Chest Pain in a Male in his 20's; Inferior ST elevation: Inferior lead "early repol" diagnosed. Is it?

A 20-something male presented from an outside facility with Chest pain.  Vital signs were normal.

History: Onset of CP 2.5 hours prior to ED arrival.  "Tight and pressure, radiates to right arm, + nausea, + SOB.  No thromboembolism risks, not pleuritic, no radiation to the back.  No cardiac risk factors, no cocaine use.


He came with this ECG from the outside facility, recorded 1 hour after pain onset:

There is at least 2 mm of inferior ST elevation, with reciprocal ST depression in aVL, ST flattening in V4-V6, and T-wave inversion in V2.

Is this inferior ST elevation due to "early repolarization"?

No.  Why not? We have found in our study comparing inferior STEMI (manuscript in preparation) to inferior early repol several distinguishing characteristics.

1. There is reciprocal ST depression in aVL.  This occurred in 0 of 66 cases of early repolarization, and 99% of patients with inferior Occlusion MI (OMI).
2. There is too much ST elevation.  In only 1 of 66 cases of early repol was there one lead with at least 2 mm STE.
3. Absence of ST elevation in V5 and V6.  In our group with inferior early repolarization, 53 of 66 had at least 1 mm of STE in V5, and 61 of 66 had at least 0.5 mm in V5.  64 of 66 had at least 1 mm of STE in V6 and 58 of 66 had at least 0.5 mm in V6.  In other words, when there is normal variant ST elevation in inferior leads, there is usually also normal variant ST elevation in V5 and V6.
4. T-waves are too tall.  T-waves in inferior leads are hyperacute, out of proportion to those in early repol
5. T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia.

95 minutes later, the patient arrived in the ED and here is the triage ECG:

There is 2-2.5 mm of ST elevation in inferior leads.  There is reciprocal ST depression in I and aVL, with T-wave inversion in aVL.  There is relative ST depression in V2 (isoelectric: in a young man it there should be at least 1 mm of ST elevation), thre is also flattening of the ST segment in V2.  There is ST depression from V3-V6.  There is a negative T-wave in V3, and biphasic T-waves in V4-V6.

There should be no doubt that this is OMI.  All of the above 5 points apply, but now all the features have evolved and are more apparent. In addition, there is ST depression, diagnostic of ischemia, in V3-V6.

Nevertheless, the cardiologist consulted diagnosed early repolarization.  The patient did not undergo immediate cath.

22 minutes later, another ECG was recorded:

It is slightly changed.  See next image for side by side comparison

Side by side comparison of leads II and III on the first two ECGs:

ST elevation is higher on the repeat ECG than on the first, especially in proportion the the R-wave.  There appears to be a diminution of the T-wave amplitude; however, not when the R-wave amplitude is taken into account.

First troponin I returns + at 0.252 ng/ml.

191 minutes after first ECG:

There is resolution of ischemic findings, spontaneously.  There are no Q-waves.  There appears to have been spontaneous reperfusion.  The minimal remaining inferior ST elevation is now consistent with early repolarization

Heparin drip started.  CCU consulted.  Admitted to CCU.  Integrilin given.  Not take directly to cath lab.

A second troponin returned at 1.71 ng/ml 3 hours later.

The patient was not taken to cath for another 6 hours after this last ECG.  It showed a 99% stenosis in the RCA, and proximal to a posterolateral branch.  A coronary aneurysm was found.  TIMI flow not reported.

Troponin I peaked at 75 ng/ml (A VERY large OMI)



Next ECG available - 2 week followup:

There are inferior Q-waves of infarction, with T-wave inversions typical of completed inferior transmural OMI.

This ECG, and the very elevated troponin, strongly suggest that the artery re-occluded during the extra 6 hour delay. 



Lessons:
1. Young people do have OMI
          a. Some of these MIs in young people are due to anomolies: aneurysm from a disorder known to be associated  with coronary aneurysms (left out to maintain anonymity) in this case.  Young women, when they have OMI, often have coronary dissection.
          b. Nevertheless, even young people have atherosclerosis and plaque rupture.  We have seen many, such as this young woman.    And young women have worse outcomes than other groups with STEMI because of the tendency to say, "Nah, couldn't be!"

2. When the ECG is unequivocally diagnostic, don't let young age or other atypical features deter you.

3. Know the features of OMI look-alikes.  In this case, early repolarization was diagnosed by the cardiologist, who clearly was unaware of important differentiating features of inferior early repol from inferior OMI (see above)

4. Once OMI is diagnosed, the patient should go immediately to the cath lab even if the ST elevation resolves, because the risk is so high.  In this case, however, the diagnosis was also simply missed.
See this case to demonstrate the danger of reperfused OMI!

5.  Finally, YOU have to be the expert and YOU have to advocate for the patient.  Cardiologists don't know everything, and in particular they don't know YOUR job, which is to differentiate the patients with benign symptoms (the vast majority) from those with Serious pathology.  If the cardiologist disagrees and is incorrect, the only way the patient will get good care is if YOU are the expert, YOU know what findings are true positives and true negatives, and YOU can explain why you are right and Advocate.

Cardiologists need to know a whole lot, but they don't do our everyday job of screening hundreds of symptomatic patients to find the one with the real thing.  They cannot be experts at that; you must be the expert.  They are much more likely to demand proof of disease than emergency physicians.  We demand proof of absence of disease.  And the cardiologists' opinions are of course often, or even usually, correct, but insist on a respectful conversation in which reasoning and evidence, rather than authority, direct the outcome.  That can only happen if YOU are well informed.


Here are two examples of early repolarization in the inferior leads:

First:

1. There is inferior ST elevation without reciprocal  ST depression in aVL.  This is because the ST axis is leftward, not down or to the right.  And thus the ST elevation in lead III is always less than or equal to that in lead II.  2. There is anterior and lateral ST elevation also; isolated ST elevation in inferior leads is relatively rare in limb lead early repol.        3. There are, in this ECG, well formed J-waves in leads V4-V6.  4. The QTc is less than 390, though we did not find this to be an accurate distinguishing feature of inferior ST elevation.  5. The ST elevation is at most 1 mm in inferior leads.

Second:

Slightly different, but the generalizations above apply here, too.

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.

Here is a series of ECGs with increasing ST elevation (STE).  They are of a young male with pleuritic, but not positional, chest pain.

Time zero:

NSR.  No remarkable findings.  Minimal STE in V2, V3, and I.  QTc 383.  LAD occlusion, early repol formula = 18.1


Time = 4.5 hours:

New, diffuse ST elevation. QTc 384, formula 19.1.  The ST axis is about 30 degrees (towards leads I and  II, such that there is STE in aVL, I, II, and aVF, but not III) and there is no reciprocal ST depression except in lead aVR).  This is very typical for pericarditis or diffuse early repolarization.  Pericarditis does not usually have T-wave voltage this high; a high T/ST ratio is more likely to be early repolarization.  Additionally, there are very well formed J-waves, typical of early repolarization.  It is highly unlikely to be acute STEMI.


There was no pericardial friction rub and echo revealed no pericardial fluid and no wall motion abnormality, and normal EF.

Time = 5.2 hours:

More ST elevation, especially in lead V2.  QTc 389, formula 20.56


Time = 7.2 hours:

No change.  QTc 389, formula 19.96



He ruled out for MI.

Diagnosis: probable dynamic early repolarization.  Could it be pericarditis?  Yes, but if there is no pericardial effusion and there is good cardiac function with negative troponins (not myocarditis with myocardial dysfunction), then pericarditis would be treated with Nonsteroidal antiinflammatory medications only.

In other words, the really important differential is this: is this STEMI, or is it a more benign etiology?  And to make this determination, it is important to know that early repolarization may be dynamic (1, 2).  And it may even change from hour to hour, or with heart rate or exercise.   We have seen this many times, though it is not common.

The use of the LAD-BER formula may be of great help and lead one to obtain an echocardiogram rather than activating the cath lab.





1. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61. 

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.











2. Mehta MC. Jain AC.  Early Repolarization on the Scalar Electrocardiogram.  The American Journal of the Medical Sciences 309(6):305-11; June 1995. 

Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1-5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in aVR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.

Found a great site for beginners in ECG, also good for experienced readers!

It's an Irish site.  It has excellent video demonstrations of the underlying pathophysiology of ECG findings correlated with simultaneous video of ECG evolution.

http://www.ecgteacher.com/

What is this irregular supraventricular tachycardia? New K. Wang Video.

K. Wang, MD
Clinical Professor of Medicine
Cardiology Division
University of Minnesota

med.umn.edu/cardiology/faculty/wang/home.html


Here is the main tracing in high resolution:

Large Transmural STEMI with Myocardial "Rupture" of Ventricular Septum

A man in his 60's presented after 4 days of chest pain, with some increase of pain on the day of presentation.  Exact pain history was difficult to ascertain.  There was some SOB.  He had walked into the ED (did not use EMS).  Here is his ECG:

There is atrial fibrillation at a rate of 95.  There is Right Bundle Branch Block with a QR particularly noted in V1-V3 (no rSR',  as there is an initial Q-wave diagnostic of infarction in the anterior wall and septum).  The Q-waves extend to V5 and are very wide (80 ms in V2).  There are also inferior Q-waves which can mimic a left anterior fascicular block, as they result in left axis deviation.  There is rather massive ST elevation, and this is not only anterior but inferior (see analysis below).  

The end of the QRS is best seen in lead V1 (and results in a QRS duration of 176 ms).  If one draws a line down to lead II across the bottom, one can find the end of the QRS in lead II.  From there, one can find the end of the QRS in all leads. This analysis shows that there is ST elevation after the end of the QRS in leads II, III, and aVF, and reciprocal ST depression in aVL.  Thus, this is both an anterior and inferior STEMI.

How old is this antero-inferior STEMI?  Could it be acute (vs. subacute or days old)?  Although the patient has had pain for 4 days, could the artery have fully occluded only within hours?  Very unlikely.  Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.) [and these are associated with larger MI and worse outcomes (2. Armstrong et al.)], the presence of such well developed anterior Q-wave suggests completed transmural STEMI.

So this patient likely has a several day old infarction, with persistent ST elevation and persistently upright T-waves.

The wide Q-waves suggest "transmural" MI (completed MI with infarction of the entire thickness of the ventricle).  This was common in the days before reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy.  When there is MI extending all the way to the epicardium (transmural), that infarcted epicardium is often inflamed (postinfarction regional pericarditis, or PIRP).  In addition, when there is full thickness infarction, especially with inflammation, the myocardium is at risk of "rupture."  The term "rupture" makes it sound like some sort of explosion or massive blowout, but it is usually a small, slow leak that, over time, can cause tamponade and death.  Rupture can be either free wall rupture (causing tamonade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock.  If detected early by ultrasound, the patient can be saved.  Our own Dave Plummer of HCMC reported on survival of 2 of 6 patients with free wall myocardial rupture diagnosed by bedside ultrasound in the ED.(3)


Oliva et al. (3) strongly associated myocardial rupture with postinfarction regional pericarditis (PIRP), and associated PIRP with persistent upright T-waves.  He found 2 patterns of atypical T-wave development in PIRP:
1) persistently positive (upright) T-waves 48 hours after AMI onset, diagnostic of PIRP; and
2) premature, gradual reversal of inverted T waves to positive (upright) deflections by 48 to 72 hours after MI onset in the presence of well formed Q-waves.

The patient was taken to the cath lab emergently and a 100% mid LAD occlusion.  It was opened but opening resulted in no flow.  The initial troponin I was 23.7 ng/ml and was falling, confirming infarction days ago.

2 days later the patient became increasingly tachycardic, hypotensive, and had a new murmur.  This was the 12-lead ECG. 

Not much change, except a slightly faster ventricular response at 110 bpm.  No resolution of ST elevation.  The T-waves are persistently positive.  This remains consistent with PIRP, as was the first ECG.

An echocardiogram showed no hemopericardium, but did show a new small ventricular septal defect with left to right shunting.

The patient was taken for immediate surgical repair.



1.  Raitt MH, Maynard C, Wagner GS, Cerqueira MD, Selvester RH, Weaver WD. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol 1995;25(5):1084-8.


2.  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 53(17):1503-9. Apr 28, 2009.


3. Plummer D, Dick C, Ruiz E, Clinton J, Brunette D. Emergency department two-dimensional echocardiography in the diagnosis of nontraumatic cardiac rupture. Ann Emerg Med 1994;23(6):1333-42.

4.  Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis: ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993;88(3):896-904.

5. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22(3):720-6

K. Wang Video: Differential Diangosis of Tall R Waves in Right Precordial Leads

Again, thanks to K. Wang and to Scott Joing of www.hqmeded.com for this fine video:

K. Wang, MD
Clinical Professor of Medicine
Cardiology Division
University of Minnesota

med.umn.edu/cardiology/faculty/wang/home.html

Young Woman with history of repaired Tetralogy of Fallot presents with chest pain

History:  This woman in her 20's (age) with history of repaired Tetralogy of Fallot presented with CP.  Here is her presenting ECG:

Sinus rhythm.  Right bundle branch block (RBBB) and left anterior fascicular block (LAFB) with very high voltage, consistent with RV hypertrophy (RVH) due to Tetralogy (remember there is a constricted outflow tract of the pulmonary artery, leading to RV hypertrophy.)  There is no initial r-wave of the  rSR' - there are initial Q-waves.  The expected ST depression in V2 and V3 is not there, and in fact there is ST elevation in V3, as well as V4-V6.  There is also some ST elevation in I and aVL.  This is all consistent with either acute or old MI with persistent ST elevation.

I was very suspicious of anterior STEMI, and found a previous ECG from 4 months prior:   

Very large RR’ in V1: RBBB and RVH, also LAFB

 Baseline ST depression in V1-V3, typical for RBBB.  There is no ST elevation anywhere, also typical for RBBB.

So there is relative ST elevation in V2 (relative to the previous ST depression) and new ST elevation elsewhere. 

An immediate echo confirmed new anterior-apical-septal wall motion abnormality, as well as RVH and LVH, and the patient was taken for angiography, which revealed fresh non-occlusive thrombus in the left main that extended down and occluded the LAD.  The patient went for bypass surgery.

Lessons:   
1. RBBB should not have ST elevation at baseline
2. In RBBB, there should be some ST depression in V2 and V3.  An isoelectric ST segment may represent relative ST elevation.
3. A previous ECG can be very helpful
4. Echocardiography did confirm the findings, but delayed therapy.  The ECG was diagnostic.
5. ST elevation can be found even when the QRS appears very distorted. 

Male in his 50's resuscitated from ventricular fib and comatose

After resuscitation, he had this ECG (the rhythm is interesting, too):

There is sinus rhythm but the sinus rate is somewhat irregular ("sinus arrhythmia")  Whenever the sinus takes longer than about 800 ms to fire, the AV node escapes (see complexes 7, 10, and 13).  Of course the most important finding is not the rhythm, but the right bundle branch block with profound ST depression most marked in leads V2 and V3, diagnostic of posterior STEMI.

The patient was taken to the cath lab and had a distral circumflex occlusion that was opened and stented.  There was a posterior wall motion abnormality.

Here is a nearly identical case but with posterior leads recorded.  You'll notice in this case that the ST elevation in V9 is very subtle.

Remarks:

1.  Notice the ST elevation is greatest in the right precordial leads (not left, which would more commonly signify diffuse subendocardial ischemia
2.  In "isolated" posterior STEMI, there is often some subtle inferior and/or lateral ST elevation.  This case is not exception: there is subtle ST elevation in aVL with reciprocal ST depression in III.
3.  Although RBBB always has some ST depression in V2 and V3, in the opposite direction from the terminal R' wave, it is usually not more than 1 mm.  See the second ECG in this post for an example of the normal ST depression of RBBB. 
4.  The exception is with RV hypertrophy. Remember: ST segments are always proportional to the QRS, so in RV hypertrophy, the R' wave is very large and the ST depression is proportionally large.  My next post will demonstrate this.