A Male in his 50’s with epigastric pain

This was sent by a recent residency graduate who works at a hospital without a cath lab.  As you might imagine, our graduates have learned to scrutinize ECGs for subtle findings:

This middle-aged male with a history of smoking and alcohol use who had not had medical contact in many years presented with sharp, severe, "indigestion" in his epigastrium.  Medics gave him nitro and aspirin without improvement.  He received more nitro and also a "GI cocktail" in the ED without improvement.

Here is his initial ECG:
There is subtle scooped ST depression in III and aVF, and subtle ST elevation in aVL  (and also I).  The T-wave in aVL is very large compared to the QRS.  There is also a "down-up" (reverse biphasic) T-wave in V2.  This finding is very suspicious for posterior MI.
Since lateral and posterior MI are in one vascular territory (the circumflex), these findings are highly suspicious for circumflex occlusion.

Remember that circumflex occlusion results in diagnostic ST elevation (1 mm in two consecutive leads) in only about 50% of cases.  The lateral wall is often referred to as being "electrocardiographicaly silent".

Part of the reason for this is that the QRS axis is often perpendicular to lead aVL, so there is often very little QRS voltage in aVL: when there is low QRS voltage, there is also low T-wave voltage.  So one must rely an subtle findings that do not reach 1 mm if one is to make the diagnosis.

Often the findings of ST elevation in aVL are best seen in the reciprocal ST depression in inferior leads.

Here is another case for contrast, in which ST elevation in aVL with reciprocal ST depression in lead III is a false positive:
 
http://hqmeded-ecg.blogspot.com/2011/12/subtle-lateral-st-elevation-false.html
This was a false positive cath lab activation.
Here there is a lot of voltage in aVL, so you can't blame subtle ST elevation on lack of QRS voltage. 


Case continued:

The physician was worried about all these findings but was reluctant to activate.  The first troponin I returned at 0.031 ng/mL (less than 99% cutoff of 0.32).

At one hour, with the patient still in pain, he repeated the ECG:
There are some subtle changes: mostly a more upright T-wave in III and V2

The physician started a nitro drip and heparin and consulted a cardiologist at a referral institution.

The patient's pain increased while waiting for transport and another ECG was recorded:
No significant change

Just after leaving, the second troponin I returned at 0.90 ng/mL (positive).  The physician called the referral hospital to recommend immediate cath given a now objective diagnosis of NonSTEMI and with pain refractory to medical therapy.

On arrival, he did not go immediately to the cath lab.

Later that night he did go.  The circumstances surrounding that delayed decision are uncertain.

He had a 100% mid circumflex occlusion with otherwise clean coronaries.  It was stented.

I do not have the peak troponin or echo results.

Learning points:

1. Many occlusions do not reach 1 mm of ST Elevation.  These NonSTEMIs with occlusion can be recognized and need immediate cath lab activation.

2. The ACC/AHA recommends immediate cath for patients with ACS who have uncontrolled symptoms.

A Male in his 50’s with epigastric pain

This was sent by a recent residency graduate who works at a hospital without a cath lab.  As you might imagine, our graduates have learned to scrutinize ECGs for subtle findings:

This middle-aged male with a history of smoking and alcohol use who had not had medical contact in many years presented with sharp, severe, "indigestion" in his epigastrium.  Medics gave him nitro and aspirin without improvement.  He received more nitro and also a "GI cocktail" in the ED without improvement.

Here is his initial ECG:
There is subtle scooped ST depression in III and aVF, and subtle ST elevation in aVL  (and also I).  The T-wave in aVL is very large compared to the QRS.  There is also a "down-up" (reverse biphasic) T-wave in V2.  This finding is very suspicious for posterior MI.
Since lateral and posterior MI are in one vascular territory (the circumflex), these findings are highly suspicious for circumflex occlusion.

Remember that circumflex occlusion results in diagnostic ST elevation (1 mm in two consecutive leads) in only about 50% of cases.  The lateral wall is often referred to as being "electrocardiographicaly silent".

Part of the reason for this is that the QRS axis is often perpendicular to lead aVL, so there is often very little QRS voltage in aVL: when there is low QRS voltage, there is also low T-wave voltage.  So one must rely an subtle findings that do not reach 1 mm if one is to make the diagnosis.

Often the findings of ST elevation in aVL are best seen in the reciprocal ST depression in inferior leads.

Here is another case for contrast, in which ST elevation in aVL with reciprocal ST depression in lead III is a false positive:
 
http://hqmeded-ecg.blogspot.com/2011/12/subtle-lateral-st-elevation-false.html
This was a false positive cath lab activation.
Here there is a lot of voltage in aVL, so you can't blame subtle ST elevation on lack of QRS voltage. 


Case continued:

The physician was worried about all these findings but was reluctant to activate.  The first troponin I returned at 0.031 ng/mL (less than 99% cutoff of 0.32).

At one hour, with the patient still in pain, he repeated the ECG:
There are some subtle changes: mostly a more upright T-wave in III and V2

The physician started a nitro drip and heparin and consulted a cardiologist at a referral institution.

The patient's pain increased while waiting for transport and another ECG was recorded:
No significant change

Just after leaving, the second troponin I returned at 0.90 ng/mL (positive).  The physician called the referral hospital to recommend immediate cath given a now objective diagnosis of NonSTEMI and with pain refractory to medical therapy.

On arrival, he did not go immediately to the cath lab.

Later that night he did go.  The circumstances surrounding that delayed decision are uncertain.

He had a 100% mid circumflex occlusion with otherwise clean coronaries.  It was stented.

I do not have the peak troponin or echo results.

Learning points:

1. Many occlusions do not reach 1 mm of ST Elevation.  These NonSTEMIs with occlusion can be recognized and need immediate cath lab activation.

2. The ACC/AHA recommends immediate cath for patients with ACS who have uncontrolled symptoms.

A Male in his 50’s with epigastric pain

This was sent by a recent residency graduate who works at a hospital without a cath lab.  As you might imagine, our graduates have learned to scrutinize ECGs for subtle findings:

This middle-aged male with a history of smoking and alcohol use who had not had medical contact in many years presented with sharp, severe, "indigestion" in his epigastrium.  Medics gave him nitro and aspirin without improvement.  He received more nitro and also a "GI cocktail" in the ED without improvement.

Here is his initial ECG:
There is subtle scooped ST depression in III and aVF, and subtle ST elevation in aVL  (and also I).  The T-wave in aVL is very large compared to the QRS.  There is also a "down-up" (reverse biphasic) T-wave in V2.  This finding is very suspicious for posterior MI.
Since lateral and posterior MI are in one vascular territory (the circumflex), these findings are highly suspicious for circumflex occlusion.

Remember that circumflex occlusion results in diagnostic ST elevation (1 mm in two consecutive leads) in only about 50% of cases.  The lateral wall is often referred to as being "electrocardiographicaly silent".

Part of the reason for this is that the QRS axis is often perpendicular to lead aVL, so there is often very little QRS voltage in aVL: when there is low QRS voltage, there is also low T-wave voltage.  So one must rely an subtle findings that do not reach 1 mm if one is to make the diagnosis.

Often the findings of ST elevation in aVL are best seen in the reciprocal ST depression in inferior leads.

Here is another case for contrast, in which ST elevation in aVL with reciprocal ST depression in lead III is a false positive:
 
http://hqmeded-ecg.blogspot.com/2011/12/subtle-lateral-st-elevation-false.html
This was a false positive cath lab activation.
Here there is a lot of voltage in aVL, so you can't blame subtle ST elevation on lack of QRS voltage. 


Case continued:

The physician was worried about all these findings but was reluctant to activate.  The first troponin I returned at 0.031 ng/mL (less than 99% cutoff of 0.32).

At one hour, with the patient still in pain, he repeated the ECG:
There are some subtle changes: mostly a more upright T-wave in III and V2

The physician started a nitro drip and heparin and consulted a cardiologist at a referral institution.

The patient's pain increased while waiting for transport and another ECG was recorded:
No significant change

Just after leaving, the second troponin I returned at 0.90 ng/mL (positive).  The physician called the referral hospital to recommend immediate cath given a now objective diagnosis of NonSTEMI and with pain refractory to medical therapy.

On arrival, he did not go immediately to the cath lab.

Later that night he did go.  The circumstances surrounding that delayed decision are uncertain.

He had a 100% mid circumflex occlusion with otherwise clean coronaries.  It was stented.

I do not have the peak troponin or echo results.

Learning points:

1. Many occlusions do not reach 1 mm of ST Elevation.  These NonSTEMIs with occlusion can be recognized and need immediate cath lab activation.

2. The ACC/AHA recommends immediate cath for patients with ACS who have uncontrolled symptoms.

Chest Pain, LVH with Incomplete LBBB, and ST Elevation

A middle aged male with history of bicuspid aortic valve and aortic stenosis complained of 30 minutes of chest pain and dyspnea.  He described it as tightness and pressure.  It resolved with nitroglycerine.   Vital signs were normal and he appeared well.

Here is the initial ECG:
There is profound LVH with incomplete LBBB, with a QRS of 118 ms.  There is marked ST elevation in precordial leads. Although this can be seen with this degree of LVH and incomplete LBBB, one must entertain the possibility of anterior STEMI.
The ST/S ratio is 5/28 in lead V2, for a ratio of 0.18.   

Though 0.18 is less than 0.25, and of course also less than 0.20, it is still quite a high ratio.   A mean maximal ST/S ratio for a cohort of patients with complete LBBB is 0.10 (95% CI: 0.9-0.11).  


Worried about STEMI, a bedside echo was immediately recorded. Here is the parasternal long axis:

There is profound LVH and good wall motion

Here is a still image:
The arrows highlight the wide aortic root

A parasternal short axis was done:


This shows profound LVH with overall good wall motion.  In particular, the anterior wall and septum have good wall motion.  This makes anterior STEMI very unlikely.

The aortic root was not initially noticed, but the physicians were confident there was no STEMI.



The initial troponin I returned elevated at 0.128 ng/mL, at which point another ECG was recorded:
No change, consistent with the interpretation that this is the baseline ECG

The on-call cardiologist was consulted for management of this patient with a positive troponin and worrisome ST segments.  Because of the history of bicuspid aortic valve, the cardiologist was concerned about possible Aortic Dissection and suggested a chest CT.

After a second look at the echo, there was more suspicion of dissection, and a CT was ordered.  Here is one image:
This shows a large aortic root aneurysm that also has a subtle dissection (low density thin lines in the midst of the contrast is a dissection flap)

A repeat ECG was essentially unchanged.

Consistent with massive LVH



The patient went to the Operating Room.

(I am not completely certain that there was no involvement of the coronary cusps, with resulting partial occlusion of the left main and resulting NonSTEMI, but the serial ECGs do not support this).

Learning points:

1) Massive LVH can evolve over time to incomplete, or complete, LBBB, and it can have ST elevation that mimics STEMI.
2) Use ED echo to confirm good wall motion when there is anterior ST elevation due to LVH
3) Don't forget aortic dissection!

Paced rhythm. Is there Ischemic ST elevation?

An elderly male with a dual chamber pacemaker and severe dilated non-ischemic cardiomyopathy presented with dyspnea.  He had not had an angiogram in 10 years.  Although he had severe heart failure, the etiology of acute dyspnea was not readily apparent.  The differential was pneumonia/sepsis, heart failure exacerbation, pulmonary embolism, or possibly ACS.

He had an ECG recorded:
There are P-waves but a ventricular paced rhythm.  The heart rate is 118.
Is there excessive discordant ST elevation in anterior leads?
ST/S ratios have not been studied for paced rhythm, but we have studied them for LBBB, and perhaps this knowledge can be applied to paced rhythm (?)  This is uncertain, but I do it frequently and I think it works. 
If we do apply these rules, the ST/S ratio is highest in V2 and V3.  In these leads, the STE at the J-point is 4 mm in V2 and 4-5 mm in V3, with a 27-28 mm S-wave, for a max ratio somewhere between 0.145 - 0.185.

These ratios are a bit higher than normal for a maximal ST/S ratio, but they are not higher than cutoffs of 0.20 (more sensitive, less specific) or 0.25 (very specific).  

So this is unlikely to represent acute anterior STEMI, but let's compare to a previous ECG:
There is much less STE here.  The ratio is closer to 0.06.

Should you worry that there is an increase in the ST elevation and ST/S ratio?  Normally, yes.

But look at the heart rate: the bottom ECG has a heart rate of 79.  The top one has a rate of 118.

Tachycardia results in increased discordant ST elevation in paced rhythm and in LBBB.  All of this ST segment shift can be attributed to tachycardia.

Outcome:

 Troponins were mildly elevated (up to 0.176 ng/mL).  The patient was diagnosed with acute decompensated heart failure.   As the heart failure was managed, and the heart rate decreased, the ST segments shifted down.  There was no wall motion abnormality.

Exacerbation of heart failure can also exaggerate ST elevation in Paced rhythm and LBBB, as demonstrated in this case.



Learning Points:

1.  Tachycardia can exaggerate the appropriately discordant ST elevation in paced rhythm (and in LBBB)

2. Heart Failure can also exaggerate this ST elevation. 

Chest Pain: What do you see on the ECG?

I saw this ECG, knowing only that there was a chief complaint of chest pain:
What do you see?



















I thought: "This looks like it could be an acute inferior MI."   This is because of the extremely subtle ST elevation in lead III, Q-wave in lead III, biphasic T-wave in aVF, and reciprocal subtle ST depression in aVL.

I went to find the providers because I thought this ECG is so subtle that it could easily be missed by anyone.

Here was the history:

A male in his 40s was eating a heavy meal when he developed "sharp" midsternal non-radiating chest pain of 10/10 severity.  Then he vomited and his pain decreased to 1/10.   About 20 hours later, his pain remained 1/10 and he presented to the ED because a friend suggested he should.  Exam was normal.

His pain resolved with both a nitro and an antacid.

Indeed, the ECG had been read as "no evidence of ischemia" by several providers.



After pain resolution, another ECG was recorded:
ST elevation and Depression is almost completely resolved. The probability of MI is increased.


The interpretation remained "no evidence of ischemia."


His initial troponin returned elevated at 0.746 ng/mL (99% cutoff, 0.030).  



He was appropriately treated for NonSTEMI.  He remained pain free, so no emergent cath was necessary.  10 hours later, this ECG was recorded:
Significant evolution of deeper T-wave inversion is present in inferior leads, diagnostic of inferior NonSTEMI.

The angiogram showed a 95% mid-RCA lesion that was stented.

Commentary

There are many NonSTEMIs that truly have normal or non-diagnostic ECGs, but there are also many that are read as negative when they are at least highly suggestive of ischemia.

In this case, the initial troponin was positive and the diagnosis therefore should not be in doubt.  

Which begs the question: Would more accurate interpretation of the ECG add any value?

I believe the answer is yes.

1. If recognized, it can heighten your suspicion of NonSTEMI and help prevent a missed MI.  The troponin might be negative (not in this case) and you might send such a patient home.  It has happened!  And unstable angina still exists, despite rumors of its demise.

2. If immediately recognized, it can speed the evaluation and disposition.  This patient, even if he had had a negative initial troponin, should not be admitted to "observation," but rather should be an inpatient.  You can order that inpatient bed right away.

3. Immediate recognition facilitates more rapid use of nitro, a P2Y12 inhibitor, and use of anti-thrombotics such as heparin.

4. In a patient with ongoing, refractory chest pain, such an ECG tells you that it is most likely ACS and puts you on notice that more rapid angiography may be necessary if symptoms cannot be resolved medically.