A 53 year old with chest pressure has a diagnostic EKG (EKG 1). What is it? Chest pressure resolves (EKG 2)

A 50-something male had onset of pain approximately 30 min prior to arrival and was still present on arrival.  The pain was described as a pressure with radiation to his back. No nausea or SOB. No diaphoresis. He had never had this pain before.

Computer and physician read:

SINUS RHYTHM

MODERATE ST DEPRESSION [0.05+ mV ST DEPRESSION]

What do you think?

After looking, compare with the patient's previous ECG (next), and then see what you think.

There is ST Elevation in V2 and V3

Previous ECG from 3 months prior, during a visit for angioedema:

This ECG is normal, with a bit of normal ST elevation in V2 and V3

The first ECG above: ST Elevation, but not enough to meet STEMI criteria of 2 mm in both V2 and V3 (for a male over age 40).  

There is also ST depression in II, III, aVF and V5, V6.  There are large T-waves.

That first ECG, by itself, without comparing with the previous ECG, is diagnostic of acute LAD occlusion.

ST elevation is sometimes normal and sometimes not.  How do you tell the difference?  See more complete discussion below.

As for this first ECG:

Normal ST elevation NEVER has associated ST depression.  This ECG has ST depression in inferior leads (it also has a touch of ST elevation in aVL) AND there is ST depression in V5 and V6.  This is diagnostic of an acute LAD occlusion.  Comparison with the previous ECG, which barely has any normal ST elevation, proves that this is New, and ischemic, ST Elevation.

Additionally: the T-waves are hyperacute!  Compare with the patient's baseline T-waves.

These findings were not appreciated for variety of reasons.  The triage physicians is particularly skilled at ECGs and did not see it.  Of course the computer did not see it either.

Patient was given aspirin and the pain resolved.

A 2nd ECG was recorded:

These were immediately recognized as Wellens' (Pattern A, biphasic) waves and thus this is analogous to Wellens' syndrome (anginal episode, resolved, preserved R-waves, and Wellens' waves)

Why is it only "analogous" to Wellens' syndrome and not the syndrome itself?  

'

Answer: in Wellens', you don't have the luxury of seeing the EKG that was recorded during pain because there was no ECG recorded during pain.

Cath team was called.  First (and only) high sensitivity troponin I returned at 53 ng/L.

Angiogram Results:

Culprit Lesion (s): 80% thrombotic stenosis in the mLAD.  This was stented.

Subsequent ECGs:

This was at 66 minutes, 33 min after ECG 2:

There is some evolution: STE in V2 is less, T-wave inversion slightly deeper.  This is typical Wellens evolution.

After PCI at 3.5 hours:

Still more deepening of T-waves.  

They are becoming Pattern B (deep, symmetric) Wellens' waves.  

Wellens did not know it at the time because he only had single snapshots in time, but Pattern A evolves into Pattern B over hours to days.  

(I have been writing about this observation for years but no one, to my knowledge, has published a peer-reviewed paper on the topic.)

Next day:

Formal Bubble Contrast Echocardiogram:

Normal left ventricular size and systolic function with an estimated EF of 60%.

Small regional wall motion abnormality--apical septal, mid anteroseptal, and apical anterior hypokinesis.  

Comment: We don't have good evidence for infarct size (as troponins were not measured to peak), but since the duration of chest pain was very brief, the artery was probably only briefly occlusion, and this is probably a small infarct.  Thus, the wall motion abnormality is probably transient ("myocardial stunning") and will recover within days to weeks.

Normal ST elevation in V2-V4 vs. Ischemic ST Elevation:

Normal STE:

--Has upward concavity in all of V2-V6.

--STE should not be more than 5 mm in any lead

--There should be no ST depression in inferior leads.

--There should be no ST depression in any precordial leads.

--There should not be any Q-waves in V2-V4.

--There should be no terminal QRS distortion in V2 or V3 (there must be either an S-wave or a J-wave -- J point notching -- in both leads)

T-waves may be tall, but should not be far taller than baseline

If any of these criteria are met, then the formula (see below) may be falsely negative.

Ischemic STE:

Even if all of the above are met, the STE may still be ischemic, due to LAD occlusion.

At this point, one can use the Formula for differentiating Normal STE from LAD Occlusion.

See this post for complete description of the formula: 

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

What would have happened if we applied the formula to this case.

Computuerized QTc was 374 ms.

STE at 60 ms after the J point in lead V3 = 3.5

R-wave amplitude in V4 = 22

QRS amplitude in V2 = 10

Formula value = 15.76  This is a VERY low value and would turn out to be a false negative!!

The most accurate cutpoint is 18.2

17.0 is a very sensitive cutpoint

19.0 is a very specific cutpoint

Beware using the formula in ECGs that have Exclusions!!

Chest pain with ventricular paced rhythm - will you be able to rise above the STEMI paradigm and figure out what to do?

 Submitted by Marie Wofford MD and Mark Kastner MD, edits by Smith and Meyers

An 86 year old with prior history of CAD and PCI, aortic stenosis, pacemaker, atrial fibrillation on warfarin, hypertension, etc., presents with sudden onset mid back pain radiating to the left shoulder and chest. His vital signs were within normal limits with the exception of tachypnea at 22/min. The EMS ECG is shown below:

What do you think?

The ECG shows ventricular paced rhythm (the pacer spikes are barely visible to me in lead V2), resulting in almost LBBB morphology (LBBB morphology would require upright usually monophasic R waves in I and aVL, which is not present in this ventricular paced rhythm). 

There is STE in V1 through V5, and in leads II, III, and aVF. The inferior leads all show concordant STE, most less than 1.0 mm. In the precordial leads, the STE is excessively discordant (greater than 25% of the preceding S wave) in many leads in a row (see exact numbers below). 

Lead V5 is the transition lead, and it is difficult to say whether the positive or negative component is greater. 

When the QRS is nearly equally positive and negative, the ST segment should be isoelectric (no STE or STD).  Any STE in this situation is indicative of OMI.  

But this is an issue only for that one lead.  Several leads meet the Smith Modified Sgarbossa Criteria, and only one is necessary to make the diagnosis of OMI.

V1: 1.0 / 6.0 = 17%

V2: 3.0 / 17.0 = 18%

V3: 5.0 / 17.5 = 29%

V4: 3.5 / 12.5 = 28%

V5: 1.0 / 2.0 = 50%

This ECG is diagnostic of transmural ischemia involving the inferior and anterior / anterolateral walls, with the most common etiology being, of course, OMI. This combination of anterior and inferior makes a large LAD the most likely culprit (or at least whatever artery is acting like the LAD usually acts, supplying both of these territories).

Initial troponin I was 25 ng/L  (URL 20 ng/L for men, 12 ng/L for women).

He was taken for cath within an hour of arrival. 

RCA: ostial lesion, 99% stenosis, prior prior prox RCA stent which was patent

LAD: mid-LAD lesion 99% at site of prior stent, with "limited" collateral flow from first RV marginal to distal LAD

LCX: minor luminal irregularities

RPDA: 100% stenosis (unclear whether this was chronic)

The RCA lesion was deemed the culprit lesion and stented. There is no comment on the acuity of the mid-LAD lesion, but judging by the fact that they did not intervene on it and did not describe any reasons why they were unable to intervene on it, it seems to me that they thought this was not an acute lesion.

In retrospect, it does make sense to me in this coronary context that the RCA lesion alone could explain the ECG findings. At baseline, his RCA supplies both the inferior and anterior walls, because there is a severely limiting stenosis in the LAD with collaterals from the RCA. When such an RCA suffers acute OMI, both the inferior and anterior walls have acutely lost blood supply, causing a pattern that is much more commonly seen in large LAD occlusion.

Here is his ECG the next day:

Resolution of prior findings, and reperfusion T wave inversion in the inferior leads, as well as likely posterior reperfusion T waves.

Troponin I levels:

1900: 8,019 ng/L

2200: 10,207 ng/L

No further troponins measured.

Formal (noncontrast) echocardiogram on day 2 showed LVEF 55%, distal inferior hypokinesis, RV systolic function mildly reduced.

He was discharged 2 days later without further complications.

Learning Points:

Use the modified Sgarbossa criteria to evaluate for OMI in LBBB and ventricular paced rhythm (stay tuned for big publication on paced rhythm coming out soon!!!) The ACC/AHA guidelines give us no advice on how to diagnose OMI in paced rhythm. 

There is huge variability in coronary anatomy, but the ECG findings don't lie about which walls are infarcting.

Troponins are least when the benefit of reperfusion is maximal! This patient's initial troponin was barely over the URL for this assay.

When there is less than 1 mm of ST depression, can you make the diagnosis of posterior OMI?

 Submitted and written by Alex Bracey MD, edits by Smith and Meyers

I went to see the next patient who had presented to the Emergency Department for chest pain. Before walking into the room I reviewed the triage ECG taken moments before.

What do you think?

Sinus rhythm with ST depression (STD) in V2-V5, with maximal STD of less than 1mm in lead V3-V4.

Close-up of the STD with red lines overlain. Compare the top of the line at the QRS onset to the top of the line at the J-point.

When there is less than 1 mm of ST depression, can you make the diagnosis of posterior OMI?

While subtle, the STD is certainly present and highly suggestive of posterior OMI. Because there is no clear evidence of concomitant OMI in the other three walls of the LV (inferior, lateral, or anterior), this could be called "isolated" posterior OMI.

In speaking with the patient, she was a woman in her 60s who had experienced 3 days of stuttering chest discomfort that radiated to her neck, described as a heaviness. She had experienced an episode that was more profound than the preceding days which prompted her presentation to the ED.

A bedside echo was performed which showed a posterior wall motion abnormality.

She was given aspirin and heparin while I discussed the case with the cardiology attending, who ultimately agreed to activate the cath lab despite the late hour. 

After the conversation concluded, the initial troponin I resulted at 4.00 ng/mL.

Angiogram:

Coronary angiogram demonstrating 100% thrombosis of the LCX with TIMI 0 flow.

 Coronary angiogram post-DES deployment to the proximal LCX with TIMI flow 3 restored.

The patient had an uncomplicated post-catheterization course, during which troponin I peaked at 32 ng/mL (large infarct -- but it could have been much larger. She was discharged home after several days without apparent limitations.

Formal echocardiogram (without contrast) was performed approximately 48 hours after arrival and did not show any wall motion abnormalities.

Discussion

Approximately 10% of OMIs will involve the posterior wall, most of which also have concomitant involvement of the lateral and/or inferior walls (though usually not meeting STEMI criteria). Isolated posterior OMI, however, manifests as STD without associated STE since the subepicardial myocardial ischemia that would normally generate STE on overlying leads is occurring in the opposing or negative vector compared to the recording ECG leads. The majority of isolated posterior OMIs will be due to occlusion of the LCX, RCA, or a variety of their posterior branches.

The 4th Universal Definition of Myocardial Infarction defines posterior OMI as STE greater than or equal to 0.5 mm in leads V7-V9 (posterior leads) and only mentions STD in V1-V3 as potentially indicating LCX OMI, though it refers to these findings as "nonspecific." Posterior leads, however, will not always demonstrate STE of even 0.5 mm even with clear evidence of OMI in standard ECG configuration, since more lung tissue separates the heart from the posterior ECG leads and air is a poor conductor of electricity. It is not surprising, then, that isolated posterior OMIs are often missed and associated with worse outcomes.

Teaching Points

 - Isolated posterior OMI may manifest as STD maximal in leads V1-V4. That STD may be less than 1 mm. Remember that the vast majority of individuals have normal, baseline, non-ischemic STE in V2 and V3 (hence the STEMI "criteria" require 1.5 - 2.5 mm for diagnosis). Thus, even an isoelectric J-point could be relative ST depression, and any ST depression in these leads is abnormal. 

 - Bedside echo with clear regional wall motion abnormality may help to confirm subtle but concerning ECG findings of OMI

 - Posterior leads may be helpful in the diagnosis of posterior OMI with STE thresholds of 0.5mm in any of leads V7-V9; however, since air is a poor conductor of electricity, even this small amount of STE may not manifest despite OMI. Our opinion is that posterior leads very rarely add information to careful inspection of the standard 12 leads for the presence of STD maximal in V1-V4, as long as one does not require a full millimeter of STD in those anterior leads.  The one exception is this: one study (Poh et al.) shows that diffuse subendocardial ischemia manifests ST depression, not ST elevation, in posterior leads, and this is consistent with electrophysiology. 

Poh K-K, Chia B-L, Tan H-C, Yeo T-C, Lim Y-T. Absence of ST elevation in ECG leads V7, V8, V9 in ischaemia of non-occlusive aetiologies. Int J Cardiol [Internet] 2004;97(3):389–92. Available from: http://dx.doi.org/10.1016/j.ijcard.2003.10.022

Saw this ECG while reading through a stack. Lots here: myocardial stunning, MRI viability, P2Y12 inhibitors and CABG.

I had just finished passing the shift off to my partner and the next shift of residents.  It was 11:30 PM.  I turned to the computer system to finish reading any EKGs from the shift and I saw this one, which had been recorded after the end of my shift at 11:11.

Usually these are brought immediately by the tech to the faculty physician.  I'm not certain whether another faculty had seen this or not.

What do you think?

I immediately saw the ST depression in V3 and V4 of at least 1.5 mm.  There is also minimal STD in II, III, aVF.  

When you see this inferior STD, you should not think "inferior ischemia" because ischemic ST depression does not localize to a myocardial territory (it usually manifests with an STD vector towards leads II and V5, with reciprocal ST elevation in aVR).

Instead, when you see this, you should be thinking that it is reciprocal (opposite) ST Elevation in the opposite lead (aVL).  So I looked at aVL and of course there is ST Elevation there; it is miniscule, but so is the QRS!

The STD in V3, V4 is diagnostic of posterior OMI, and this would usually be due to the circumflex or a branch thereof.  And when the circumflex is involved, it is likely that the high lateral wall (aVL) will also be involved.

Therefore, the entire picture presented by this ECG is a circumflex (or branch) OMI.

But it must be in the context of a clinical presentation consistent with ACS.

So I looked at the chief complaint on the computer: "lightheaded".  Hmmm.....

So I went to see the patient.  He stated that he had come in tonight because "felt something right here" and pointed to his chest.  After coaxing, he did admit that the discomfort was still going on.

So we activated the cath lab and obtained another ECG, recorded 33 minutes after the first: 

Yikes

Translation: looks very worrisome!

We did an bedside echo while waiting for the cath team in the middle of the night:

Here you can see that the wall closest to the transducer is contracting and thickening vigorously.  The wall opposite (posterior/lateral wall) is barely moving.

The patient received aspirin, heparin, and ticagrelor.

The first high sensitivity troponin I returned at 22 ng/L (URL = 34 ng/L, so it was normal)

The patient went to the cath lab.

Angiogram (detailed results at the bottom):

Severe 3 vessel disease, with very severe stenoses throughout the circumflex and its branches.  They did not find a specific culprit, and the patient’s pain was gone by the time of the angiogram, so I suspect one of those severe stenoses had a transient thrombosis that autolysed before the angiogram.

There was also distal left main disease.

Due to all this coronary disease, it was determined that bypass surgery (CABG) would be required.

Here is the post angiogram ECG:

Much better than the 2nd ECG; it looks like the first one

The 2nd troponin was over 1000 ng/L, and no more troponins were measured after that.

Formal echocardiogram with contrast:

Normal LV size & wall thickness w severely decreased systolic fct: 

Ejection Fraction = 33%.

Wall motion abnormalities involving basal-mid segments of the inferior, inferoseptum, inferolateral, anterior, and anterolateral walls. The apex is relatively spared.

 

Regional wall motion abnormalities in multiple vascular territories with relative sparing of the apex suggestive of multivessel coronary disease, predominantly involving the RCA and Left circumflex.

Case continued

The patient was considered for Coronary bypass surgery, and so an MRI viability study was done which showed preserved viability and normal ejection fraction.

In other words, the wall motion abnormalities and the low ejection fraction on the day after admission were "myocardial stunning," and NOT due to completed infarction.  It often takes days to weeks for ischemic myocardium that is NOT infarcted to regain function.  One can assess the amount of completed infarction from: Peak troponin (estimate), ECG findings of completed infarction (estimate), or viability studies such as MRI (more exact).  Also, one can do a "convalescent" echocardiogram at 6 weeks after the event, at which time the stunning should be resolved.

A subsequent echo showed EF of 78%.

He underwent Coronary Artery Bypass Surgery 5 days after admission.  The delay was a result of having received ticagrelor in the ED, which makes for bleeding complications.  There is some controversy over the use of P2Y12 inhibitors in ACS.  They are generally recommended for STEMI, but with poor evidence (I would consider this OMI to be analogous to STEMI).  They are discouraged for Non-STEMI.  See below for a brief discussion of P2Y12 inhibitors. 

Learning Points:

1. In the right clinical setting (chest discomfort), ST depression maximal in V1-V4 is posterior OMI until proven otherwise.  STD in V5 and V6 is usually due to non-occlusive etiologies (subendocardial ischemia, including ACS with partial coronary obstruction)

2. Inferior ST depression is reciprocal to high lateral ST Elevation

3. High lateral ST elevation may be minimal, especially when the QRS is small

4. Triple vessel disease without an identified culprit does not mean there was no culprit and no OMI.  It means that the culprit could not be identified and that the artery was open by the time of the angiogram.

5. P2Y12 inhibitors can delay CABG surgery

6. Wall motion abnormalities and poor ejection fraction can reverse if the myocardium is not infarcted.  This is called "myocardial stunning."

Full angiogram results 

Three vessel CAD including distal left main disease and CTO of RCA with left to right and right to right collaterals.

 

Disposition

 

CV surgery consult for CABG due to three vessel CAD and diabetes.  

Potential targets include LIMA-LAD, SVG to OM1, OM2 and dRCA.

No evidence of plaque rupture in any of the large epicardial vessels.

Heparin gtt ACS protocol overnight after removal of TR band.

Nitro gtt in case of chest pain.

Echocardiogram tomorrow am.

 

Coronary Angiography (Note: All Coronary Angiograms were done in the usual views)

 

LMCA: Moderate to large caliber vessel with moderate diffuse disease distally with calcification extending into LAD.

 

LAD: Moderate caliber vessel with severe diffuse disease with calcification in the proximal to mid LAD. The rest of the LAD has diffuse disease without focal stenosis. There are multiple small diagonal branches with diffuse disease. There are septal collaterals supplying RPDA.

 

LCx: Large caliber vessel. There is severe serial stenosis in the proximal to mid segment with calcification. There is moderate caliber bifurcating OM1 with severe ostial stenosis. OM2 is moderate caliber vessel and has moderate to severe proximal stenosis. OM3 is small caliber with diffuse disease.

There are epicardial collaterals supplying the RPLAs.

 

RCA: Large caliber vessel with severe diffuse calcification. It is chronically occluded in the proximal segment. The distal RCA, RPDA and RPLA are filled by right (conus, SA nodal and RV marginal branch) collaterals and also septal collaterals from LAD and epicardial collaterals from LCx.

P2Y12 inhibitors, brief discussion.  

This is copied from a section I (Smith) wrote in the EmRap CorePendium (Dr. Meyers and I wrote the section on Acute Coronary Syndromes)

Here is the section on "Upstream" use of P2Y12 inhibitors, upstream meaning in the ED or ambulance, prior to angiogram "defining" the coronary anatomy: if the anatomy mandates CABG, then they will not be given.  On the other hand, if there will be PCI, a P2Y12 inhibitor must be given.

“Upstream” (pretreatment, in the ED or prehospital) administration of P2Y12 inhibitors and of glycoprotein IIb-IIIa inhibitors.※

• Should dual antiplatelet therapy be given in the ambulance or ED prior to the angiogram? Or should the practitioner wait until the angiogram “defines” the coronary anatomy and the choice of therapy (PCI, CABG, or neither)?
• American College of Emergency Physicians clinical guideline: “P2Y12 inhibitors and glycoprotein IIb/IIIa inhibitors may be given in the ED or delayed until cardiac catheterization” (Level C recommendation).※
• Only prasugrel (NSTEMI with PCI only) and ticagrelor (STEMI with PCI only) have been studied in dedicated trials comparing pretreatment vs. no pretreatment.
  • For patients who are sent immediately for an angiogram (eg, STEMI/occlusion MI):
    • ATLANTIC trial: Ticagrelor
      • Prehospital (31 min earlier than the controls) treatment resulted in 5% more patients (47.5% vs. 42.5%) with ST resolution after PCI (P = .05), a secondary outcome. The outcomes of this trial were considered negative.※
  • For patients undergoing delayed angiogram/PCI (eg, for NSTEMI):
    • For NSTEMI with PCI, P2Y12 inhibitors are typically not given “upstream” (in ED) unless by interventionalist or per interdisciplinary protocol.
    • ACCOAST trial: Prasugrel
      • 30 mg upstream followed by 30 mg at angiography as compared with 60 mg at angiography, had more bleeding with the same ischemic outcomes.※
      • The median was 19 h from symptom onset to angiography.
    • Unstudied problem: Patients who must wait over the weekend, up to 72 h, for an angiogram. Does upstream dual antiplatelet therapy, along with anticoagulants, decrease preprocedure re-infarction?

Here is the section on CABG and P2Y12 inhibitors in Unstable angina/NSTEMI with PCI:

• Only give before PCI with institutional approval due to CABG bleeding risk. CABG is required in up to 16% of NSTEMI cases.※
• However, good evidence of safety and efficacy has been documented even in the CABG group:
  • ACUITY (non-randomized).※
    • Editorial※
  • 1,539 of 13,800 had CABG, with a 5-d washout before CABG
  • A longer length of stay by 3 d was recorded
  • 30-d death/MI/revasc: 17.3% vs. 12.7%, favoring clopidogrel pretreatment
  • No CABG bleeding difference

Sudden CP and SOB with Inferior ST Elevation and in STE in V1. Is it inferior and RV OMI?

A 60-something had been having chest "soreness" on and off for one month when she presented with sudden chest discomfort and dyspnea starting about an hour prior to arrival.

Here is the triage ECG.

It was texted to me along with concern for inferior ST Elevation and STE in V1, possible inferior and right ventricular OMI:

There is a negative P-wave in lead II.  

You'll notice that the P-wave is abnormal everywhere.  

This is an ectopic atrial rhythm, and it is low in the atrium such that the atrium is depolarized AWAY from lead II and is inverted.  

In any ECG, there might be an atrial repolarization wave, or not.  When there is sinus rhythm, with conduction towards lead II, the atrial repolarization wave is negative, resulting in PR depression and depression of the first part of the ST segment (see schematics below).  This is why we measure the ST segment relative to the QRS onset (PQ junction): both intervals may be depressed by a normal atrial repolarization wave.  

In pericarditis, the atrial repolarization wave is exaggerated; hence, we get excessive PR depression.

In low atrial rhythms, on the other hand, when the atrial impulse is traveling from inferior to superior, the atrial repolarization wave is positive, and can result in a mimic of ST Elevation.  

This is what is happening in inferior leads, but ALSO in V1.

Ken Grauer says this is called the "Emery Phenomenon," but I can't find that in any search.

Here is a magnification of V1:

Here it is with the atrial repolarization wave outlined by a circle:

Case continued:

I responded that this was unlikely to be OMI, that it was probably an atrial repolarization wave, and to get serial EKGs and troponins.

The patient ruled out for MI, and probably had chest wall pain.

See below for more Learning about the Atrial Repolarization wave.

Here are some schematics:

Normal atrial repolarization wave

This schematic is from my book, The ECG in Acute MI

Here is another recent case:

A man in his sixties with chest pain

At this link, there is an extensive discussion by Ken Grauer

Here you can see how the atrial repolarization wave can mimic what appears to be significant ST Depression:

Look at this ST Depression (It's not real)