What kind of AV block is this?? And where is the coronary occlusion??

For couple very interesting related posts, click here.

A 76 year old male presented with chest pain.  Here is the initial ECG:

Rhythm: slow and regular.  p-waves are not conducting down to ventricles.  This was initially diagnosed as complete AV block.  What is it really?
ST segments: There is obvious inferior STEMI, with ST elevation (and Q-waves and T-wave inversion) in II, III, aVF and reciprocal depression in I and aVL.  Where else is there ST elevation?  Where is the occlusion?    

Here the p-waves are highlighted by arrows:

Answer to artery:
First, the patient was hypotensive, which should clue you in to Right ventricular infarction.  The ECG diagnosis of RV MI is made by ST elevation in lead V1.  Indeed, at angio, there was a proximal RCA occlusion.

Answer to rhythm:
Notice the p-waves are inverted!  Thus, they are retrograde.  (or there is a low atrial pacemaker and 3rd degree block, and sinus brady, and junctional escape).  Look closely: p-waves are progressively later after each QRS.  Thus, the R-P interval is increasing.  This is junctional rhythm with retrograde Wenckebach (RP interval steadily increasing).  Unfortunately we do not have a long enough rhythm strip; if we did, it would eventually show a dropped p-wave!!

For a comprehensive explanation, I have copied below (with permission) from Kyuhyun Wang's great Atlas of Electrocardiography.  Here he explains it in the context of an "echo beat".  First, he explains the echo beat, then he shows a case of retrograde Wenckebach with an echo beat.

Pericarditis vs. MI #2

Posterior Leads Fail to Diagnose Posterior STEMI

For more cases of posterior MI:

http://hqmeded-ecg.blogspot.com/search/label/posterior%20STEMI

A 54 year old male with recent angiogram that showed only scattered coronary lesions of less than 50% developed chest pain at 11:30 AM.  It became progressively worse, so he decided to drive to the ER.  The pain became so intense that he flagged a passing fire truck. They called the medics.  En route to the hospital, the patient went into ventricular fibrillation.  He was defribillated.  It happened again and he was shocked again.

In the ED, here was his first ECG:

Sinus rhythm with a slightly prolonged QRS, but not bundle branch block.  There is ST depression in V2-V4, maximal in V3.  There is also ST depression in II, III, and aVF.   This should always alert to ST elevation in aVL, and, sure enough, aVL has minimal ST elevation. 

This is diagnostic of posterolateral STEMI.  When precordial ST depression is maximal in V1-V3, in contrast to V4-V6, then posterior infarct is the usual etiology.

As stated many times in this blog, high lateral STEMI may show itself primarily through "inferior" reciprocal ST depression.

On the contrary, with ST depression in II, III, aVF and also in precordial leads but maximal in V4-V6, then subendocardial ischemia is fairly certain, often accompanied by ST elevation in aVR.  In such cases (not this one!), the "inferior" ST depression is not reciprocal to ST elevation.

A consulting cardiologist requested posterior leads, but these showed no ST elevation (not shown).  Nevertheless, the patient was taken to the cath lab and found to have a 100% acutely occluded obtuse marginal off the circumflex supplying the posterior and lateral walls.


Why were posterior leads negative?  One must remember that it is a long way from the heart to the back, with a lot of air (lung) interposed.  So the voltage is far less.  A lot of indirect evidence suggests that 0.5 mm of ST elevation in just one of leads V7-V9 is quite sensitive and specific for posterior STEMI, but even 90% sensitivity misses 1 in 10.

Here is a case in which absence of ST elevation in posterior leads helped to diagnose subendocardial ischimia:  http://hqmeded-ecg.blogspot.com/2010/12/st-depression-v2-v4-posterior-leads.html


Here is a worthwhile paper: Wung SF, Drew BJ. New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction. Am J Cardiol 2001;87(8):970-4; April 15 2001..

The 12-lead ECG, without the posterior leads, is so clearly due to posterior STEMI that in spite of negative posterior leads, I was certain that this was posterolateral STEMI because:

1) nothing else causes ST depression in II, III, aVF and in right precordial leads greater than left precordial leads
2) high pretest probability for STEMI (chest pain followed by cardiac arrest)

Pretest probability:
--Nearly half of all ventricular fib arrests are due to STEMI
--MI is nearly certain if arrest preceded by chest pain
--Non STEMI can of course also cause ventricular fibrillation, but not nearly as commonly.

An academic note on terminology of posterior MI: Bayes de Luna determined by MRI that what was thought to be posterior MI as manifested by enlarged R-waves in V1-V3 is really "lateral."  One Society changed the terminology; here is the article:
http://circ.ahajournals.org/cgi/content/extract/114/16/1755

The committee on standardization of electrocardiography prefers to keep the term "posterior" for acute MI (I think appropriately):
http://content.onlinejacc.org/cgi/reprint/53/11/1003.pdf  page 1007

LBBB: is there STEMI?

A 45 year old male with no history of cardiac disease presented with new onset pulmonary edema.  He was intubated prehospital.  BP before and after intubation was 110 systolic, with HR of 120.

Click on this ECG and try to interpret it yourself before reading the answer below:

There is sinus tach with LBBB.  There is no concordant ST elevation.  V4 has 2 mm of discordant ST elevation (at the J-point, relative to the PR segment) following a 5 mm S-wave.  The ST/S ratio is 0.40 in this lead.  Lead II has proportionally excessively discordant ST depression, with 1.25 mm STD and only 4.0 mm R-wave, for a ratio of 0.31.  This is also a sign if ischemia (reciprocal inferior ST depression).              
Also, look at V3: complexes vary slightly: 2nd complex has approx 2.5-3.0 mm STE following a 14 mm S-wave; complex 4 has 2-2.5 mm STE following a 10.5 mm S-wave.   So these are significantly higher than the normal maximum (of V1-V4) ratio, which is about 0.10. 

Definitions in LBBB:
Concordance: ST segment is in the same direction as the majority of the QRS
Discordance: ST segment is in the opposite direction to the majority of the QRS
Rule of appropriate discordance: ST segments in all leads should be discordant to the majority of the QRS.
Smith rule: Discordance should be proportional to the QRS, with an ST/S or ST/R ratio no greater than 0.25.  Even anything greater than 0.20 is probably STEMI.

In a study of 20 patients with LAD occlusion, vs. 129 controls with ischemic symptoms and LBBB, at least one complex in V1-V4 with at least 2mm of STE and an ST/S ratio greater than or equal to  0.20, and especially if greater than 0.25, was highly specific for LAD occlusion (1).  

Cases with excessive discordance of at least 5mm [Sgarbossa criteria 3] that did not have proportional discordance, did not have LAD occlusion.  The mean highest ST/S ratio for those without occlusion was 0.10 (95% CI: 0.09-0.11); the mean highest ST/S ratio for those with occlusion was 0.44 (95% CI: 0.19-1.05)

Because of this study, I believe the following rule is as good for diagnosis of STEMI in the setting of LBBB as standard interpretation of STEMI in the absence of BBB (and that it is more sensitive and specific than the Sgarbossa rule):

Smith modified Sgarbossa rule:

1) at least one lead with concordant STE (Sgarbossa criterion 1) or
2) at least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2) or
3) proportionally excessively discordant ST elevation in V1-V4, as defined by an ST/S ratio of equal to or more than 0.25 and at least 1 mm of STE. (this replaces Sgarbossa criterion 3 which uses an absolute of 5mm)

It is important to remember that this is not sensitive for "MI" which is diagnosed by biomarkers. The lack of sensitivity of the Sgarbossa rule in previous studies is because the ECG is always (even without BBB) insensitive for MI.  It is, however, much more sensitive for occlusion.

Followup (Answer):
Because of proportionally excessive discordance in lead V4, (and, of course, clinical instability), the patient was taken for immediate angiography, which confirmed a 100% mid-LAD occlusion.

For a case with more than 5 mm of ST elevation in V1-V4, but without excessive proportional discordance, see this post:
http://hqmeded-ecg.blogspot.com/2011/02/new-lbbb-and-massive-st-elevation-do.html

Tom Bouthillet of EMS 12-lead has done a great job of describing my ratio rule here:
http://ems12lead.com/2010/12/29/excessive-discordance-as-a-marker-of-acute-stemi-in-lbbb/

To learn more about the meaning of New LBBB, look here:
http://hqmeded-ecg.blogspot.com/2010/03/new-left-bundle-branch-block-is-poor.html

Here is the reference in full text

 

29 year old, healthy, with pleuritic chest pain

A 29 year old male presented with 6 hours of stuttering chest pain, constant for the last hour, worse with breathing.  He had no medical history.

 What is the diagnosis?






Diagnosis:

There are Q-waves, ST elevation, and hyperacute T-waves in V2 and V3, diagnostic of acute LAD occlusion (STEMI).

Take home point here:

Obtain an ECG on anyone with chest pain. Sometimes you will find an obvious STEMI.

Clinical Course:

He was taken for immediate PCI of a 100% LAD occlusion with thrombus; door to balloon time was less than 60 minutes and symptom onset to balloon time was approximately 2 hours.

Nevertheless, he suffered a large infarction with peak troponin of 110 and the following ECG the next AM:

There are now deep QS-waves, with persistent ST elevation in precordial leads.  The shallow T-wave inversion is typical of completed transmural infarction, and contrasts with the deep T-wave inversion seen with quick reperfusion of an MI with much remaining viable myocardium.

He did not regain his R-waves after reperfusion.  Whether he will do so over the next months or not is uncertain now.   He has persistent ST elevation.  This may resolve over a couple weeks; if it does not, then he is at high risk of developing an LV aneurysm, or diastolic dysfunction of the anterior wall.  He is also at risk of a mural thrombus.

Q-waves in acute MI:

1) QR-waves are common early in anterior MI.
2) QS-waves are uncommon early in anterior MI; they are common in late presentation.
3) Q-waves are independently associated with worse outcomes (78% relative increase in 90-day mortality in Armstrong et al.)
4) Q-waves alone do not necessarily imply irreversibly infarcted myocardium; they should not dissuade from reperfusion therapy.

References:

Armstrong PW et al.  Baseline Q-wave surpasses time from symptom onset as a prognostic marker in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention.  J Am Coll Cardiol 2009;53(17):1503-9.

Raitt MH et al.  Appearance of abnormal Q-waves early in the course of acute myocardial infarction: implications for efficacy of thrmoblytic therapy.  J Am Coll Cardiol 1995;25(5):1084-8.

Is it MI or pericarditis?

I had a recent comment on this post, which was put up 7 years ago (850 posts since then!).  I was reminded of it.  And so I thought I would repost it.

Case

This is a 48 y.o. male with a history of Bipolar disorder, polysubstance abuse, spontaneous pneumothorax x2, who presents for chest pain x 4 hours. The patient was in his usual state of health until this afternoon when he noticed the gradual onset of bilateral chest pain. He had a relapse of crack use this AM. He describes the pain as bilateral, radiating to the left arm, worsening over time, and associated with mild SOB and also some pleuritic chest pain. There is no relation of pain to exertion or meals, and no associated diaphoresis, nausea or vomiting. No recent long sedentary periods. No recent trauma, but has been doing more manual labor than usual. Pt has not had chest pain with crack use before.

Here is his initial ECG:

Sinus.  Normal QRS.  QTc 375.  ST elevation in all leads that is not inconsistent with early repol or pericarditis, especially since there is J-wave notching (in lead aVL).  However, look closely at aVL: there is actually a bit of ST depression here.  That should not happen with pericarditis or with early repol, especially when there is J-wave notching.  It could be present in myocarditis but that may only be diagnosed after an angiogram shows no culprit.  One should suspect that this is reciprocal ST depression.

Here is his previous ECG for comparison, recorded 7 months prior:

Here there is none of the ST elevation seen in the above ECG.  In fact, the T-waves are normal here, whereas they are large above.  The ones above, then, are not necessarily due to early repol.  There is a change.  The most important change, though, is the ST elevation in inferior leads and the reciprocal depression in aVL.

 Here I place them on the same page for better comparison:

This comparison makes it obvious that the new ST elevation is diffuse: inferior, anterior, lateral. aVL is NOT elevated! .  

Here I have magnified II, III, aVF, and aVL for better comparison:

Now the difference in ST segments become more evident: new ST elevation in II, III, and aVF, with reciprocal ST depression in aVL.

Here I have magnified V1-V3 for better comparison:

Now the new ST elevation in V1-V3 is obvious

The Emergency physician started therapy for NSTEMI.  The first troponin returned at 2.25 ng/mL. The cardiology fellow then opined that this was myopericardititis and instructed to stop the heparin. However, myopericarditis is a diagnosis of exclusion and much less common than acute MI.  One must undertake treatment for ACS, including an angiogram.  Only if the angiogram is normal would one then consider myocarditis and probably obtain an MRI.

The reciprocal ST depression in lead aVL and the T-wave enlargement in V2 and V3 are all but diagnostic of MI.

Follow up:

The troponin I peaked at 23.6 ng/mL.  The echo showed an inferior and anterior wall motion abnormality.  Thus, it was not pericarditis, though myocarditis is possible..  Angiogram showed a ruptured plaque in the proximal LAD, with distal embolization of thrombus to the apex.  This was a "type III," or "wraparound" LAD which supplies both anterior and inferior walls.  This accounts for the transient hyperacute T-waves in anterior leads and for the ST elevation in inferior leads.

Even without the angiogram, the rapid rise and fall of troponin is highly suggestive of MI, not myopericarditis.

The stenosis was minimal, and the ACS occurred in the setting of cocaine use, so the therapy was eptifibatide and heparin for 72 hours, with no PCI.

Learning Points

1) Pericarditis should never be assumed when there is even a hint of reciprocal ST depression.  Only localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare.  I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.

2) Wraparound or Type III LAD ACS mimics pericarditis because it leads to diffuse ST elevation.

Wide complex tachycardias: 2 cases. What is the diagnosis and management?

This is the most widely misunderstood problem in Emergency tachydysrhythmia care.  There are many textbooks and articles and preparatory tests that get this wrong.  So read carefully!

Case 1.

This is a 37-year-old male who states that he has paroxysms of chest palpitations which usually last about 15 minutes and get better with cough or changes in position. The previous evening at approximately 11 p.m., he began to have chest palpitations which lasted through the night until the morning of admission. Along with these palpitations, he had some headache with dizziness. He denied any chest pain or shortness of breath.  He did admit to crack cocaine use over the past several days.

There are no p-waves.  The rate is 180 and constant.  It is regular.  It is wide.

What is your differential diagnosis?
What are the treatment options in the ED?


Case 2.
This is a case that comes courtesy of Dr. Kyuhyun Wang (long time Hennepin EKG wizard and my mentor, now at the University of Minnesota).   It is from his marvelous Atlas of Electrocardiography, with permission.

This is an irregularly irregular rhythm.  The QRS is wide and bizarre, with multiple QRS morphologies and very short R-R intervals

What is your differential diagnosis?
What are the treatment options in the ED?

Answer to Case 1:

Regular wide complex tachycardia.  It could be:

1) Ventricular tachycardia (VT)

2) PSVT [AV nodal re-entry tachycardia (AVNRT, 60% of PSVT), orthodromic WPW (30% of PSVT)] with aberrancy  (RBBB, LBBB, IVCD)

3) Antidromic AtrioVentricular Reciprocating Tachycardia (AVRT)

--Since it is not irregular, it cannot be atrial fibrillation. 

Use of adenosine

--PSVT would usually terminate.  

              --The QRS does not look like any recognizable aberrancy (briefly, it does not look like RBBB or LBBB.  Furthermore, the first 40 ms of the QRS is conducted slowly, unlike SVT with aberrancy).  

              --It looks more like VT, but could be AVRT, except that this is relatively rare

--VT would not terminate with adenosine, but it also would not be dangerous.  

--AVRT is a reentrant rhythm that goes down an accessory pathway (bypass tract), causing a wide complex, and up the AV node; therefore AV nodal blockade (adenosine) will terminate it.  Thus, adenosine is safe in a patient with this ECG (whether VT or ART) and usually will terminate the rhythm if it is AVRT. 

             --Of course, one can also use electricity, but that requires sedation and is not required unless adenosine fails (and one should try 6mg, then 12mg, then probably also 18 mg before it is true failure).

If the patient were unstable, which he is not, then one would immediately use electrical cardioversion.

Re-entrant tachycardia in WPW, whether orthodromic or antidromic (AVRT), usually starts with a premature atrial beat (PAC) that is able to go down one of the tracts while the other is still refractory.  In this case, cocaine may have contributed by leading to a PAC.

The patient was electrically cardioverted, and this was his ECG after:

There is sinus rhythm with a very short PR interval and widespread delta waves.  This confirms that the first ECG was antidromic reciprocating tachycardia.  There are secondary repolarization abnormalities (ST depression) very typical of WPW.

For another example of WPW with repolarization abnormalities that mimic acute MI, go here:

http://hqmeded-ecg.blogspot.com/search/label/wolff%20parkinson%20white%20WPW



Answer to Case 2:

This is irregularly irregular.  Only MAT and atrial fibrillation are irregularly irregular.  Since there are no p-waves, this is atrial fibrillation.  There is a wide complex.   Atrial fibrillation with a wide complex can be atrial fib with RBBB or LBBB or nonspecific intraventricular conduction delay, but these do not have extremely short R-R intervals and do not have multiple QRS morphologies. 

The shortest R-R interval is less than 200 ms, which is very short; this atrial fibrillation is able to be conducted to the ventricles at an extremely fast rate.  This and the multiform QRS can only be due to a bypass tract, as in WPW.  Any AV nodal blocker (adenosine, Ca channel blocker, beta blocker, digoxin) is contraindicated because it may increase the conduction rate through the bypass tract and result if ventricular fibrillation.  To treat this, one must convert the atrial fib to sinus, either chemically (e.g. procainamide) or (my preference) electrically.  If any R-R inverval is less than 220 ms, the patient has a very short pathway refractory period and is at risk for ventricular fibrillation. [Sharma AD, Bashore TM, Sellers TD, Prichett EL, Smith WM, Gallagher JJ. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med 1979;301:1030–5]

The post cardioversion ECG of the second case is unavailable but might look similar to the one above, depending on the location of the bypass tract.



Literature: This paper established adenosine as safe in ventricular tachycardia and led to new ACC/AHA guidelines which state that adenosine may be given in regular wide complex tachycardia:

Marill KA et al. Adenosine is safe and effective for differentiating wide-complex supraventricular tachycardia from ventricular tachycardia.  Crit Care Med 2009 Sep 37:2512. 

There are those who warn that if you give adenosine to a wide complex tachycardia thinking it is AVRT or SVT with aberrancy, but it is really adenosine responsive fascicular VT, that it will convert and you will miss the diagnosis of VT.  
I argue that:
1) this is very rare and 
2) it doesn't matter, as fascicular VT occur in otherwise well hearts and are not any more dangerous that SVT with aberrancy and 
3) all patients will get a follow up in any case. 

Summary of points

1) Any fast rhythm which worries you may be treated with electrical cardioversion.  If confused, use electricity.  If the patient is unstable, use electricity.
2) AV nodal blockers are only contraindicated when there is atrial fib with WPW
3) In regular tachycardias due to WPW (even wide ones!), AV nodal blockers are safe and effective.  They block the limb of the re-entrant rhythm which goes through the AV node, thus interrupting the circuit.
4) Atrial fib with WPW is very recognizable: there are bizarre QRS with multiple morphologies, and very fast rhythms with short R-R intervals.  If you can find any R-R interval shorter than 240 ms, then AV nodal blockers are definitely dangerous.

Stuttering thrombus in the LAD, dynamic hyperacute T-waves, Q-waves, full resolution at 3 months

A 70 y.o. woman who presented with L arm pain that started at 6:45 in the morning when she woke up. Pain was also in the upper back with some discomfort in the L chest. Described as "Achy" pain. She initially thought she must have slept wrong.  No associated SOB, diaphoresis, or dizziness. No similar pain previously.  No h/o CAD. She sat and rested but the pain got stronger, so she took 2 ASA. She felt a little "clammy."  The pain went away after ~15 min. She lay down for ~20-25 min and while lying down the pain returned and persisted x 10 min prior to resolving again.  She called 911. 

She was pain free when the medics recorded 3 ECGs over 40 minutes.  They all were similar to the first:

V6 is missing.  There are Q-waves in leads V3 and V4, with ST elevation and a large T-wave.  Normally, one might think this ST elevation and T-wave is early repolarization, but early repol like this should 1) not occur in a 70 yo woman 2) never have Q-waves.  Therefore, this is old MI with acute ischemia or acute STEMI.

In the ED she was pain free.  This was her ECG at presentation:

QTc 442 ms.  The T-waves in V3 and V4 are still large, but definitely smaller than in the prehospital ECGs.  This is typical of hyperacute T-waves during reperfusion.  You can compare the T-waves with her baseline (next ECG below).  Additionally, there are new Q-waves in V2 and V3.

look here for more on hyperacute T-waves:
http://hqmeded-ecg.blogspot.com/search/label/hyperacute%20T-waves
These ECG indicate that, at the time the patient was having pain, her LAD was occluded or nearly occluded.  Old ECG from 3 years prior:

QTc 405 ms.  Normal previous ECG.  No Q-waves.  No ST elevation. No large T-waves.

So the patient has a spontaneously reperfused LAD.  Antiplatelet and antithrombotic therapy was begun.

At 113 minutes after presentation (first troponin was less than 0.04):

QTc 447 ms.  T-waves continue to diminish.  Q-wave in V2, V3.

Just before cath, time = 240 minutes:

QTc 447 ms.  T-waves very diminished now

Here is a composite of V4-V6 from previous to prehospital to ED:

2 hours after LAD intervention (80% stenosis with hazy LAD thrombus):

QTc 450.  T-waves begin to invert.  If this was the first ECG you had recorded in the ED, it would be Wellens' syndrome.

Next Day.  Troponin I peaked at 2.28 mcg/L.  The septum, anterior wall, and apex are akinetic on echo (myocardial stunning):

T-waves evolve to become deeper and more symmetric

3rd day, 48 hours.

T-wave evolution continues

6th day, 120 hours:  Normal echocardiogram now:

T-wave evolution continues

7 weeks later:  

R-waves present, T-wave inversion gone

3 months later:

Complete recovery of ECG

Summary:
1) With a large amount of myocardium at risk, there is a large wall motion abnormality
2) Hyperacute T-waves are a sign of a large amount of myocardium at risk and that it is still viable
3) With minimal actual myocardial cell death (infarction), as shown by a low peak troponin, the myocardium will recover:
a) The myocardial function (as shown by echo) will recover (this may take weeks)
b) The ECG will recover (this may take months, as in this case).

Wellens' missed. Then returns with Wellens' with dynamic T-wave inversion

This 53 year old woman presented with increasing intermittent substernal chest discomfort similar to her GERD, but not relieved by the usual therapies.  She was given an aspirin.  She had the following ECG recorded in the ED:

A very astute physician read this as "biphasic T-waves in V3 and V4."  There is also T-wave inversion in aVL.  This is very suggestive of Wellens' syndrome with a proximal LAD lesion.

 A subsequent ECG was recorded:

There is now a bit less of the biphasic T-waves.

The patient was admitted to observation.  Her troponins [Ortho Clinical Diagnostics, Limit of detection is 0.012 mcg/L, 99% reference value ("positive" troponin) of 0.034 mcg/L] were less than 0.012, then 0.015, then less than 0.012.  Since these are all below the 99% reference, and thus they are technically "negative;" however, a detectable rise and fall is suggestive of unstable angina.


The ECG findings were not commented upon by the inpatient team, and the patient technically "ruled out".  After a careful evaluation that did not suggest an ischemic etiology, she was sent home without doing a stress test and with a diagnosis of "reflux."

2 weeks later, the patient presented with the same symptoms, happening 5 times between 6 AM and noon, never lasting longer than 15-20 minutes.  Here was here initial ECG:

This time there are full blown Wellens' T-waves in V2-V5, I, and aVL, nearly diagnostic of a proximal LAD stenosis.  When the patient has pain, it is likely that the artery is briefly closing.

25 minutes later, this ECG was recorded:

There are PVCs, but the Wellens' T-waves have resolved.  This is typical of unstable angina; usually when there is significant infarction, the T-waves will evolve by becoming deeper and more symmetric over many hours' time.  See link below.

She was started her on heparin and eptifibatide.  105 minutes later (uncertain whether the patient had another episode of pain that she did not report), the Wellens' T-waves were back.

Wellens' T-waves return

The next day at 7 AM this was recorded:

Wellens' T-waves are again less prominent

Troponins never became "positive:"  The first level was "normal," the second was "normal," then 3rd was 0.021, 4th 0.029, 5th 0.032, never climbing above the 99% reference value of 0.034 mcg/L.

Later that day, the patient underwent an angiogram and had a 95% stenosis of the proximal LAD, and another of the first diagonal off the LAD.  Both were stented.

This is an unusual case of "Wellens' syndrome."  The amount of myocardial infarction (necrosis), as measured by troponin, was so small that the T-waves did not have the typical evolution (T-waves become deeper and more symmetric) seen here:

http://hqmeded-ecg.blogspot.com/2011/03/classic-evolution-of-wellens-t-waves.html

Instead, the T-waves were dynamic, inverting, then normalizing.  One might be tempted to call these normalizing T-waves "pseudonormalization."  But this term is the name for the becoming-upright of a T-wave when the artery is re-occluding.  See these posts:
http://hqmeded-ecg.blogspot.com/search/label/pseudonormalization

In this case, the ischemia is resolving without significant infarction, so that the T-waves truly normalize.

1) Even ACS with negative troponins may be strongly suspected by ECG analysis.
2) Troponin rise and fall, even below the 99th percentile, strongly suggests ACS
3) Dynamic T-waves are an infrequent but potentially important sign of ACS.
4) Unstable Angina is alive and well!  Troponins do NOT rule out ACS.