Reciprocal ST depression in II, III, aVF. What is the diagnosis?

A colleague approached me with this ECG of a middle aged male with this ECG; my colleague was worried about acute ischemia.  There was no old ECG for comparison.

There is STE in V1-V3, with preceding deep QS-waves, and some T-wave inversion in V3.  This is basically diagnostic of anterior LV aneurysm.  But there is also ST depression in II, III, and aVF, suggestive of reciprocity from high lateral ST elevation, and one can imagine a bit of ST elevation in aVL.  What is going on?  Answer below. 

Answer:

Lead aVL also has a Q-wave, so there is an old lateral MI.  Put this together with the anterior LV aneurysm, and the fact that many (old or acute) anterior MIs are due to an occlusion of the proximal LAD, with involvement of the lateral wall (and thus with reciprocal ST depression in II, III, and aVF), and it becomes apparent that this is probably part of his LV aneurysm.  LV aneurysm, just like acute STEMI, may have reciprocal ST depression.  In this case, the old high lateral MI manifests as chronic reciprocal ST depression in II, III, and aVF.

His echo confirmed dyskinesis and myocardial thinning diagnostic of LV aneurysm.  The troponin was negative.

Pseudo Right Ventricular MI

This most recent post will help you understand this post here:

I was nordic skiing out in the wilds of the Upper Peninsula of Michigan when I received a call on my iPhone from some colleagues.  They texted me the following ECGs, which I viewed in the shade of a pine tree on a glorious sunny snowy landscape.  AT&T surprised me with their reach.

A 52 year old woman presented with chest pain.   There was some pulmonary edema.  This ECG was recorded at 1144:

There is ST Elevation in aVR and diffuse ST depression (I, II, aVF, V3-V6).  Thus the ST elevation axis is towards the right, not posterior, not inferior.  There is no ST elevation or depression in lead III, so the ST axis is perpendicular to III, towards aVR.  This is typical for subendocardial ischemia, not STEMI, and often means left main ischemia or 3 vessel ischemia.

A right sided ECG was recorded 3 minutes later.  Right sided ECGs are best recorded in the context of inferior STEMI.  There is little utility to them in other situations, unless you suspect an isolated RV infarction.  I'll post one of those later.

There is quite a bit of ST elevation in V4R-V6R.  Some is due to baseline wander, but not all.  It looks like a right ventricular MI.  There was no RVMI, though.  This ST elevation is a reciprocal view of the left lateral ST depression.  The ST vector is to the left and so this is what I would call a pseudo right ventricular MI.

The physicians were very worried about RV MI.  But STE in Right sided leads is to be expected when there is left sided ST depression and STE in aVR!!

Because of precordial ST depression, clinicians were also worried about posterior STEMI.  But posterior STEMI is not likely when there is diffuse ST depression, with STE in aVR.  It is likely when there is ST depression primarily in V1-V4.  Posterior STEMI may also be accompanied by lateral STEMI, with ST depression in inferior leads (mostly lead III), but not in lead I. 

Nevertheless, they recorded posterior leads [V4-V6 are moved to V7 (posterior axillary line), V8 (between V7 and V9), and V9 (paraspinal) (all are at the level of the tip of the scapula)].

There is no ST elevation in V7 "V4" to V9 "V6".  Positive would be 0.5 mm in just one lead.

The patient was treated with NTG, aspirin, eptifibatide, heparin, and became pain free.  Clopidogrel was avoided due to the high likelihood for need for bypass surgery, which can be complicated by the prolonged platelet inhibition of clopidogrel.

This is her ECG 1.5 hours later:

STE in aVR and diffuse ST depression are still present but less marked.

Perusal of her charts revealed that she had an LAD stent that was very close to the ostium of the circumflex.  Troponin I was positive and peaked at 4.88 ng/ml.  Echo revealed inferior but mostly lateral hypokinesis.  Cath the next day revealed that both the proximal LAD and the ostial circumflex had tight culprit lesions with intact flow.  They were not amenable to PCI.  She underwent successful CABG.

The RCA and the right ventricular branch were normal.

Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents.

Here are some basic concepts before we get into the ECGs:

• STEMI and NonSTEMI are arbitrary terms that may confuse the clinician.
• "STEMI" should mean "coronary occlusion" (or near occlusion, without good collateral circulation -- in other words, it needs thrombolytics or emergent angiogram with PCI).  
• NonSTEMI should mean "MI without occlusion."
• "STEMI-equivalent" is a good term for "coronary occlusion".
• Many STEMI-equivalents have no significant ST elevation, as you may have seen from many of my posts.
• In some STEMI-equivalents (posterior STEMI, lateral  STEMI, posterolateral STEMI), ST depression is the only, or most visible, feature of the ECG.
• So how do we tell if ST depression represents a STEMI-equivalent or NonSTEMI/subendocardial ischemia?
• As I see it, there are 5 primary patterns of ST depression.  I outline them below and demonstrate them to show which are STEMI equivalents and which are NonSTEMI.
• NonSTEMIs/subendocardial ischemia may need immediate angiogram and PCI (or emergent CABG) if the patient is hemodynamically unstable or if the ischemia (as measured by chest pain and ECG findings) cannot be controlled medically (aspirin, GP IIb IIIa inhibitor, antithrombotic, nitroglycerin).
• NonSTEMIs should never get thrombolytic therapy.
• Clopidogrel should probably be avoided in NonSTEMIs that have a high likelihood of needing CABG (ST elevation in aVR)

ST elevation axis (vector) is the opposite of the ST depression vector, though not necessarily the same magnitude (millivolts or millimeters).  Once you understand this, it makes everything simple.  It is worth a few moments to concentrate and learn it.

First, there are countless ways ischemic ST depression (STD) presents.  Check here, for instance. 

But I like to classify 5 primary STD patterns in ACS in which there is ST depression without any significant ST elevation.  Some are STEMI-equivalents, and some are Non-STEMI.  The diagnosis depends on the ST axis.  Which direction does ST elevation go?  Sometimes it is better to ask: what is the opposite of the ST depression vector?

If the ST depression is directly anterior (V1-V4), then the ST elevation axis is directly posterior, and there is a high likelihood of posterior STEMI.

If the ST depression vector is inferior and leftward, there is a lot of ST depression in inferior and left lateral leads, and corresponding ST elevation in aVR (superior and rightward), towards the base (top) of the heart. (There may also be ST elevation in right sided leads but NOT due to RV MI).   Unless there is a concomitant anterior STEMI (high occlusion resulting in STEMI of anterior and basal walls), STE in aVR is not a STEMI in lead aVR; rather the STE in aVR is reciprocal to a leftward and inferior ST depression axis caused by diffuse subendocardial ischemia.

• Thus, an ST elevation axis that is anterior, posterior, inferior, or left lateral is likely to be a STEMI-equivalent.  Anterior-Superior axis (anterior STE + V1 and aVR) is also STEMI
• An ST axis which is rightward (ST depression V3-V6) or superior (ST elevation in aVR) is likely to be a NonSTEMI. 

In all this, it is important to realize that ST depression does not localize subendocardial  ischemia.  On the other hand, reciprocal ST depression does help to localize the area with ST elevation.   For instance, if there is ST depression in V4-V6, it does not necessarily mean that the ischemia is of the lateral wall.  The ischemia might be in that location, but not necessarily.

This is a mystery I cannot explain, but has been proven by comparing ECG findings to angiography.

Examples

1. Severe subendocardial ischemia, nonlocalized: Diffuse ST depression, including leads I, II, aVF, III, V3-V6, with STE in aVR.  This one was severe acute left main stenosis.  One might also find this in severe 3 vessel disease with ACS.

A patient who lives through Left Main Occlusion is not common.  Acute left main ACS with critical stenosis is the much more common issue, and this causes subendocardial ischemia.  So no thrombolytics.  Both severe 3 vessel ACS and acute left main ACS are likely to need CABG and thus you might want to avoid clopidogrel.  So the fact that 3 vessel ACS and left main cannot be differentiated on the ECG is not so important.

ST elevation is in aVR.  The ST axis is towards aVR, but this does not mean there is STEMI in aVR!  Instead, this elevation is reciprocal to global subendocardial ischemia with the negative ST axis inferior and lateral, towards the apex (I, II, aVF, III, V3-V6).  There is no occluded artery here.  There is no STEMI.  The precordial ST depression is not maximal in precordial leads V1-V4, therefore there is no posterior ST axis and no posterior STEMI.

2. Isolated posterior STEMI: Leads V1-V4 primarily 

Standard 12-lead ECG:

ST depression is limited to precordial leads and is maximal in V2-V4 precordial leads.  Thus the ST axis is posterior.

Posterior ECG: Leads V4-V6 replaced by leads V7-V9:

ST elevation in V7-V9 confirms posterior STEMI.  There was a circumflex occlusion.

3. Posterolateral STEMI: Precordial leads V1-V3 +/-V4 with STD in II, III, aVF, but no ST depression in I and minimal STE in aVL

Example 1:

The ST axis is away from inferior and anterior leads, and so is posterior and superior.  With a bit of ST elevation in aVL, it is also lateral.

Example 2:

There is ST Elevation here, in aVL, but it is much less obvious than the ST depression  in inferior leads and in V2, V3.

4. Subendocardial ischemia, non-localized, usually not as severe as #1 above: ST Depression in V3,V4-V6.  ST axis is rightward, with little posterior or inferior components.

77 yo presented with pulmonary edema.  Troponin I peaked at 6.7 ng/ml.  There was an inferoposterior wall motion abnormality.  All arteries were diseased but there was no obvious culprit.  This is not a posterior STEMI.  This is a NonSTEMI.

In this case, the ST axis is perpendicular to III and  aVF and towards aVR, and away from I and II (leading to ST depression in I and II).  So it is upward and rightward.  If this were inferior STEMI, the ST axis would be towards III and aVF (which also give ST depression in I and aVL).

5. Isolated High Lateral STEMI: II, III, aVF only (ST Depression is reciprocal to minimal STE in aVL)

Example 1.

Acute Circumflex occlusion (also old inferior MI with Q-waves, and early repol giving anterior STE)

Example 2.

Acute First Diagonal Occlusion.

Example 3.

This patient presented with DKA and an acute STEMI with first diagonal occlusion.  The peaked T-waves are due to hyperkalemia, which was immediately treated.  Notice that the ST elevation in aVL is far less obvious than the reciprocal ST depression in II, III, aVF.  The ST axis is towards aVL and away from inferior leads; thus there is ST depression in inferior leads.  There was a 100% acute occlusion of the first diagonal, with peak troponin I of 110 ng/ml, new lateral wall motion abnormality, and ejection fraction decreased to 55%.

The LAD occlusion formula did not work here. Why?

I received this from a reader, who applied the LAD occlusion (anterior STEMI) formula.

The patient presented with chest pain and dyspnea.  Here is his ED ECG.

There is anterior ST elevation, so they were worried about STEMI. The QTc was 429 ms.  ST elevation at 60 ms after the J-point is 4.5 mm.  R-wave amplitude in V4 is 14 mm.  The old 3 variable formula value is 26.1 (>23.4), suggesting anterior STEMI.

What do you think about this ST elevation?

I received this from a reader as a possible false positive case because he ruled out for MI by troponins and echo.

This, however, is a case of LVH on the ECG.  There is high voltage and the typical repolarization abnormalities of LVH, with the "hockey stick" ST depression (formerly called "strain") in I, aVL, V5 and V6, and the very high S-wave voltage in the leads with ST elevation (V3 = 3mm at J-point, and 4.5 mm at 60 ms after the J-point).  However, this is an expected amount of ST elevation for such a large preceding S-wave.

The old 3-variable formula was not derived using a control group with LVH, and does not work for LVH.  It is only to be applied when differentiating normal variant ST elevation (early repolarization) from anterior STEMI.

The new 4-variable formula also has a falsely elevated value at 19.56 (greater than most accurate cutpoint of 18.2) in spite of the fact that it accounts for large QRS voltage in V2 (25 mm)

(It is also important to remember that the sensitivity and specificity of the formula was not perfect, at about 90% and 90%)

I am working on a formula for differentiating the ST elevation of LVH from that of anterior STEMI.  It will involve a ratio of ST Elevation to preceding S-wave.  We have a large group of LVH patients, some with and some without STEMI, whom we are comparing.

One thing I hypothesized based on my experience, and that we are indeed finding in our data, is that when there is LVH on the ECG with large S-wave amplitude, the patient almost never has a STEMI!  This is because those who do have LVH with a large S-wave amplitude lose that amplitude when the LAD is occluded!!!

Weakness and Bradycardia

A 70 yo man with a h/o DM, HTN, CAD, chronic renal insufficiency and recent NonSTEMI with pulmonary edema who is on carvedilol and amlodipine called 911 for weakness.  His pulse was 40.  BP was about 100 systolic.

Here is his prehospital ECG:

There is sinus bradycardia with Giant T-waves. 

Bradycardia and large T-waves should immediately make you want to know the K.  The K was 6.8 mEq/L.  Creatinine was elevated at 5.0 mg/dl and the patient stated his urine output was low.  He also had melena and a low hemoglobin.  We placed a dialysis catheter and he went to the ICU for dialysis.  The next AM this ECG was recorded:

Normal sinus rhythm and normal T-waves.

Learning point: Bradycardia should always make you think of hyperkalemia, especially when on beta blockers and/or calcium channel blockers.

In patients receiving one or more agents that depress SA node and atrioventricular (AV) node function, a syndrome of bradycardia, renal failure, AV block, shock, and hyperkalemia (BRASH), has been described. Patients with BRASH are generally taking therapeutic doses of SA and AV node blocking medications, and the level of hyperkalemia may be mild. However, the severity of bradycardia (caused by sinus arrest and/or AV block) is generally greater than expected for either the dose/level of SA and AV node blocker or the level of hyperkalemia.