Validation of Smith Modified Sgarbossa Criteria Published in American Heart Journal

We have completed and published the external validation of the Modified Sgarbossa Criteria for Diagnosis of Acute Coronary Occlusion in the Presence of Left Bundle Branch Block.

H. Pendell Meyers had just graduated from college when he took this project on.  Now he is a 4th year student at Duke, interviewing for Emergency Medicine Residency Positions.

He did amazing work on this project.

Here is a link to the abstract:

A quick summary:

Sgarbossa criteria:

1. at least 1 mm of concordant ST elevation in at least one lead (5 points)
2. at least 1 mm of concordant ST depression in at least one of leads V1-V3 (3 points)
3. at least 5 mm of discordant ST elevation in at least one lead (2 points)

Weighted criteria (the actual Sgarboss criteria): At least 3 points required to make the diagnosis of acute MI.  Thus, criterion 3 is not sufficient.

Unweighted criteria: any one of the above

Derived Smith-Modified Criteria, published in 2012 in Annals of EM (amazing work on this was done by Dr. Ken Dodd, who was a medical student at the time and is one of our emergency medicine/internal medicine residents now):

1. at least 1 mm of concordant ST elevation in at least one lead (5 points)
2. at least 1 mm of concordant ST depression in at least one of leads V1-V3 (3 points)
3. at least 1 mm of discordant ST elevation AND an ST elevation to S-wave ratio of at least 25% in at least one lead.

Validation Results:

There were 45 patients with LBBB and acute coronary occlusion and 249 controls:
The Modified Criteria (ST/S ratio of greater than or equal to 25%) was far more sensitive than either the weighted or unweighted Sgarbossa criteria 

Formula positive for LAD occlusion. But echo shows no wall motion abnormality! What is it?

Dr. Josu Abecia Valencia, from Spain, asked me my opinion on this case.  He has a great Spanish language blog.  You can find this case in Spanish at his blog here:

He gave his permission for me to post it here.

A 35 year old complained of typical substernal chest pain:
What do you think?
My opinion is below.
Notice the computer reads early repolarization.

Here is my response:

Dr. Abecia,
This is highly suspicious for LAD occlusion, though not diagnostic.
Have you used my formula?
ST elevation at 60 ms after the J point in lead V3 = 4 mm
computerized QTc = 405
R-wave amplitude in V4 = 14.5 mm
Formula value = 23.9, which is > 23.4 which is pretty specific for LAD occlusion.

I would do frequent serial EKGs, every 15 minutes, for several hours.
I would do an emergent formal contrast echocardiogram.

If still non diagnostic, consider immediate angiography.

What was the outcome? 

Here is the outcome (slightly limited because I don't read Spanish very well):

Time zero: Troponin T drawn, returns later at 43 ng/mL (slighlty elevated)
Serial EKGs unchanged.
Thoughts: myopericarditis vs. early repolarization vs. possible MI
Time 5 hours: Troponin T returns at 151 ng/mL.
Still thinking myocarditis
Time 11 hours: Troponin T returns at 350 ng/mL
Echo shows EF of 67% and no Wall Motion Abnormality

But symptoms persisted, and with the positive troponin, they sent him for angiogram.  Here are the results:
Occlusion of the very distal LAD.  So in this case, it was a small infarct territory.
The thrombus was suctioned out and it was stented.
Symptoms resolved.

The formula to differentiate benign ST elevation from LAD occlusion worked perfectly, even though it was a small anterior MI.  It outperformed serial ECGs and formal echocardiogram.

One might argue, with good rationale, that such a small MI can wait until the next day for angiogram.  I will not oppose the argument strongly, but the patient did have ongoing chest pain that was relieved by intervention.  

What is the treatment for this subendocardial ischemia?

This elderly patient had an accidental carbon monoxide poisoning.  The patient did not have ischemic symptoms, but we do an ECG routinely to look for ischemia.  Here it is:
There is ischemic ST depression, typical of diffuse subendocardial ischemia.

The CO level returned at 28%.

Carbon Monoxide displaces oxygen from hemoglobin, and thus effectively decreases oxygen saturation, in this case by 28%, down to 72%.  But it also binds with cytochrome oxydase to inhibit ATP formation.  Thus, its effect is the same as ischemia.

We consider cardiac ischemia (on the ECG, or by elevated troponin), by itself, to be an indication for emergent hyperbaric oxygen (HBO) even if there are no other indications such as neurologic disability, loss of consciousness, level greater than 40%, pregnancy, or other indications.

We happen to have one of the world's finest hyperbaric oxygen facilities here at Hennepin County Medical Center (HCMC).  Dr. Cher Adkinson designed and built the center, and it is now run by our director of Hyperbaric Therapy, Chris Logue, MD.

We treat many chronic conditions with , but are open 24/7/365 for emergencies including CO poisoning, air embolism, decompression sickness, and central retinal artery occlusion.

The patient underwent hyperbaric oxygen therapy.  Here is her ECG afterwards:
There is only minimal residual ST depression.

The troponin I peaked at 5.1 ng/mL.

Dr. Adkinson's research here at HCMC, published in JAMA, found that myocardial injury (as indicated by troponin elevation, but also by ischemia on the ECG) is common in carbon monoxide poisoning and is independently associated with an increased risk of mortality at 7-year followup (38% vs. 15%).  A subsequent publication in JACC reported that myocardial injury was not at all predicted by CO level.

Echo after HBO showed:
Normal estimated left ventricular ejection fraction - 65%.
No wall motion abnormality
Normal left ventricular size.

The patient did well.

STE in aVR and diffuse ST depression: It can be ACS or demand ischemia. If ACS, either posterior STEMI or subendocardial ischemia!

A middle-aged male with a history of 2-vessel coronary bypass called 911 because of the relatively sudden onset of severe SOB.  He had had more mild SOB for the past 2 days.  The medics found him in respiratory distress with coarse breath sounds, a BP of 196/132, oxygen saturations of 90%, and a pulse of 130.  They put him on CPAP for respiratory support.  He denied chest pain.

Here is his prehospital ECG:
There is diffuse ST depression, with ST elevation in lead aVR

The patient arrived in the ED and was put on Noninvasive ventilation (BiPAP).  Blood Pressure was 200/110.  A nitroglycerin drip was started and this ECG was recorded:
Same as prehospital

The ischemia could be due to supply/demand ischemia from hypoxia, tachycardia, and hypertension, or it could have been initiated by ACS.  The ECG cannot differentiate.   If ACS, it could be diffuse subendocardial ischemia, or posterior STEMI.  Does that matter?

Bedside echo showed diffuse B-lines of pulmonary edema.

The plan was to completely control the blood pressure and re-assess for ischemia.

BP was controlled to 120/70 with very high dose Nitro, and the patient's respiratory distress was improved, and another ECG was recorded:
Continued ST depression

Now we have controlled the excessive demand but the ischemia persists:
the BP is not elevated, the heart rate is only mildly elevated, there is no more hypoxia, the hemoglobin returned normal, and there is no evidence of valvular dysfunction (at least no murmur).

Thus, ACS is very likely the initiating factor.  So we have ACS with both refractory symptoms and pulmonary edema, both of which are indications for cath lab activation.

ST depression in the precordial leads can be either posterior STEMI or diffuse subendocardial ischemia.  Does this matter?  No!  This is ACS that needs the cath lab now because it is refractory to medical management.

There are those who think this ECG pattern in ACS is due to left main occlusion.  This is not accurate.  See this exhaustive post on the topic.

The cath lab was activated.

Normally, a P2Y12 inhibitor (clopidogrel, ticagrelor) would be given, but in this case with STE in aVR and diffuse ST depression, there is high potential for left main insufficiency or severe 3 vessel disease.  Thus, there was approximately a 50% likelihood that the patient would need CABG (surgical bypass), although this probability is less in a patient with previous bypass.  Clopidogrel or even ticagrelor would increase the risk of severe bleeding at surgery.

Thus, eptifibatide was given instead of ticagrelor.  Eptifibatide can be turned off.

The patient could not lie flat and so was intubated.

The patient went to the cath lab and had a 100% mid circumflex occlusion that was opened.  Since bypass would not be needed, ticagrelor was initiated.

The outcome was good except for some bleeding complications, during which time his P2Y12 inhibitor (ticagrelor) needed to be held.

The echocardiogram confirmed a posterior wall motion abnormality.  The troponin I peaked at 20 ng/mL.


The patient returned a few weeks later with the identical presentation: respiratory failure, pulmonary edema, and severe hypertension.  His ECG is shown here:
There is diffuse ST depression and ST elevation in aVR, although not as profound as the first time

After treatment with BiPAP and IV Nitroglycerin, his symptoms greatly improved and this ECG was recorded:
The supply/demand issues are gone and the ST depression is resolved.

Because of the recent stent and the time off of clopidogrel, an angiogram was done and showed no in-stent thrombosis (no new ACS).  The troponin peaked at 1.5 ng/mL and there was no new wall motion abnormality.

This ST Depression was due entirely to supply/demand mismatch, not due to ACS.  The second presentation was purely a type II MI.

Learning Points:
1.  In the setting of ischemia, before diagnosing ACS, manage the oxygen supply and demand issues first.  Use supportive care.  Then re-assess.  If ischemia persists, then it is ACS.

2. If ACS and symptoms are refractory, it does not matter whether it is a posterior STEMI or diffuse subendocardial ischemia.  Emergent angiogram and PCI if indicated should be undertaken.

Slightly Peaked T-waves, What is it?

I saw this as I was reading a large a stack of ECGs:
What do you think?

There is sinus tachycardia.  The T-waves are slightly peaked, suggesting hyperkalemia.  But what is atypical is that the T-wave in V3 towers over the R-wave.  And there is terminal QRS distortion in lead V3 (meaning there is neither a J-wave nor an S-wave).  The QTc is 462 ms.  These are suspicious for hyperacute T-waves and anterior injury.  The formula score is 24.8 (>23.4), also consistent with anterior injury.

The above is what I thought when I saw this, so I went to the chart and found this history:

A type I diabetic aged approximately 35 years old presented with chest pain, nausea, vomiting and diffuse abdominal pain.  The patient was in DKA with an anion gap of 35, a glucose of 1128, and a K of 5.5 mEq/L. 

pH = 7.17, pCO2 = 24, HCO3 =  8.  

Her T-waves were attributed to hyperkalemia, without further investigation.

What do you think of this?
T-waves are much more normal, less peaked, but also with better R-wave amplitude.  The ST segment is back to 0.  Equation value is 23.0.  There is an S-wave in V3 now, although small.

One would not expect such profound T-wave changes from a K of only 5.5.  

The patient did have a serial troponins (they are automatically ordered on critically ill patients) and they rose to a peak of 12.4 ng/ml, which is too high for a typical critical illness without MI.  

Here is her ECG the next day (with a normal K):

Because of the high troponin, echocardiography was done and showed a wall motion abnormality in the anterior, anterolateral, and apical walls, consistent with LAD myocardial infarction.  Therefore, she underwent angiography and had a 95% LAD thrombotic culprit that, fortunately, had reperfused on its own (that's why the troponin was only 12).  It was stented.  Had it not opened on its own, it could have resulted in a very large anterior wall MI.

The possibility of anterior STEMI was not noticed during patient care.  I noticed it much later on looking through a random stack of EKGs.  I mention this only to point out that these findings can be noticed, and differentiated from more benign etiologiesprospectively.  

This is NOT a retrospective finding.

Learning point

Hyperacute T-waves and hyperkalemia may be confused, and they may be simultaneous.  Here the potassium was barely high enough to result in a change in T-waves, so one should be especially suspicious in this case.

Is this Coronary Occlusion? Cath lab?

This patient presented with cardiac arrest:
There is RBBB and ischemic ST elevation in V1-V3.  There is ST elevation in aVL and ST depression in III.  This is all consistent with a proximal LAD occlusion.
Should the patient go to the cath lab?

The answer depends on the clinical situation, of course!

This is a young patient who had pulseless, non-shockable cardiac arrest.  He was found with heroin paraphernalia.  He was resuscitated with ventilation and epinephrine.

So this is a type 2 MI with ST Elevation.  Not all ischemic ST elevation is due to plaque rupture.  Only if it is a result of plaque rupture is there an indication for emergent coronary angiogram.

The etiology of cardiac arrest was respiratory, with hypoxia as the etiology.  The ischemia on the ECG is due to a combination of hypoxia from hypoventilation and severe hypotension while in arrest.  It is not due to coronary obstruction.