Before diagnosing STEMI, try to find a previous ECG!

A man in his 50's complained of typical chest pain.  Here is his ED ECG:

There is a Q-wave in V2, with ST elevation and hyperacute appearing T-waves in V2 and V3.  This is all but diagnostic for anterior STEMI.  The anterior STEMI equation should not, strictly speaking, be used, because the presence of a Q-wave makes STEMI very likely.

The physician was about to activate the cath lab.  However, he found out that the patient had been seen in the ED for chest pain 6 months prior, and had the following ECG:

Nearly identical to the first.  However, the first one has slight straightening of the ST segments in V2 and V3, which are suspicious.

The patient had been ruled out by serial troponins at the previous hospitalization.  He had not had an echocardiogram or any stress testing or angiogram.  The etiology of the abnormal baseline ECG is uncertain.  Is it due to a previous anterior MI?  Very likely.

Because there was no significant change, the cath lab was not activated.  Serial ECGs were recorded and showed no evolution.  The patient ruled out for MI by serial troponins, but, again, did not have a stress test or echocardiogram.

Lesson:

1. Always check old ECGs, if available, when there is a subtle ECG with possible STEMI.
2. Serial ECGs can help to clarify the situation.

Middle Aged Male with Chest Pain and Previous MI

A middle aged male with h/o CAD presented with chest pain.  He had a recent previous stent in the circumflex.  Here is the ECG at time = 0:

What do you think?

Here is the previous ECG from one month prior:

Now  what do you think?

The first ECG shows Q-waves in lateral leads, and T-wave inversion as well, wit ST elevation in I and aVL.  There is ST depression in V2-V5, 1 mm in V3, diagnostic of posterior STEMI.  Thus, this is posterolateral STEMI.  The Q-waves may lead one to believe that this is a subacute STEMI with a prolonged duration, long enough to result in infarction in addition to injury.  But the pain duration was only 1 hour.

Comparison with the previous ECG confirms that this is acute STEMI superimposed on a previous lateral MI (old lateral Q-waves, old T-wave inversions).  The ST elevation in I and aVL is definitely new.  And now it is clear that the ST depression in V2-V5 is very marked, as there is 3.5 to 4 mm of relative ST depression in V3.

It is not clear that the treating physicians saw the previous ECG.  They were uncertain of the diagnosis and called  an immediate cardiology consult.  Hydromorphone relieved all the pain, which helped ease the anxiety of the physicians.  The cardiologist arrived  immediately, but did not immediately activate the cath lab.  They ordered this repeat ECG at time = 51 minutes:

Now it is very clear that there is an acute posterior STEMI.  

An unusual feature of this case is the persistent negative T-waves in the affected leads.  Normally, with occlusion of the infarct-related artery, negative T-waves from previous MI will become upright (pseudonormalization).  So one would expect, if this is indeed STEMI, upright T-waves in I, aVL, V5 and V6.

An immediate echocardiogram was ordered which confirmed new posterolateral wall motion abnormality and old anterior and apical wall motion abnormality.  The patient underwent PCI with stent of occluded proximal circumflex near the ostium of the first obtuse marginal where the previous stent had been placed.  The maximum troponin I was 80 ng/ml.

Here is the post-PCI ECG:

Notice the tall and large precordial T-waves.  These are what I call Posterior reperfusion T-waves.  They are the analog of Wellens' T-waves and if recorded from the posterior wall would look like Wellens' T-waves.  But because the leads are over the anterior wall, then they are large and upright, rather than inverted!

Opiates in Acute Coronary Syndrome:

Opiates are associated with 1.5x mortality in ACS.  Why?  Probably because they lead the physician to a false sense of security.  In this case, the absence of any further chest pain was reassuring to the physicians.

See this reference with full text link:

American Heart Journal, Volume 149, Issue 6 , Pages 1043-1049, June 2005

STEMI: Which coronary artery is occluded?

This middle aged male with chest pain had this recorded by the medics at t = 0:

ST elevation in I and aVL and reciprocal ST depression in III, but also with STE in V2, and subtle ST depression in V3 and V4

What artery do you think is occluded?  Answer below.


The medics activated the cath lab prehospital, and then recorded this at t = 8 minutes:

There is now more STE in I and aVL, but also new STE in V3


In the ED, this was recorded at t = 28 minutes:

Now there is STE throughout the precordial leads.



The pattern of ST elevation in I and aVL and V2 (also usually with some ST depression in V3-V5) has been described as a "Midanterolateral MI" (see article below) due to occlusion of the first diagonal (branch of the LAD, also known as D1, or LADD1) artery.  The D1 branches off from the LAD to the lateral wall and may also supply some of the anterior wall.

In this case, as time and ischemia progressed, this became a full anterolateral MI, but the infarct-related artery was indeed a very large LAD D1.  It was rapidly treated and the maximum troponin was low, but there was an anterolateral wall motion abnormality on Echo.

Literature:

Isolated mid-anterior myocardial infarction: a special electrocardiographic sub-type of acute myocardial infarction consisting of ST-elevation in non-consecutive leads and two different morphologic types of ST-depression

Sclarovsky S. International Journal of Cardiology. Volume 46, Issue 1, August 1994, Pages 37–47



Abstract


We describe eight patients with a distinct electrocardiographic pattern of anterior wall myocardial infarction characterized by three main features: (1) a pattern of ‘transmural ischemia’ (ST-elevation with positive T-wave) in nonconsecutive leads: aVL and V2, and two different types of ST-depression; (2) a pattern of ‘true reciprocal changes’ (ST-depression and negative T-wave) in III and aVF; (3) a pattern of ‘sub-endocardial ischemia’ (ST-depression with positive T-wave) in V4–5, while ST in V3 was either isoelectric or depressed. We characterize the electrocardiographic features and correlate them with the echocardiographic, radionuclide, and angiographic data. All patients admitted to the coronary care unit from January 1990 to April 1992 with evolving acute myocardial infarction were evaluated prospectively. Patients whose admission electrocardiogram met the description above were included. The electrocardiographic evolution, echocardiographic, Technetium MIBI tomography, and coronary angiography are described. Of 471 patients with acute anterior wall myocardial infarction, admitted to the coronary care unit during the study period, eight patients met the inclusion criteria (1.7% of acute anterior wall myocardial infarction). Echocardiographyic studies revealed mid-anterior hypokinesis in two patients, anterior and apical hypokinesis in one, and no wall motion abnormality in four patients. Technetium MIBI tomography, done in five patients, was consistent with mid-anterior or mid-anterolateral infarction without involvement of the septum or apex. Coronary angiography, performed in seven patients, demonstrated significant obstruction of the first diagonal branch in all of the patients. In four patients, the diagonal occlusion was the only significant coronary lesion in the left coronary artery. Conclusion: Most of the anterior myocardial infarctions also involve the septal and apical regions. Anterior wall myocardial infarctions limited to the mid-anterior or mid-anterolateral wall, without apical or septal wall involvement are relatively rare. This study describes a special electrocardiographic form of anterior wall acute myocardial infarction. This distinct electrocardiographic pattern represents true mid-anterior wall myocardial infarction, caused by occlusion of a first diagonal branch of the left anterior descending coronary artery. The septal and apical regions are not involved because the blood supply via the left anterior descending artery is not interrupted.

Two patients with chest pain and ST elevation. Are they STEMI?

Both of these patients presented with chest pain.  What do you think of the ECGs?

 


For the answer, go to the free pdf of this paper I authored in Annals of Emergency Medicine, p. 52 (the 8th page of the paper).   There is a full explanation of the formula which helps to differentiate these two entities. 

There is an online excel spreadsheet on the right sidebar of the front page of this blog which can be used to calculate the formula value and help you to assess your patient's ECG.

The picture below shows where to find the online calculator.  It is important to read the limitations in red above the calculator:

Back pain radiating to the chest in a man in his 40's

A man in his 40's presented with severe back pain radiating to the chest.  Here was his ECG, with pain:

What is your diagnosis?

This is diagnostic of hyperacute T-waves and LAD occlusion or subtotal occlusion.  There are subtle de Winter's T-waves in V4-V6, in which the large T-wave is preceded by ST depression.

Apparently, it was not recognized (which is not unusual, this is subtle and difficult).  Aortic dissection was on the differential diagnosis, and a CT of the chest ruled this out.  Troponins were negative, the pain was resolved, and the patient was discharged.

He returned the next day with 9/10 back pain.  Here was his ECG:

What do you think?

The fact that the T-waves are so different from the previous day's confirms the ischemia of the previous day.  There is ST segment elevation in precordial leads.  Is it normal variant ST elevation ("early repolarization")? 

Even without a previous ECG for comparison, this is unlikely to be normal STE because of the poor R-wave progression.  In our study of early repol vs. subtle anterior STEMI, only 5% of early repol had an average R-wave amplitude from V2-V4 of less than 5 mm.  Here it is 1 + 2 + 9 = 12 divided by 3 = 4mm average.   If you use the formula (see sidebar) which incorporates the ST elevation at 60 ms after the J-point in lead V3, and the QTc (393ms), then the result is 23.8, which is greater than 23.4 which indicates anterior STEMI.

His pain resolved spontaneously, and he had the following ECG:

This is now obviously diagnostic of MI, and with T-wave inversion and absence of pain, the artery is likely to be open.  The Q-waves indicate that the MI has probably been going on for quite some time.

The troponin returned positive this time and the patient went for cath and had subtotal stenosis of the LAD just distal to the first diagonal.  It was stented.

I don't know the peak troponin, or echo results, or how much myocardium was lost.  But here again is a "NonSTEMI" that really should be treated like a STEMI.  The ECG 1 week later is consistent with significant myocardial loss:

Near total loss of R-waves from V2-V4