Chest pain and ST-segment Elevation

This was provided by Casey Parker at Broome Docs Blog, with permission.

A 23 year old presented with pleuritic left chest pain radiating to the left arm.  He had a recent sore throat. 

Here is his ECG:

Sinus rhythm with inferolateral ST elevation.  There is no ST segment depression in aVL.  Therefore, it is highly unlikely to be inferolateral STEMI.  Correspondingly, the ST elevation in lead II is greater than lead III.  There is slight ST elevation in lead I.  The ST axis is directly towards lead II, and thus also V5.

Along with the age, pleuritic chest pain, and viral symptoms, there is no doubt that this is peri- (or myo-) carditis.  Occasionally, pericarditis can be localized to one wall or the other, in which case the ST elevation is also localized, as in MI, and it can mimic STEMI.  Most pericarditis is diffuse, covering the entire epicardium, and thus the sum of the ST vectors is towards lead II.

We compared the ST segments of patients with early repolarization, pericarditis, and inferior STEMI, and found that ST depression in aVL was nearly perfect at distinguishing the benign entities from STEMI.

Of course, no rules are perfect, and if this patient had more typical pain and/or were a bit older, or had a positive troponin, I would get a stat echocardiogram to be certain there is no wall motion abnormality.

The initial troponin (they say troponin T??) was 0.88 and rose to 16 (which is very unusual for Trop T, so maybe they meant troponin I).  An echocardiogram showed no wall motion abnormality. 

Thus, the diagnosis is myocarditis.

What is the Diagnosis?

This 65 year old woman presented in cardiogenic shock:

Some will find this easy (if so, sorry!), but some might be confused.  See below.

Well, 2 cardiologists and one emergency physician thought that there was high lateral ST elevation with reciprocal ST depression in inferior leads.  They did not see that it was atrial flutter.  When you are tuned into reading atrial flutter, though, as I am, this is regognizable within seconds as atrial flutter.  The flutter waves distort the baseline and can make it appear to have ST elevation or depression.

Diagnosis: Atrial flutter.   There is no ST elevation or depression, only flutter waves that mimic ST deviation.

There was very poor LV function causing the shock, but made worse by poor filling due to atrial flutter with 2:1 block and a ventricular rate of 130.

The angiogram was completely normal.

Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH)

A 52 year old male presented with epigastric pain, continuing in the emergency department.  He has a history of hypertension, and is on amlodipine.  Thinking that epigastric pain might be an anginal equivalent, this ECG was recorded:

There is LVH.  There are T-wave inversions in aVL and V3-V6. 

The physicians were worried about Wellens' syndrome and treated for ACS.  He was placed on a nitroglycerine drip.  Initial troponin was negative.  A followup ECG was done 3 hours later.

Perhaps slightly less T-wave inversion.  Nonspecific.

He was admitted.  All troponins were normal.  A formal echo showed concentric LVH and there was also a subtle abnormality which the echocardiographer thought suspicious for LAD distribution ischemia.  So he underwent a coronary angiogram which was completely normal.

This is not Wellens'.  Why?

1.  LVH frequently causes T-wave inversion which mimics Wellens'
2.  In Wellens', the chest pain is nearly always resolved by the time of the ECG.  It is reperfusion that results in the T-wave inversion and the pain is thus resolved by this time.
3.  Wellens' is defined by chest pain and ECG abnormalities.  Though Acute MI can present as epigastric pain, it is not at all common and T-wave inversion in the setting of epigastric pain is not high risk for ACS.
4.  T-wave inversion in Wellens' is primarily V2-V4.  When T-wave inversion is V3-V6, one should think more about LVH or Benign T-wave Inversion (this post on Benign T-wave Inversion is worth reading)

Dynamic inferior MI: STEMI or Non-STEMI? Does it matter?

A 63 year old with no cardiac history developed substernal chest burning while exercising, relieved with rest.  It later woke him from sleep and was constant.  He walked into the ED and had this ECG recorded at 0140:

There is subtle ST elevation (STE) in leads II, III, and aVF, with reciprocal ST depression in lead aVL (this must be present in inferior MI, or you should think of something else, like early repolarization or pericarditis).  There is thus injury, but there is not 1 mm of ST elevation in 2 consecutive leads.  (V2 also suggests posterior ischemia.)
This ECG is diagnostic of inferior MI

He was given aspirin, clopidogrel, sublingual nitro x 3 and IV nitro, and his pain improved but did not entirely resolve.  This ECG was recorded at 0157:

Most STE and ST depression is resolved.  There is now T-wave inversion in III, suggesitive of some reperfusion.  The artery is probably open.

The patient began having more pain again, and this was recorded at 0220: 

There is even more STE than on ECG #1, maybe 1 mm in 2 consecutive leads (in case it matters to you).  The T-wave is upright again.  This is called pseudonormalization because the T-wave is normally upright, but when T-wave inversion due to reperfusion reverts to upright, then it is "pseudo-" and implies re-occlusion.  (V2 again suggests posterior ischemia.)

He was taken for PCI of a distal RCA, found to have a 95% thrombotic occlusion.  Peak troponin I was less than 5 ng/ml.  Whether the artery was 100% occluded at the time of the 3rd ECG is not known.


STEMI or Non-STEMI?

This was called a Non-STEMI because there was not (depending on the person doing the measuring) 1 mm of STE in 2 consecutive leads.  But there was injury, and it was due to coronary occlusion or subtotal occlusion, and the pain was refractory to medical therapy.  So no matter what you call it, the patient needs immediate reperfusion therapy. 

Nature does not follow the metric ruler system nor does it adhere to graph paper.  That was invented by engineers and doctors and there is no magic to these numbers.

So where does the "magic" of 1 mm in 2 consecutive leads come from?  The randomized trials of thrombolytics vs. placebo enrolled patients with suspected MI and 1 mm of STE in 2 consecutive limb leads and found that the patients who received the drug had lower mortality than those receiving placebo.  The enrollment criteria were based on previous studies of MI, as diagnosed by CK-MB, that found that 1mm in limb leads had the best sensitivity, but at only 46%.

Thus, this non-angiographic data does not mean that some patients with less ST elevation would not benefit.  (In fact, in none of these thrombolytic trials did the authors specify the method of measurement of the ST segment!)

Schmitt et al. found that only 77% of RCA occlusions have at least 1 mm in 2 consecutive leads.  I recently showed that millimeter criteria are nearly worthless in differentiating subtle anterior STEMI from normal variant ST elevation.

Likewise, there are no randomized trials of therapy for refractory ischemia (definite ACS with ECG ischemia with medically uncontrolled symptoms).  In fact, since these patients should go immediately, they were excluded from all trials of emergent angiography for NonSTEMI.

The consensus, as documented in the ACC/AHA AND the Eurpean Soc of Cardiology Guidelines is that these patients should undergo immediate angiography [but thrombolytics only in the case of injury (STE) on the ECG].

Learning point: STEMI or Non-STEMI is an arbitrary definition, and doesn't always help direct therapy.

ST depression after cardiac arrest is frequently not due to ACS

Case 1

A 22 yo male had a cardiac arrest with ventricular fibrillation recorded.  He was resuscitated.  He was comatose.  Here is his initial ECG:

There is widespread ST depression, with ST elevation in aVR.   There are also lateral Q-waves.

 Is this ACS with 3-vessel disease or left main stenosis?  No, and one should not make such an assumption.  The initial ECG after a cardiac arrest frequently shows ischemic ST depression which resolves on subsequent ECGs.  So we waited and recorded a second ECG 27 minutes later:

The ST depression is resolved.  The Q-waves persist.

The patient had myocarditis and no coronary disease.  He underwent therapeutic hypothermia and fully recovered. 



Case 2

A young man presented after resuscitation from asystolic cardiac arrest.  In spite of immediate bystander CPR, he had no brain function on arrival.

There is ST depression in V2-V6.  Is this ACS?

The total absence of brain function in spite of immediate CPR suggested a CNS etiology of arrest.  CT of the brain revealed aneurysmal subarachnoid hemorrhage.  The patient went on to brain death. 

Cardiac arrest was likely due to massive catecholamine surge and stress cardiomyopathy.

Do all cardiac arrest patients need emergent angiography and PCI?

We studied all our cardiac arrests over a 3 year period (Acad Emerg Med 17(S1):S194. Abstract 580) and found that the majority did not have need for immediate PCI.  The incidence of STEMI was only 28%: 38% for those with VF or VT, and only 20% for those with PEA.   We did not assess the incidence of ACS without STEMI as an etiology; however, unless there is instability, these do not need emergent PCI.  In another study in which all arrest patients underwent immediate aniography, just under 60% had any Acute MI (Non-STEMI + STEMI).  In this large study from France, 31% of 435 arrest patients with no obvious extracardiac cause of arrest had STEMI; 170 other patients had at least one significant coronary lesion, as defined by a >50% stenosis.  However, stenoses are not necessarily related to ACS, do not necessarily need PCI, and, if they do, do not necessarily need it emergently.  Studies which associate a very high rate of coronary thrombi with with sudden death are frequently studies of unresuscitated victims.  Similarly, unresuscitated ventricular fibrillation is frequently due to Acute MI.  However, ACS may be more common in patients who are not resuscitated than in those who are.  In  this study, 68% of resuscitated victims were judged to have Acute MI (STEMI + Non-STEMI); given that about 45% of patients with Acute MI in the CK-MB era had STEMI, then perhaps about 30% had STEMI.

Finally, many or most patients with cardiac arrest and positive troponins have "Acute MI" by the new 2007 definition, but do not have type I AMI due to ACS.

Therefore, don't always think "STEMI", or even "cath lab," when you take care of a patient with resuscitated cardiac arrest, and even if they have ST depression; the cath lab need only be emergently activated for definite STEMI-equivalent, persistent ischemia, electrical instability, or hemodynamic instability. 

I know there are differing opinions on this, and no randomized trials.  I would be interested to hear your evidence-based feedback on this.

ST changes due to limb lead LVH?

This was a middle aged female with a h/o CAD who presented to the ED by EMS sudden onset of central chest pressure 45 min prior to ED arrival with associated diaphoresis and SOB.    


There is LVH and there are ST-T abnormalities (large inferior T-waves and ST elevation, with reciprocal findings in aVL).  There are also suspicious T-wave inversions in V2-V5; they look like Wellens' waves in V4 and V5. 
Though the ST Elevation does not meet STEMI criteria, it is an obvious OMI.



In LVH, just like in BBB, the ST segment (and T-waves) are often discordant to the majority of the QRS (ST elevated if QRS negative, as in inferior leads, or depressed if QRS mostly positive, as in I and aVL).  Here is a previous post that demonstrates this.  

In this case, the inferior ST elevation appears to be too much to attribute it to LVH alone. 

The cath lab was activated but the interventionalist cancelled the activation.  

However, then a previous ECG was located:

Previous ECG has LVH in aVL, but no "secondary" ST-T abnormalities.  This demonstrates that the precordial T-wave inversion is new as well.

This confirms that the inferior ST elevation is new and thus due to acute OMI.

This case was written in 2012, before we changed the paradigm to OMI/NOMI and years before the Queen of Hearts was in use.

Now, in 2023, I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:

The culprit was 100 % thrombotic occlusion of the mid RCA.  The Peak troponin I was 47 ng/ml (equivalent to 47,000 ng/L) --  a very large infarct.  There was a regional wall motion abnormality in the inferior and posteriorior walls.   The LAD was not involved.

Here is the ECG after PCI:

This was called an NSTEMI by the cardiologists.  Of what use is this nomenclature if a case such as this is called a NonSTEMI?  There is occlusion of the infarct-related artery and ST elevation, but because it is not 1 mm at the J-point, it is arbitrarily called a NonSTEMI.

Had the patient not undergone immediate reperfusion therapy, much more myocardium would be lost.

That is why using any millimeter criteria for diagnosing STEMI is very insensitive (it is also nonspecific, as in LVH, BBB, early repol, etc.)