvenile T-waves (PJTWP). These are slightly asymmetrically inverted T-waves in V1-V3, but not beyond.  The bottom line is that there is little firm guidance on the topic.  


PJTWP important considerations:

1. Patients are typically African American women under age 30.  It is rare in males over 19 years of age to have T-wave inversion beyond lead V1, unless there is lead misplacement or also possibly deep inspiration during recording (1).

2. T-waves are slightly asymmetrically inverted in V1-V3.  T-wave inversion that extends out to V4 and beyond should only be seen in patients under age 12.

3. "Benign T-wave Inversion" is a different form of non-pathologic T-wave inversion.  It does often extend out to V4 and beyond, has some ST elevation, and biphasic T-waves.  It is seen primarily in young African American males.

4. There are no structural cardiac abnormalities.

5. The primary life-threatening pathologies on the differential diagnosis are 
         a) Anterior ischemia (from pulmonary embolism or ACS)
         b) ARVD, Arrhythmogenic Right Ventricular Dysplasia (ARV Cardiomypathy).  It is relatively rare, but causes deadly dysrhythmias.

ARVD: T-wave inversion in V1-V3, with the typical PJTWP morphology, but associated with
 i)  Syncope without a prodrome, 
ii)  PVCs with an LBBB morphology, 
iii) Ventricular dysrhythmias, or 
iv)  Epsilon waves of course are very specific but insensitive for ARVD
v)   Males over age 19, definitely need further evaluation.

6.  Although it is called "persistent", these T-waves may not always be persistent.  Instead, like all benign findings, including early repolarization, it seems that they may be absent on a previous ECG and still be benign.

Persistent juvenile T wave pattern (PJTWP) – persistent confusion?

A 32-year African-American female came to the ED complaining of episodes of palpitations and a “racing” heart. She had a history of DM and HTN. Vital signs and the physical exam were unremarkable. An ECG was obtained:
Figure 1.  There are assymetric T-wave inversions in V1-V3.  Are these normal variants?  Persistent Juvenile T-waves?  Are these pathologic?  Does she have "anterior" ischemia?
This was compared with an ECG recorded 7 years prior:
Figure 2. This previous ECG also has TW inversions in V1 and V2 and a biphasic TW in V3.  
Does the ECG demonstrate a PJTWP?  Does the fact that it was not fully present before preclude the diagnosis of PJTW?
This is a difficult question to answer, but there have been a number of publications in the last few years that shed some light on PJTWP. I’ll review 5 issues that this literature highlights, then circle back to our patient.

Issue 1. Definition of PJTWP
A clear description of the PJTWP is surprisingly difficult to find.

Defining true juvenile T wave patterns
It is worth revisiting the “true” juvenile T wave pattern. Recall that the RV of the neonate has spent 9 months fighting the high-resistance pulmonary circulation, and so the RV is (non-pathologically) hypertrophied. As a result, there may be ECG findings of right ventricular dominance, including T-wave inversion (TWI) in leads V1-V3 or V4 in young children. Generally, this pattern evolves to the adult pattern (i.e. TWI limited to V1) by about 10 years of age.

Characteristics of “true” juvenile T wave pattern include shallow inversions, limited to V1-V3/V4, an asymmetric morphology of the inverted T wave, and no significant ST segment deviation. For example, here is the ECG of a healthy 3 year-old female:

Figure 3. We call these slightly asymmetric T-waves in V1-V3.
Some would call these symmetric, in contrast to the very asymmetric T-waves of, for instance, Left Ventricular Hypertrophy below.

Figure 4. These are T-wave inversions that everyone would call asymmetric

For comparison, here are the symmetric T-waves of Wellens' Pattern B syndrome:
Figure 5. Note the near perfect symmetry of V2 and V3. This is NOT normal, not PJTWP.

The ECG of another healthy 3 year-old, taken from Chan et al. (2)
Figure 6. Notice the inverted T-waves in V1-V3 are slightly asymmetric.

An example of a juvenile T wave pattern in a healthy 11 year-old male is provided in an article by Sharieff and Rao:(3)
Figure 7.  Here the T inversion is limited to V1 and V2; it is slightly asymmetric.

Defining “persistent” juvenile T wave pattern in adults
There are no consistent definitions of this adult variant of TWI. While one author proposed “asymmetric T-wave inversions in right precordial leads, without any other abnormalities”(4) as criteria, not all researchers agree.

For example, at least three articles suggest that PJTWP is typically associated with significant ST segment elevation in those same leads.(5, 6, 7)     

Look at these closely, as we do not agree that this is PJTWP!

Figure 8. One complex of domed ST elevation preceding the TWI.  This is not PJTWP, rather it is Benign T-wave Inversion (BTWI), also known as ST-T Normal Variant (STTNV) (8).

Choo 2002
Figure 9.  Domed ST elevation preceding TWI -- we do not believe this is PJTWP, rather it is BTWI, the other normal variant

2009 Papadakis
Figure 10.  Domed ST elevation preceding TWI -- we do not believe this is PJTWP, rather it is BTWI, the other normal variant

All three of these ECGs show domed ST Elevation that precedes the TWI in the precordial leads, a feature that is not usually seen in children. This pattern has been termed “benign T wave inversion” (BTWI) or “ST Elevation and Inverted T Wave” or ST-T Normal Variant (STTNV) by various authors.   See numerous examples of BTWI here.  In contrast to PJTWP, this STE/TWI pattern of BTWI is found more often in males than females,(8) and is considered by some to be a training-related variant.  It is especially common in African American males.(8)

Issue 2. PJWTP is found more often in women.
Most studies show that anterior TWI is found more often in women than men. In a Finnish study, the distinct majority (87%) of the people with right-precordial TWI were women (9), and a retrospective review done in New Jersey also found a similar proportion.(4). On the other side of the world, in a population of Israeli Bedouins, only women showed this pattern (10).

Issue 3. TWI (PJTWP or BTWI?) is found more often in people of African heritage

Similar to other atypical patterns of repolarization abnormalities, PJTWP appears to be seen more common in patients of African heritage. In a cohort of black and white females in the UK, 15% of the black females manifested TWI in anterior leads, while only 4% of the white females did.(11).  Similar results were seen in a cohort of British and French athletes.(12).  In a group professional American football players, 4.3% of the black players showed this pattern, while only 1% of the white players did.(6)  A 2008 study found that TWIs (of unspecified location) were far more common in black athletes than white.(13)   Unfortunately, these studies are complicated by the confusion between PJTWP and BTWI patterns.

Issue 4. It may not be part of the “athlete’s ECG.”
A number of ECG variants have been described in highly trained athletes; e.g. low-grade AV blocks, pseudo-LVH patterns, RSr', and early repolarization.(14) It is unclear, however, if anterior TWI is part of this group of variants.

A number of studies have suggested that anterior T wave inversions are more common in athletes, and that they resolve with cessation of intense training.(15)  However, Sharma found an equal incidence of anterior TWI  greater than 2 mm in both athletes and non-athletes.(16)

Other experts agree with this perspective.(17) Accordingly, at least 3 different groups have recommended that athletes who have TWI in V2 and V3 should receive further evaluation, even if currently asymptomatic.(5, 18, 19)

Issue 5.  PJTWP is considered after ischemia, PE, and ARVC have been excluded.
A diagnosis of PJTWP should be arrived at only after consideration of more dangerous causes of anterior TWI. Such ECG changes could reflect severe COPD, PE, or pulmonary hypertension. Posterior MI or anterior ischemia should also be ruled-out.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare disease, with ECG manifestations that could be mistaken for PJTWP.  Criteria for recognizing ARVC on the standard ECG include “inverted T waves in right precordial leads (V1, V2, and V3) or beyond in individuals greater than 14 years of age (in the absence of complete right bundle-branch block QRS ≥120 ms)” as a major criterion for diagnosis.”(20) Clearly, in the right context such as syncope, palpitations, or tachycardia, ARVC must be considered before diagnosing PJTWP on the ECG.  

Here are diagnostic criteria for ARVD from Eur Heart Journal Task Force (full text link): Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria.

So, does our patient have persistent juvenile T wave pattern?
The 2014 ECG shows asymmetric T wave inversion in leads V1 – V3, without ST segment elevation or other concerning findings on the ECG. A review of her old ECGs showed, however, that this TWI was not unchanged from prior, and was more pronounced than 7 years ago. In particular, the T wave in V3 is now over 2 mm deep.

A cardiology consultation was obtained, serial troponin levels were negative, and an echocardiogram from 3 years prior was found to be normal. She was discharged from the ED with plans for outpatient follow-up with cardiology.
Figure 11.  Note that the T-wave inversions in 2014 are deeper than in 2013.  Can we prove that this is still normal?  Or Abnormal?

Multiple ECGs were obtained in each patient, so that the chance of a technical error (lead placement) causing this pattern is unlikely.  In case #1, 2 ECGs were obtained in different months of 2007 and 2014 and were consistent.

One may object that without definitive evaluation using echocardiography, angiography, MRI, etc., that we cannot be certain that the TWI is not due to an undiagnosed structural disorder, including ARVD.  Evaluation was pursued only to the degree that the indivudual clinician felt was warranted for the presenting complaint.  

On the other hand, we are not aware of any longitudinal studies of normal populations which confirm that what appears to be PJTWP does NOT develop later.  We do know that many T-wave inversion patterns are benign.

Given that this pattern is commonly presumed to be benign, clinicians may have "underinvestigated" the ECG findings in this case.  Biases about TWI in female African American patients may play a role in limited investigation, leading to premature diagnostic closure.  

These limitations argue for reconsidering the benignity of PJTWP.

So – can you diagnose PJTWP if the pattern is not, in fact, persistent? Despite the number of new articles on the subject, there is no guidance here.

Furthermore, as discussed in Issue #1 above, much of the literature regarding PJTWP includes ECGs with significant ST elevation in the anterior leads, a distinctly unjuvenile pattern. How distinct is this STE/TWI pattern from “true” PJTWP? Is it a minor variant, or is it clinically important? Again, the answer isn’t clear from the recent results.

I guess you could say that our case and review suggest that “persistent juvenile” T wave pattern may be neither persistent nor juvenile.

1.            Marcus FI.  Prevalence of T-Wave Inversion Beyond V1 in Young Normal Individuals and Usefulness for the Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia.  Am J Cardiol 2005;95:1070-1071.
2.            Chan TC, Sharieff GQ, Brady WJ. Electrocardiographic Manifestations: Pediatric ECG. J. Emerg. Med. 2008;35(4):421-430. doi:10.1016/j.jemermed.2007.09.039.
3.            Sharieff GQ, Rao SO. The Pediatric ECG. Emerg. Med. Clin. North Am. 2006;24(1):195-208. doi:10.1016/j.emc.2005.08.014.
4.            Kaid KA, Maqsood A, Cohen M, Rothfeld E. Further characterization of the “persistent juvenile T-wave pattern” in adults. J. Electrocardiol. 2008;41(6):644-645. doi:10.1016/j.jelectrocard.2008.08.028.
5.            Uberoi A, Stein R, Perez MV, et al. Interpretation of the Electrocardiogram of Young Athletes. Circulation 2011;124(6):746-757. doi:10.1161/CIRCULATIONAHA.110.013078.
6.            Choo JK, Abernethy III WB, Hutter Jr. AM. Electrocardiographic observations in professional football players. Am. J. Cardiol. 2002;90(2):198-200. doi:10.1016/S0002-9149(02)02454-2.
7.            Papadakis M, Basavarajaiah S, Rawlins J, et al. Prevalence and significance of T-wave inversions in predominantly Caucasian adolescent athletes. Eur. Heart J. 2009;30(14):1728-1735. doi:10.1093/eurheartj/ehp164.
8.            Roukoz H.  Wang K.  ST Elevation and Inverted T Wave as Another Normal Variant Mimicking Acute Myocardial Infarction: The Prevalence, Age, Gender, and Racial Distribution.  Annals of Noninvasive Electrocardiology 16(1):64-69, January 2011.   doi:10.1111/j.1542-474X.2010.00410.x.
9.            Aro AL, Anttonen O, Tikkanen JT, et al. Prevalence and Prognostic Significance of T-Wave Inversions in Right Precordial Leads of a 12-Lead Electrocardiogram in the Middle-Aged Subjects. Circulation 2012;125(21):2572-2577. doi:10.1161/CIRCULATIONAHA.112.098681.
10.          Assali A-R, Khamaysi N, Birnbaum Y. Juvenile ECG pattern in adult black arabs. J. Electrocardiol. 1997;30(2):87-90. doi:10.1016/S0022-0736(97)80014-3.
11.          Malhotra A, Dhutia H, Gati S, et al. 103 Prevalence and significance of anterior T wave inversion in females. Heart Br. Card. Soc. 2014;100 Suppl 3:A60. doi:10.1136/heartjnl-2014-306118.103.
12.          Rawlins J, Carre F, Kervio G, et al. Ethnic Differences in Physiological Cardiac Adaptation to Intense Physical Exercise in Highly Trained Female Athletes. Circulation 2010;121(9):1078-1085. doi:10.1161/CIRCULATIONAHA.109.917211.
13.          Magalski A, Maron BJ, Main ML, et al. Relation of Race to Electrocardiographic Patterns in Elite American Football Players. J. Am. Coll. Cardiol. 2008;51(23):2250-2255. doi:10.1016/j.jacc.2008.01.065.
14.          Wu J, Stork TL, Perron AD, Brady WJ. The athlete’s electrocardiogram. Am. J. Emerg. Med. 2006;24(1):77-86. doi:10.1016/j.ajem.2005.04.009.
15.          Wilson MG, Sharma S, CarrĂ© F, et al. Significance of deep T-wave inversions in asymptomatic athletes with normal cardiovascular examinations: practical solutions for managing the diagnostic conundrum. Br. J. Sports Med. 2012;46(Suppl 1):i51-i58. doi:10.1136/bjsports-2011-090838.
16.          Sharma S, Whyte G, Elliott P, et al. Electrocardiographic changes in 1000 highly trained junior elite athletes. Br. J. Sports Med. 1999;33(5):319-324.
17.          Corrado D, Biffi A, Basso C, Pelliccia A, Thiene G. 12-lead ECG in the athlete: physiological versus pathological abnormalities. Br. J. Sports Med. 2009;43(9):669-676. doi:10.1136/bjsm.2008.054759.
18.          Drezner JA, Ackerman MJ, Anderson J, et al. Electrocardiographic interpretation in athletes: the “Seattle Criteria.” Br. J. Sports Med. 2013;47(3):122-124. doi:10.1136/bjsports-2012-092067.
19.          Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur. Heart J. 2010;31(2):243-259. doi:10.1093/eurheartj/ehp473.
20.          Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia Proposed Modification of the Task Force Criteria. Circulation 2010;121(13):1533-1541. doi:10.1161/CIRCULATIONAHA.108.840827.
21.          Dalal D, Nasir K, Bomma C, et al. Arrhythmogenic Right Ventricular Dysplasia A United States Experience. Circulation 2005;112(25):3823-3832. doi:10.1161/CIRCULATIONAHA.105.542266.
22.          Jha AK, Varosy PD, Kanaya AM, et al. Differences in Medical Care and Disease Outcomes Among Black and White Women With Heart Disease. Circulation 2003;108(9):1089-1094. doi:10.1161/01.CIR.0000085994.38132.E5.

A Young Woman with A Wide Complex Regular Tachycardia.

A woman in her early 30s with no past medical history presented with palpitations.  She had no chest pain, SOB, shock, hypotension.  She felt otherwise well.

Here is her 12-lead ECG:
How would you treat this patient?

Far less important: 
What kind of regular wide complex tachycardia is it?

First, the patient is otherwise healthy and in no distress.  She tolerates this very well.  Thus, whether it is 1) Ventricular Tachycardia (VT), 2) SVT (AVNRT) with aberrancy, or even 3) antidromic AV reciprocating tachycardia (AVRT) does not matter for the emergency management.   (Atrial flutter and atrial tach are far less likely.)

You have a minute to think.  If it is VT, you won't hurt her by giving adenosine, and it is AVNRT or AVRT, it is likely to successfully terminate it.  If at any time she becomes unstable, then electrically cardiovert.


She was given adenosine and she converted to normal sinus rhythm, with a subsequent normal ECG (not shown).

(see bottom of page for approach to 12-lead diagnosis of regular wide complex tachycardia):

--Was it VT, and the conversion was just coincidence?
--Or did she have AVNRT or AVRT, and the termination at the time of adenosine was causal?
--Or something else, like Fascicular VT?

What do we get from analysis of the ECG?

1.  There are some elements which favor SVT (or fascicular VT):
     a) In the precordial leads, the QRS width is only 120 ms, which among VT cases only happens in fascicular VT.
                In non-fascicular VT, the initial part of the QRS must travel through slow conducting myocardium, and the QRS, especially the beginning of the QRS, is slow.
     b) In the precordial leads, from the onset of the r-wave in V1 and V2 to the nadir of the S-wave is only 40 ms, which is very fast for non-fascicular VT.  Among VT, only fascicular VT would have a such a rapid initial deflection.

2.  There are other elements in favor of VT:
    a) Concordant QRS in the precordial leads (no RS pattern, all in the same direction)
           --Concordance comes in two varieties:
                  --upright  QRS in V1 (RBBB type).  This is almost always VT or AVRT (antidromic, lateral accessory pathway)
                  --negative QRS in V1 (LBBB type).  This is VT at least 90% of the time, but not 100%.
    b) The QRS duration in the limb leads seems to be about 140 ms.

So why is the QRS 120 ms in precordial leads, and 140 ms in limb leads?  And what is the QRS duration actually?

The QRS duration is the longest QRS duration of the 12 leads.  Shorter durations can be due to recording angles.  In this case, the frontal plane (limb leads) is more able to capture the entire QRS duration that the precordial leads.  So the QRS duration is closer to 140ms, and the initial deflections are longer than 40 ms, so VT remains in the differential.

What VT responds to adenosine?

Right ventricular outflow tract VT, also known as Repetitive Monomorphic VT (RMVT).  RVOT originates from the "base" or top of the heart and thus has and LBBB morphology (as here), but also an upright R-wave in all inferior leads (unlike this ECG).  So this is not RVOT, at least not typical.

The other common "idiopathic" VT is Posterior Fascicular VT, which originates in the posterior fascicle, and thus has an RBBB/LAFB morphology.  It responds to verapamil.

Here is one case of Posterior Fascicular VT.

Here is a 2nd case of Posterior Fascicular VT.

In reality, fascicular VT can originate in any fascicle (anywhere in right or left bundle, etc.).  Re-entrant rhythms can originate anywhere (they only require a second pathway with a different conduction velocity and refractory period).   All of them will be narrower that VT that comes from a structurally abnormal heart.  Any of them can (rarely) respond to adenosine.

The "idiopathic" VTs occur by definition in structurally normal hearts and have a relatively benign prognosis.

Probable Diagnosis

This is a rare non-RVOT fascicular VT that responded to adenosine.  It will require EP testing to confirm.

When determining VT vs. SVT, here is the sequence of analysis I use:

Consider in the context of clinical scenario.  
(None of this applies to fascicular VT or RV outflow VT, which are associated with normal heart structure and originate in or near conducting fibers.  However, these are rare exceptions):

a. VT is more common than SVT among WCT
b. Older patients are more likely still to have VT
c. Any history of cardiomyopathy, MI, structural heart disease, or coronary disease makes VT much more likely

And then consider the ECG.  

The unifying principle of most VT is that the first part of the QRS is initiated in myocardium, NOT in conducting fibers, and thus conducts slowly.  Therefore, the initial part of the QRS changes its voltage SLOWLY (wide).  This is what I look for to diagnose VT:

1. The longer the QRS, the more likely it is VT.  A QRS duration greater than 140 ms is likely VT, though it is not a terribly reliable differentiator.  However, a QRS duration of 200 ms is almost always VT or aberrancy with hyperkalemia.  
2. Obvious AV dissociation?  then VT, if not:
3. Obvious fusion beats?  If so, then VT, if not:
4. Leads V1-V6 unidirectional (no RS or SR) and "concordant" (in the same direction)?  Then VT (but in this case concordance is less convincing because the QRS duration is only 120 ms.
5. If there are RS complexes (they are not concordant): is there any precordial RS that has a duration from onset of R to nadir of S that is greater than 100 ms?  Then VT.  Here it is very short (40 ms)
6. Abnormal LBBB or RBBB pattern (see this link for a figure from the Brugada paper):
----a normal RBBB or LBBB pattern makes SVT very likely: both have a rapid initial deflection, the r-wave in LBBB and the rS in RBBB, followed by a slowly conducting latter part of the QRS.
     a.  If there is LBBB pattern, is the initial r-wave greater than 50 ms?  Or is the onset of the QRS to nadir of the S-wave in V1-V3 greater than 60-70 ms?  If so, this is not true LBBB. 
     b. If there is RBBB pattern, is there a monophasic R-wave?  Or is the first R of the Rsr' larger than the second one?  Then VT.
7. Initial R-wave in aVR (not an r-wave, not preceded by q-wave)?  Then VT
8.  If the initial deflection in aVR is an r-wave or q-wave, is it greater than 40 ms?  If so, then VT