What is the infarct artery? (Complex analysis, in this case)

This case was put on Twitter by Elisha Targonsky, who has a nice EM blog (http://thechartreview.org).  He provided it for posting here.  On Twitter, he asked for an analysis of the infarct artery.

Analysis of the infarct artery is mostly an academic exercise.  The patient clearly needs cath lab activation.  However, it is of some clinical value: interventionalists like to know what artery is affected because it often determines which artery they will investigate first with angiography.

So it does have some value, but is not critical.

But moreover, it is an exercise which helps one understand all the ST vectors at play in an ECG.
What is your analysis?  See mine below.

Notice this is a 15 lead ECG, with posterior leads V8 and V9 and also Right sided lead V4R.

Here was my Twitter response without any other information:
Tweet 1: Prox large RCA, also to lateral and posterior walls. Ant MI is RV, not LV. V2 less STE b/o posterior MI.
Tweet 2: In other words: pseudo anterior MI (RV: V1-V4) from large RCA, to post & lat also. V2 STE attenuated by post

One must explain several findings:
1. Inferior ST elevation
2. Anterior ST elevation (V1 and V3), but very little in V2
3. ST elevation in V4-V6 (but also ST depression in aVL)
4. Posterior ST elevation
5. ST elevation in V4R

--One is tempted to call this LAD occlusion with anterior MI and wraparound LAD to the inferior wall.  But then how do you get a posterior STEMI also?

--One might say: OK, it is left main, and that is why there is BOTH anterior (LAD) and Posterior (Circ) STEMI.

Why the inferior STE?  Maybe it is a left dominant system, so the circ also goes to the inferior wall.

But then one must still explain 2 findings: the patient is still alive AND there is ST elevation in V4R.

ST elevation in V4R can conceivably be caused by LAD occlusion, as some individuals have the RV supplied by rightward branches of the LAD.  This is a possibility, but you would expect such a patient to be in shock.

What was the clinical scenario?

A middle-aged male with h/o CAD, HTN, DM, hyperlipidemia.
Previous LAD stent, then 2 years later had bare metal stent to RCA.
Presented without shock, with 10/10 substernal CP.  Diaphoretic and nauseated.

--So left main is very unlikely.

--What then?   The ST elevation in V4R is the big clue.  This is almost always due to Right Ventricular MI.  RV MI also may cause anterior ST elevation mimicking anterior MI ("Pseudoanteroseptal MI").  In these cases, the maximum ST elevation is in V1 or V2, and becomes less as one goes out to V3, V4, etc.

So the IRA is the RCA.

--What does this RCA supply besides the RV?  It supplies the inferior wall, the posterior wall, the inferolateral wall (STE in V4-V6 without high lateral STE in aVL)

--Why is there less STE in V2 than in V1 or V3?
1. The posterior ST elevation is exactly reciprocal to V2 and is attenuating the STE in V2.
2. That downward pull is not as opposite V3 as it is opposite to V2.
3. The RV ST elevation is greater in V1 than in V2
4. The lateral ST elevation has more "upward" pull on V3 than there is downward pull from posterior.

--Why is there ST depression in aVL but ST elevation in precordial lateral leads V5 and V6?
V5 and V6 are situated more inferior than aVL.  Many inferior MI have ST elevation in V5 and V6.  And all inferior STEMI have ST depression in aVL.  In our series of 150 inferior STEMI, 27 had ST elevation in V5 and V6.  All had ST depression in aVL.

What direction is the ST vector?
There is diffuse ST elevation, except towards leads I, aVL and V2:
To the right
Left inferolateral
Left anterior
Right anterior

Angiography Results:

No disease in LAD or circ
RCA dominant with acute thrombosis
Thrombectomy and stent.

Good outcome.

Read this ECG

What is the diagnosis here?
The computer read was ****Acute STEMI****What is really going on?
See Answer Below

This is a trauma patient (motor vehicle collision) who arrived with a temperature of 27 degrees Celsius.  Among many injuries was a traumatic diaphragmatic hernia, which may also affect the ECG.

The prominent features are: relative bradycardia (one would expect in this ill trauma patient) and Osborn Waves in V3-V6.  The most common finding in hypothermia is atrial fibrillation with a slow ventricular response (not seen here).  The computerized QTc was 489 ms (accurate).

After warming, another ECG was recorded:

The ECG in hypothermia 

Rhythm: The most common rhythms in hypothermia are sinus bradycardia, junctional bradycardia, and atrial fibrillation.  Shivering artifact is common.  Atrial flutter may also be seen.  At temperatures below 30 C, the patient is at risk for ventricular fibrillation.   In this study of 29 humans cooled to 28-30 C for cardiac surgery, 19 developed atrial fibrillation and 2 ventricular fibrillation.

QRS: Osborn waves are thought to be pathognomonic of hypothermia, but can also be seen in normothermic patients.  "J-waves" or "J-point notching" is very common in early repolarization.   Very narrow Osborn waves were reported in severe hypercalcemia (level 16.3).  Sometimes a short ST segment of hyperCa can be misinterpreted as an Osborn wave; that is not the case in the aforementioned case report.   J-wave syndromes are proposed to give a unifying pathophysiology to Osborn waves of hypothermia and early repolarization, as well as Brugada syndrome.

Cold symptoms and bradycardia. What is this pre-excitation?

A young man presented to the ED for cough and runny nose and was bradycardic, so an ECG was recorded:
There is sinus rhythm with complete AV dissociation due to complete (third degree) AV block.  The escape has a slurred upstroke.  Is this a delta wave?

The patient stated that he knows he has this and that whenever he feels weak he just takes some methamphetamine and he feels fine!  He refused any treatment or evaluation.

The rhythm is interesting, though, and we have some disagreement about whether it is an nodal escape with a fasciculo-ventricular accessory pathway, or a ventricular escape with "Pseudo" Delta waves.  In any case, there must be some pre-excitation.

If it is fasculo-ventricular, as our EP expert says (and I defer to him), then this is a potential ladder diagram, as drawn by Christopher Watford:

K. Wang has graciously offered to let me insert pages 212 and 213 on Pseudo Delta waves from his great Atlas of Electrocardiography:

It seems to me that Pseudo Delta waves are only "Pseudo" in that the do not necessarily represent an accessory pathway, the way we normally associate delta waves with WPW.

However, it also seems that any delta wave implies some pre-excitation.  Ventricular beats often take some time to reach the conducting fibers and will thus often have pre-excitation of some sort.

A Young Woman with Chest Pressure and Subtle, Focal ST Elevation/Depression

A very healthy woman in her 20's (who, however, is a heavy smoker) presented with 4 days of waxing and waning substernal chest pressure radiating to the throat and both shoulders.  It was not sharp, not pleuritic.  There were no myalgias, no viral symptoms, no F/C/S.

Looking at her, she was the picture of health, and I thought to myself: "Is there any possible way she could have an MI?".  My answer, of course was yes.  

I've seen it too often before in young women, as for instance:
in this case, and 
in this case, and others.

So we ordered an ECG, of course:
I found this very interesting and worrisome.
--The most obvious is ST elevation is in V3-V6. This could be normal, myopericarditis, or MI.
--However, there is another finding which had me very worried: ST depression in lead III and opposing ST elevation in I and aVL.
--There is PR depression that is within normal limits
--The ST elevation in aVL is only 0.5 mm, but the QRS has even less amplitude.

Let's look at III and aVL enlarged:
Notice the QRS voltage is less than 0.2 mV (less than 2 mm) in aVL, and the ST segment is nearly 1 mm.  So the proportional ST elevation is quite high.
This is only partly due to the difference in axis between the QRS and ST segment.  QRS axis is 60 degrees, towards lead II, and the ST axis is 0, towards lead I.

Pericarditis only manifests ST depression in lead III if it is focal to the high lateral wall. Focal pericarditis is unusual, but focal myocarditis is not.  Most pericarditis is electrocardiographically diffuse, with an ST vector towards leads II and V5 and no reciprocal ST depression except in aVR.

A bedside echo was normal.  Troponin I was sent.  Chest X-ray was normal.  She was given aspirin and sublingual nitroglycerine, and her pain subsided slightly.  Another ECG was recorded:
The ST deviation is less.  Thus it is dymamic, which is not usually associated with myo-pericarditis, but probably because serial ECGs are not frequently obtained for this condition. 
Here is the enlargement:

The troponin I returned at 18.9 ng/mL. 

Is it MI or myocarditis?

See this excellent study of patients with suspected MI and normal angiograms (from 2001, it is still the best study I can find).

Of 45 patients, 35 had myocarditis by Indium scintigraphy (unfortunately, I don't know how accurate this test is, and it seems that no diagnostic test is terribly accurate for myocarditis. Even the reference standard, endomyocardial biopsy, often misses the involved myocardium).
--Half of them had focal myocarditis and half diffuse.
--28% had reciprocal ST depression.
--62% had regional wall motion abnormalities.
-- In the U.S. Myocarditis treatment trial, 89% of these highly selected patients (not ED patients) had a syndrome consistent with a viral prodrome.

Thus, unfortunately, if there is a wall motion abnormality, one is really unable to differentiate acute MI from myocarditis in the emergency department. 

Case Progression 

I consulted our cardiologist, who sent his echo tech, and we obtained a high quality, Definity contrast echo.  This was done and showed a lateral wall motion abnormality.

So we activated the cath lab.  The interventionalist was very pleased to come evaluate this young woman's coronary arteries, agreeing wholeheartedly that you can't "sit on" someone all night who has chest pain and a positive EKG and troponin.

The angiogram was completely normal.

The left ventriculogram showed a dense lateral regional wall motion abnormality, very highly suggestive of focal myocarditis.

Serial troponin I went from 18.9 ng/mL, to 19.7 at 6 hours, to 16.8 at 9 hours, to 16.1 at 24 hours to 11.5 at 42 hours.

An ECG was recorded the following morning:
Now there is much more widespread ST elevation, with no reciprocal ST depression. This is classic myopericarditis.
An MRI of the heart confirmed inflammation of the lateral wall, all but diagnostic of myocarditis.

She was treated with colchicine and ibuprofen.

A final ECG at 42 hours was resolving:

Learning Points:

When the differential diagnosis is myocarditis vs. acute MI, it is difficult to make any conclusions without an angiogram.  In half of myocarditis, there will be a wall motion abnormality (focal myocarditis) and it will be impossible to distinguish from MI.  If there is no wall motion abnormality, one can be reasonably confident that it is diffuse myocarditis and avoid the emergent angiogram.

I am not at all troubled by activating the cath lab to be certain that she was not having a coronary thrombus.  It put everyone's mind to rest.

What happened after the PCI?

A middle-aged male with h/o CABG x 3, previous stents, and aortic valve and aortic root replacement presented primarily with headache, but also told the medics that he had chest pain (for 6 hours) because he "knew they would respond faster than if he said headaches."  The chest pain was right sided rib and shoulder pain, worse with inspiration, sharp, and sometimes 7-8/10.  But the headache was much worse.   Chest pain was not relieved by sublingual NTG.

He has noticed worsening exertional dyspnea, such that he feels he can only walk about a block before experiencing "chest tightness. 

Here is his ED ECG (compare with the 2 month previous ECG below it):
--Is there a new Q-wave (tiny r-wave) in III?  
--There is new ST elevation in III, with new STE also in aVF.  
--There is reciprocal ST depression in aVL.  
--There is STE in V1, suggesting RV MI, but this was present on the old one.  
--There is some ST depression in V5 and V6.  
--This is almost certainly an acute inferior MI, though does not meet mm "criteria" for STEMI 
--The beginnings of T-wave inversion suggest an open artery.

Previous ECG from 2 months prior:
Previous, does not have the same ST deviations

CT head was negative for acute bleed.  The patient was managed medically with ASA 325 mg, heparin, and Plavix, and nitroglycerine, but his pain did not improve.  A troponin I returned at 7.7 ng/mL (diagnostic of MI).

A repeat ECG was recorded:
There is slightly more STE in III and reciprocal STD in aVL

Cardiology was consulted for NSTEMI that needs the cath lab now (objective evidence of ischemia and ongoing pain).  The cath lab was activated.

Cath results:

It was a complex cath and anatomy.  The RCA was diffusely diseased and had an acute on chronic occlusion that was opened.

A Post Cath ECG was obtained an hour later:

What is going on?

I ran across this case and this ECG while reading through a series of ECGs and it alarmed me.  The inferior ST elevation is now gone, but there is new DIAGNOSTIC ST elevation in V1-V3.  Look closely: the ST elevation is greatest in V1 and V2, and does not extend out to V4.

Why?  Because this "anterior" MI is due to STEMI of the right ventricle (RV), not of the LV.  

Case Progression

The cardiologist quickly went to evaluate the patient, who found that the chest pain was unchanged and that the patient was hemodynamically stable.  A formal echo showed some RV dysfunction and normal LV anterior wall.

This was presumed to be an isolated acute RV infarction and due to the patient stability and the difficulty of the coronary anatomy, no intervention was undertaken.  Presumably, the procedure induced a thrombus in the RV marginal branch.

This was recorded 3 hours post cath:

The RV infarct appears to be resolving spontaneously.

5 hours post cath:

More resolution of ST elevation, with some T-wave inversion.  This is good evidence of spontaneous reperfusion of the RV marginal branch

Next day:

The troponin I peaked at 29, fell to 20, then rose again just a little to 21.5 ng/mL due to the brief RV STEMI.

The patient did well.

Learning points:

1. NonSTEMI often need immediate cath lab activation. as I have often discussed.
2. STEMI in V1-V3 is anterior, but not necessarily due to LV anterior STEMI.  It may be due to RV STEMI, which is also anterior.  
3. When the RCA is the vessel involved, new anterior ST elevation is likely to be RV STEMI
4. When the ST elevation is greatest in V1-V3 vs. V2-V4, RV STEMI is more likely than LV

Detailed cath results:

1) 2 vessel CABG [Left internal mammary (LIMA) to LAD, and Saphenous Vein Graft (SVG) to left posterolateral artery (L-PLA)]
months ago.
3) The SVG to the L-PLA is occluded. The LIMA to the Mid-LAD is widely
4) The RCA was patent on the cath of 6/10/13. The occluded RCA currently
likely represents acute on chronic obstruction in light of the patients
clinical presentation and the collaterals to the R-PDA.
5) Balloon angioplasty only due to noncompliance with clopidogrel, 
reducing the sub-total occlusion to diffuse 30-40% stenosis. The R-PDA is
occluded proximally and was probe with a wire.

Coronary Angiograms 

LMCA: 60% calcified mid to distal LM stenosis.
LAD: Multiple stents in the LAD system. Sub-totally occluded LAD after the
first major septal and diagonal. D1 has an instent 70% take-off stenosis.
LCx: Co-dominant system. 80% circ take-off stenosis. Scattered 30% stenosis
throughout the circ system. The L-PLA that received the SVG has a 70%
stenosis on the native vessel just at the proximal insertion of the graft.
Only a small remnant of the SVG is visible at the insertion site consistent
with occlusion.
RCA: Stent noted in proximal portion. Sub-total occlusion proximally. A
R-PDA fills faintly by L to R collaterals.
Lesion on Prox RCA: 99% stenosis.