Chest pain in an 80 year old: What is the diagnosis?

An 80 year old male with h/o CABG presented with CP.  Here is his initial ECG (which was identical to his prehospital ECG) at 1517:

There is evidence old inferior MI.  What is the acute finding? Answer below.

This is another acute LAD occlusion.  There is slightly more than 1 mm of ST elevation in V2 and V3 at the J-point.  Is this normal or is it pathologic (STEMI or even LVH)?  First, it is clearly not LVH.  Second, normal variant ST elevation always has good R-wave progression.  If you add up the R-wave amplitudes in V2-V4 and it is less than 15 mm (here it is 11 mm), it is almost never early repolarization.  Finally, using the equation (see sidebar excel spreadsheet) and the computerized QTc of 399 ms, the value is 24.4 which is greater than 23.4 and heavily favors STEMI.

The resident saw this but the faculty was not convinced.  Chest pain continued and this repeat ECG was recorded at 1652:

There is slightly more ST elevation

A 3rd ECG was recorded at 1720:

There is still more ST elevation and the T-waves are larger.

At this point, the cath lab was activated.  Angiogram revealed an acutely occluded saphenous vein graft to the LAD which was opened with PCI.  Here is the post cath ECG:

Now there are T-wave inversion analogous to Wellens' syndrome.  These are reperfusion T-waves, also seen in I and aVL, indicating involvement of the lateral wall from a proximal LAD.

The next day ECG is here:

T-wave inversion is evolving as it normally does after reperfusion.

Troponin I peaked at 38 ng/ml.  Notice how important serial ECGs are if the initial ECG is nondiagnostic or not recognized.

Chest pain and hypotension in a patient who is 3 weeks post STEMI

A middle aged patient who was 3 weeks s/p STEMI came from cardiac rehab where he developed some chest pain, dyspnea and weakness on the treadmill.  In the ED he had some continued chest pain and hypotension. Here was his ECG:

There are inferior and lateral Q-waves with T-wave inversion in the corresponding leads.  There is minimal ST elevation.  There is no acute STEMI.  This is diagnostic of recent, reperfused STEMI.  The T-inversions are "reperfusion T-waves." 

This looks like the typical ECG of someone who had a recent Q-wave MI.  The small amount of ST elevation is persistent, not acute.  Acute STEMI would have upright T-waves.  With re-occlusion, the T-waves become upright (pseudonormalize, as in these cases).  The patient might be having cardiac ischemia, but if he is, it is unstable angina or non-STEMI, or perhaps he has not YET pseudonormalized, so serial ECGs may be important.

Below are his presenting STEMI ECG and his post-PCI ECG from 3 weeks prior:

Because of the hypotension, chest pain, and T-wave inversions, the physicians were worried about MI, took the patient to the critical care room, and called the cardiologists.  However, these T-wave inversions should be expected at one month after MI.  This is normal for these patients.

They also did an ED bedside ultrasound, shown here:

This shows a large amount of pericardial fluid, with some echogenic structures that appear to be thrombi or fibrinous exudate. The RV free wall collapses, indicating tamponade.  If you are uncertain where the pericardial fluid is, I have annotated still images with arrows at the bottom of the post.

The differential includes hemopericardium from myocardial rupture, or from coronary artery rupture from PCI, or Dressler's syndrome of post-MI pericardial effusion. 

After pericardiocentesis was unsuccessful, he was taken to the OR for a pericardial window.  300-450 ml of serosanguinous fluid was drained.  The patient was given a probable diagnosis of Dressler's syndrome.

Differential of peri-infarct pericardial fluid
The differential includes 1) pericarditis with effusion or 2) hemopericardium.
1) Pericarditis with effusion:
   a) If 3 weeks after MI, then Dressler's syndrome (Dressler's syndrome is also known as post-myocardial infarction syndrome, post-cardiac injury syndrome and postpericardiotomy syndrome), which is a late post-MI autoimmune pericarditis occurring about 3-4 weeks after the MI.  Dressler's syndrome appears to be quite rare, according to Shahar and Lichstein. 
   b) Nonspecific pericarditis
2) Hemopericardium would be due to myocardial rupture, which could be due to:
   a) Rupture of a coronary artery due to PCI or
   b) Free wall Myocardial rupture (see below, next paragraph).  

Myocardial rupture is not uncommon. It is found on 1% to 3.5% of autopsies of patients who died of MI. It is associated with transmural MI; since most STEMI are aborted with reperfusion therapy, it is not as common as it once was. It is more common in women, and in patients who have a first MI and have a good EF, as it requires a pump force from the healthy myocardium to produce high pressure which ruptures the infarcted myocardium. The "rupture" is not an explosion, rather a small tract through the myocardium which leaks blood into the pericardium, and kills by tamponade.
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Myocardial rupture is usually preceded by postinfarction regional pericarditis (PIRP). PIRP is indicated on the ECG by 2 findings: 1) persistently positive (upright) T-waves at 48 hours, or 2) premature reversal of inverted T-waves to positive deflection by 48 to 72 hours after STEMI. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual. There should be QS-waves indicative of completed transmural MI.
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Patients who present with chest pain or cardiac arrest and have an ECG diagnostic of STEMI could have myocardial rupture. Obviously, administration of heparin and/or lytics is hazardous. These patients may survive. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. 5 of 6 presented with chest pain and an ECG indicating reperfusion therapy, but were detected by bedside ultrasound.
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Plummer D et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of EM 23(6):1333-1342; June 1994.
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For more information, see chapter 28 of Smith's "The ECG in Acute MI."

Below are still images of the ultrasounds.  White arrows point to pericardial fluid.

Left ventricular Aneurysm Morphology Distorted by Right Bundle Branch Block, Mimicking Acute STEMI with RBBB

This is a complex case that I have reprinted from my article in the EMRA publication, EM Resident, with their permission.  I'm starting with some didactics.  If you want skip to the case, page down, but it is difficult to understand without knowing the background information.

GENERAL BACKGROUND

Prior Myocardial Infarction/Left Ventricular Aneurysm

Approximately 60% of patients with a previous anterior transmural MI, and fewer inferior MI patients, may have persistent ST Elevation (STE),¹ mimicking acute STEMI.  Of those with anterior persistent STE, approximately 80% have an anatomic left ventricular (LV) aneurysm (LVA), which can be seen on echocardiogram as “diastolic distortion” or myocardial wall thinning.^{2, 3}  In the reperfusion era, transmural MI is uncommon, and so the incidence of persistent STE is less than it once was.  In a 1987 series of patients with a prior MI presenting with chest pain and STE, only 50% proved to have an acute MI.⁴   Persistent STE may also be associated with systolic dyskinesis, akinesis, or a large area of myocardial necrosis, even in the absence of anatomic ventricular aneurysm.⁵

LVA of the anterior wall results in Qr-waves (deep Q followed by a small r-wave) or QS-waves (single deep negative wave) in V1-V4, followed by a moderate degree of STE.  The QS-waves indicate complete loss of anterior electrical forces during depolarization.  The T-wave may be upright (but not large or hyperacute as in acute STEMI) or inverted (but not deeply inverted, as in acute Non-STEMI).  Inferior LVA has STE and QR-waves, not QS-waves, and is thus much more difficult to differentiate from acute inferior STEMI.

We found the best discriminator of LVA vs. acute MI is the T wave amplitude/QRS amplitude ratio, and derived and validated this ratio: if (sum of the T wave amplitude) ÷ (sum of QRS amplitude) in V1-V4 is greater than 0.22, it favors AMI with good sensitivity and specificity.⁶  If any one lead has a ratio greater than 0.36, it is acute STEMI with equal accuracy.  False negatives had a long time between symptom onset and ECG, so that the T-wave was no longer tall.  We also validated this rule, published as an abstract (7).  Just as useful is evaluation of an index ECG (prior ECG), but these are not always available.  Echocardiography may also be useful if it shows dyskinesis (diastolic dysfunction); unfortunately, persistent STE after old MI also occurs without anatomic aneurysm.  STE with echocardiographic regional wall akinesis or hypokinesis is present in both acute STEMI and old transmural MI.  In some cases, coronary angiography will be required to make the diagnosis.  New STEMI in the same location as previous Q-wave MI may also have deep QS-waves, but also has tall T-waves and an increase degree of STE.

An example of classic LV aneurysm morphology (figure 1).

There is QS pattern in V1-V3 with anterior STE.  The T-wave amplitude is not sufficient for acute MI.  If you apply either ratio rule, it turns out to be LV aneurysm.  This is a classic LV aneurysm morphology.

Normal Right Bundle Branch Block (figure 2)

This is normal RBBB, with rSR’, slight ST depression in V2 and V3, and no ST elevation anywhere.

A non-pathologic RBBB has an rSR’ in V1-V3 and no ST elevation anywhere on the ECG.  In RBBB, an absence of an r-wave in lead V1 only may be normal, but if it extends to V2 and beyond it is always abnormal, and the differential includes not only RBBB with MI but also RBBB with left ventricular hypertrophy, and RBBB with cardiomyopathy.   There is usually up to 1 mm of ST depression in V2 and V3, discordant (opposite direction of) the positive R’ wave (see figure 2).  If there is a very large voltage R’ wave, as in right ventricular hypertrophy, this ST depression may be greater than 1mm in the absence of acute ischemia.  To determine the presence or absence of STE in RBBB, one must first determine the end of the QRS, which is the beginning of the ST segment (the J-point). 

 

Case presentation: Right bundle branch block (RBBB) transforms a QS- into a QR-pattern, obscuring diagnosis of left ventricular aneurysm, and suggesting acute STEMI and RBBB.

A 79 year old man presented with dyspnea.  He stated that he had sustained a recent myocardial infarction and that it had been painless.  His presenting ECG is shown here (figure 3):

There is sinus rhythm at almost 100 beats per minute.  There is a large R-wave at the end of the QRS complex in V1, and wide S-waves in lateral leads I, aVL, V5 and V6, with a QRS duration greater than 120 ms, diagnostic of RBBB.  There is absence of r-wave in V1-V4, resulting in a QR, rather than an rSR’ wave.  If the r-wave is absent, then it is a Q-wave, which strongly suggests a Q-wave MI (whether due to acute or old MI).  Figure 4 magnifies V1-V3 and shows how to find the end of the QRS, which is the J-point and beginning of the ST segment.

 Here is a magnification of V1-V3 (figure 4):

Arrows show the end of the QRS and thus the beginning of the ST segment; this is the J-point. It is apparent, then, that the ST segment is elevated.

Case continued:

Thus there are anterior Q-waves and anterior STE.  So it is an acute STEMI, right?  I saw this patient in the late 1990’s (and have seen others since) and administered tPA for acute MI.  Before the tPA had time to work, the rate slowed and the RBBB disappeared and showed the ECG in figure 1 above. 

Old records were retrieved, and indeed the patient’s previous ECG was the same.  In fact, he had presented one week earlier with the exact symptoms and exact same RBBB ECG and received tPA from one of my partners!

How is this possible?  Normally, anterior LVA has no or little R-wave amplitude.  However, this patient has rate-related RBBB.  His right bundle has a long refractory period so that when his rate increases, his right bundle is refractory and does not conduct.  In RBBB, there is automatically a large R’-wave even if there the anterior wall is dead, simply because of the sequence of depolarization.  So the LVA morphology gets replaced and distorted.

How can you suspect this?  On the ECG, it is nearly impossible, as far as I can tell.  So you must use other clinical data.  First, you have to know that this is possible.  Second, you can use echocardiography to assess for aneurysm (diastolic dysfunction or bulging), but if you see only systolic dyskinesis, it could be either LVA or acute STEMI.

In contrast to LVA, patients with acute STEMI who have Q-waves have a larger T-wave.  See figure 5 for an example of a patient with QS-waves but with hyperacute T-waves, such that the T/QRS ratio is high.  It was an acute LAD occlusion.

Figure 5. There are QS-waves as one would see in LV aneurysm, but there are large T-waves, as is seen in acute STEMI.  The T/QRS ratio is high.  It was an acute LAD occlusion.

References

1.            Mills RM, Young E, Gorlin R, Lesch M. Natural history of S-T segment elevation after acute myocardial infarction. Am J Cardiol 1975;35(5):609-14.

2.            Visser CA, Kan G, David GK, Lie KI, Durrer D. Echocardiographic-cineangiographic correlation in detecting left ventricular aneurysm: A prospective study of 422 patients. Am J Cardiol 1982;50(2):337-41.

3.            Visser CA, Kan G, Meltzer RS, Koolen JJ, Dunning AJ. Incidence, timing and prognostic value of left ventricular aneurysm formation after myocardial infarction: A prospective, serial echocardiographic study of 158 patients. Am J Cardiol 1986;57(10):729-32.

4.            Miller DH, Kligfield P, Schreiber TL, Borer JS. Relationship of prior mycardial infarction to false-positive electrocardiographic diagnosis of acute injury in patients with chest pain. Arch Intern Med 1987;147:257-61.

5.            Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnormalities: a two-dimensional echocardiographic study. Am J Cardiol 1984;53(11):1542-6.

6.            Smith SW. T/QRS amplitude ratio best distinguishes the ST elevation of anterior left ventricular aneurysm from anterior acute myocardial infarction. American Journal of Emergency Medicine 2005;23(3):279-87.

7.            Beeman W. Shroff G.  Smith SW.  T/QRS Amplitude Ratio Is Significantly Higher In Acute Anterior ST Elevation Myocardial Infarction Than In Previous Myocardial Infarction With Persistent ST Elevation (left Ventricular Aneurysm Morphology): A Validation (abstract 371).  Annals of EM Oct 2011 Suppl 58(4): S302. 

 

Subtle Anterior Transient Injury Pattern, Not Appreciated, LAD occlusion spontaneously reperfused

This 41 yo male was cleaning using a chemical and experienced sudden substernal chest burning radiating to both arms with SOB, relieved by sublingual NTG.  He called 911 immediately.  Here is the prehospital ECG at 1143:

There are precordial hyperacute T-waves.  The QTc is only 392, but there is very poor R-wave progression and the ST elevation, though less than 1 mm at the J-point, is 3 mm at 60 ms after the J-point, which indicates a steep ST segment.  The equation value (see side bar of blog, with excel spreadsheet) is 25.1.  A value greater than 23.4 indicates that this ST elevation is not a normal variant early repol, but anterior STEMI.  More importantly, there is ST depression in "inferior" leads and this is reciprocal to extremely subtle STE in aVL and a T-wave that is massive when compared to the QRS. (There is also some subtle STD in V5 and V6, which is another clue to STEMI).  The QRS is so small in aVL that the ST elevation can barely register.  The computer had nothing to offer.  The medics were worried.

Here is aVL blown up so you can see the relative size of the T-wave and QRS:

Tiny T-wave in aVL is giant when compared to the QRS. This is a hyperacute T-wave

On arrival, the pain was resolved and this ECG was recorded at 1201:

Notice the R-wave amplitude has recovered.  STE at the J-point is no different, but it is less at 60 ms after the J-point because the T-waves are not hyperacute any more.  The QTc is 401.  The T-waves are less hyperacute.  Equation value is now 22.5.  There remain some abnormalities in "inferior" leads.

So we have here a patient with a proximal LAD occlusion that has reperfused on its own (or due to NTG).

The findings of the first ECG, and their difference from the 2nd ECG, were not entirely appreciated, so the cath lab was not activated.

A while later, the first ECG was shown to me without any clinical data and, due to all the characteristics I have described, I was able immediately to say that it is an anterior STEMI.  Then, upon looking at the ED ECG, I immediately knew it was reperfused.  I knew there was a 90% unstable proximal stenosis with thrombus.

A reperfused anterior STEMI is a dangerous situation.  I once had a patient who reperfused the LAD, so I deactivated the cath lab, then he re-occluded and I re-activated the cath lab.  The delay caused his death. 

This could happen in this case, so it is imperative to at least treat aggressively with antiplatelet and antithrombotic therapy.  The cath lab was in use, so this therapy was started, and cardiology was consulted.

Cardiology did an echocardiogram.  I was worried that they would find a normal echo.  This occlusion was so brief that the anterior wall, though it would have had a motion abnormality during occlusion, could completely and rapidly recover after reperfusion.  Thus, a normal echo would give a false sense of security: if normal, it would not rule out previous anterior injury pattern.  The ECG does not lie, and in the right hands is better than an echo.  This is an unequivocal ECG, especially with the serial findings.

Fortunately, the echo showed some subtle abnormality in the septum, but it was read by one of the world's experts in echocardiography and perhaps most would not have seen this abnormality and would have dismissed the ECG findings.  Then the patient might be admitted and re-occlude (and die?).

The first troponin was normal (so that is of no help).

The two of us talked and arranged for a cath.

Before his cath, this ECG was recorded at 1321:

There is further resolution of the findings and it is now normal.

Cath showed a 95% proximal LAD stenosis with thrombus.  A stent was placed.

Here is the ECG the next AM:

QTc is 378, there is no ST elevation whatsoever.  T-waves are much smaller than they were.  This probably represents the patient's baseline ECG, but we can't know for certain.

The peak troponin I was 0.9 ng/ml.  It is interesting that the ECG did not evolve any T-wave inversion, as might be commonly seen with Wellens' syndrome.  This goes to show that not all brief LAD occlusions result in Wellens' pattern of reperfusion T-waves.

This was called by the interventionalist and cardiologists a "Non STEMI."  Had the ECG findings not been seen in the ED, no one would ever have known that STEMI was missed.

Serial ECGs confirm initial suspicion of anterior STEMI (LAD occlusion)

A 52 yo man began having substernal chest discomfort and presented 2 hours later.  His prehospital ECG, which I cannot find, reportedly had some ST depression in precordial leads.  He had this ECG recorded at 0658:

There are hyperacute T-waves in V1-V4.  There is minimal ST elevation, almost 1 mm in V2 and less than 0.5 mm in V3, but this is diagnostic of anterior STEMI even without ST elevation.  Using the equation (which may not be applicable because there is not enough ST elevation to even qualify for early repol), and the computerized QTc of 424, the value is 25.995 (greater than 23.4 is LAD occlusion).

The clinicians who saw this patient do not, like me, spend their lives analyzing the minutiae of ECGs, so they were not certain of the diagnosis, but they did suspect it, so they did the entirely appropriate management of obtaining serial ECGs, and a repeat ECG was done at0713:

Still suspicious for hyperacute T's but no ST elevation or significant evolution.  The T-wave in V2 is less prominent, suggesting some reperfusion.  QTc is 436 and equation remains greater than 23.4

So another was recorded at 0720:

Now there is ST elevation in V2 and V3, diagnostic of LAD occlusion

 Another at 0726:

Not much changed

 Another at 0744:

Now it is unequivocal

 At this point, the cath lab was activated. 

This is the post cath ECG:

Cath showed a complete mid-LAD occlusion.  Peak troponin I was 120, even with a short door to balloon time, and even though the initial ECG was not striking.  The echo showed a large anteroapical wall motion abnormality.

I suspect the prehospital ECG had de Winter's ST depression and T-waves. 

12 hours of Chest pain in a 40-something

A 40-something yo woman with several coronary risks but no history of coronary disease developed 10/10 "gnawing" retrosternal chest pressure at rest at 7:30 PM.  She thought it was reflux, but antacids did not relieve it.  She did not arrive in the ED until she had had pain all night (not certain if it was constant or intermittent).  Here is her ECG that next AM:

There is sinus bradycardia with a PVC, and an artifact on the 8th complex.  There is a significant Q-wave in lead III, with very subtle ST elevation in leads III and aVF, and, importantly, some reciprocal ST depression in aVL.  There is also high voltage suggestive of LVH, but no repolarization abnormalities that are typical of LVH.

Let's look at the limb leads enlarged:

Here the ST elevation in leads III and aVF is more clear, with reciprocal ST depression in aVL are more apparent

This is very suspicious for inferior MI of unknown age.  It could be old MI with persistent ST elevation, or it could be subacute MI with new Q-wave, but is unlikely to be very acute (with a Q-wave and without large T-waves).  If it is a subacute MI, there should be a positive troponin.

The first troponin I returned at 0.74 ng/ml, diagnostic of acute MI.  Is this STEMI or NonSTEMI?  That is an arbitrary definition, based on millimeters of ST elevation.  Every physician should know that biologicial systems do not follow millimeter rules, so many "NonSTEMIs" are due to coronary occlusion.

The important thing is whether the patient has ongoing ischemia after almost 12 hours of chest pain, and as long as the ST segments are elevated or depressed, or the patient has chest pain, one must assume there is ongoing ischemia and do something about it.  She did receive antithrombotic and antiplatelet therapy, and nitroglycerine, but her pain did not subside until she received hydromorphone.  Then it was not until a second troponin returned at 4.40 ng/ml 4 hours later, that she was taken to the cath lab.

Cath revealed a 100% occlusion of the mid- first obtuse marginal (OM-1).  Troponin I peaked at 49 ng/ml.  Echo showed an inferolateral wall motion abnormality and concentric hypertrophy.

Here is her post cath ECG for comparison:

ST segments are back to baseline

Here it is enlarged:

Learning points:

1. Any ST depression in aVL is abnormal.   We studied consecutive inferior STEMI patients and 100% (154 of 154) had some ST depression in aVL; among pericarditis controls, zero of 49 had any ST depression).   What we don't no for certain is how many inferior early repol cases have some ST depression in aVL, but it is, in my experience, exceedingly rare, and this case does NOT qualify for early repolarization, which must have good R-wave amplitude in all of II, III, and aVF (here there is a Q-wave in III).

On occasion ST depression in aVL may lead you stray, as in this recent post (which is an anomoly).

Here is an example of inferior (and lateral) ST elevation due to early repolarization:

Notice there is 1. Excellent R-wave amplitude, 2. No ST depression in aVL, 3. Proportional T-waves.  There is also 4. a short computerized QTc (in this case very short at 354 ms).  Notice there is also 5. normal atrial repolarization wave (PR depression); this is not a case of pericarditis!

2. "NonSTEMIs" may be large and due to complete persistent coronary occlusion that needs emergent reperfusion.  Millimeters do not measure occlusion.  Large MI may be very subtle on the ECG.  This was not a small MI, with peak troponin I of 49.0 ng/mL (large MI).

3. Inferior MI does not always mean Acute MI. This patients initial ECG could represent old MI with persistent ST elevation, subacute MI, or old MI with superimposed acute MI.  When the patient has such typical pain, and especially when you have a positive troponin, assume it is acute or subacute.  With such a minimal troponin elevation, this was NOT subacute.  As it turned out, the myocardium had been ischemic, with only minimal infarct, during those 12 hours, as evidenced by the only minimally elevated troponin.

4. Opiates will obscure the diagnosis of MI.   Morphine has been associated with higher mortality in ACS and this is at least partly because the relief of pain is confused by physicians as relief of ischemia. There may even be other mechanisms.

5. If in doubt, get an immediate echocardiogram.  In this case, it would have confirmed MI and allowed for earlier cath lab activation.  It may not differentiate old MI from acute MI, but absence of WMA would be helpful in finding a false positive.  However, they can produce false negative results even in very large MI!

6. Positive troponins alone are not grounds for cath lab activation.  There must also be ongoing ischemia as evidenced by either the ECG or ongoing pain, both of which were positive in this case.

The Same Theme: Large Lateral STEMI is Subtle on the ECG

This is a 34 yo female with no history of CAD who had the onset of chest pain at 0900.  It was constant, achy, substernal, 7/10, non-radiating, aggravated by smoking and movement and relieved with short deep breaths.  She took analgesics without relief.  She had had an episode one week prior.   She smokes 2 packs per day and has a family history of early CAD.  She has diet controlled DM.  She presented at 1930 and had this ECG recorded:

There is just under 1 mm of ST elevation in I and aVL, with reciprocal ST depression in inferior leads, especially III.  This should alert you to the high probability of lateral MI.  This STE is more pronounced than in this case which was a false positive, posted a few days ago.  Notice also that there is less than 1 mm of ST depression in V1-V3. This is highly suspicious for concomitant posterior MI, and should raise  your index of suspicion very high because lateral MI is frequently accompanied by posterior MI when the circumflex artery is involved.

The clinicians did not appreciate these findings.  They administered aspirin and arranged for a telemetry bed.  The patient continued to have pain and 2 more ECGs were recorded at 2145 and 2225, without any evolution.  At 2059, the first troponin I returned at 14.19 ng/ml, confirming AMI of considerable duration.  Apparently, the clinicians must have believed at first that it was a NonSTEMI because they waited until 2245 to activate the cath lab. 

At cath, there was a 100% occluded proximal circumflex which was opened and stented.  The troponin peaked at 300! (very large MI).  Echo the next day showed a posterolateral wall motion abnormality and an ejection fraction of 40%.  Here is the post cath ECG:

ST segments have resolved, confirming good microvascular reperfusion.

One week later, this was recorded:

Now there are clearly inverted T-waves in I and aVL (lateral reperfusion T-waves).  If there were posterior leads, the T-waves would be inverted, but since they are recorded in anterior leads, we see instead a phenomenon that I call "posterior reperfusion T-waves"--the T-wave which would appear inverted on posterior leads appears larger on anterior leads.

Learning point: Lateral MI may be very large but electrocardiographically subtle.  Inferior ST depression is nearly always seen in lateral MI.  Concomitant right precordial (V1-V3) ST depression makes the case for lateral MI, as the posterior wall is often supplied by the circumflex.