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)

A 30-something with inferior ST Elevation. OMI? Pericarditis? Normal Variant ST Elevation?

This ECG was texted to me with the information that it was recorded on a 30-something male who presented to the ED with bilateral chest tightness.  

There is some inferior ST elevation.  There is a Q-wave in lead III.  

The ECG is certainly suggestive of inferior OMI.

Or is it Normal ST Elevation?  Or Pericarditis?

The physician had only moderate suspicion due to absence of ST depression in aVL

What do you think?

Meyers interpretation: (all I know is 30-something male with bilateral chest tightness): The lack of hyperacute T waves and lack of STD or TWI in aVL makes this inferior STE not definitive for OMI for me yet. I am not sure between normal variant and possible pericarditis, there are some features of each. I would need more clinical info, repeat ECGs, trops, echo, etc.

Smith: I agreed and thought that it was probably not inferior OMI due to (see references):

1) Absence of ST depression in aVL [99% sensitive for inferior OMI in our study (1, 2)]

2) Absence of T-wave inversion in aVL [also 99% sensitive in our study (1)]

3) Small T-wave in lead III

However, I was not entirely certain because of:

1) Straight ST Segments in all of II, III, and aVF (absence of upward concavity is unusual in normal variant STE and in pericarditis. [Convex ST segments were seen in only 7% of pericarditis in Amal Mattu's study; did not assess straight segments. (2)]

2) Terminal QRS distortion in aVF (I have previously studied terminal QRS distortion in lead V2 and V3 as never occurring when normal variant STE is in leads V2-V4, but have noticed more and more that it is at least a soft sign of OMI in other leads).  See this blog post.  This appears to be what Amal Mattu calls the "RT Checkmark Sign"(2, 3) (I will ask Amal and edit it later if I'm wrong.) 

There is Spodick's sign, which is a downsloping of the baseline T-P segment, in several leads.  This has long been associated with pericarditis but without much evidence until recently.  In the 2020 study by Amal Mattu, referenced below, it occurred in 5% of OMI and 29% of pericarditis).(2)  They did not study normal variant STE; it may be very difficult even in the setting of a study to differentiate normal variant from pericarditis as an outcome measure.

Clinical Course

I recommended a formal bubble contrast echocardiogram, serial troponins, and serial ECGs.

Serial ECGs were unchanged.

The echo was normal.

All Abbott high sensitivity troponin I were below the level of detection.

Epilogue

The pain resolved.  The patient had had some viral symptoms, and for this reason was diagnosed with pericarditis and treated with colchicine.

Comment: I have my doubts about pericarditis here: 

1) Pain was not pleuritic, positional, or sharp, and also was not persistent.  Pressure pain where MI is ruled out is more likely to be esophageal.

2) There is no PR depression

3) The ST elevation is far more in inferior than in lateral leads.

4) The ST/T ratio in V6 is less than 25%

I think that normal variant ST elevation (early repolarization) is more likely.  

Final thoughts and New Study differentiating Pericarditis from OMI

Is it important to differentiate pericarditis from normal variant ST Elevation?  It can be!

Read this important post written by Pendell Meyers when he was a medical student:

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

3 References

2 Studies comparing acute OMI to pericarditis, one by Smith, one by Amal Mattu.  Unfortunately, since it is very difficult to make a definite diagnosis of pericarditis, neither study could even attempt to differentiate pericarditis from normal variant ST Elevation, and it is possible that a large percentage of patients in both studies had normal variant STE and non-cardiac chest pain.

1) Bischof JE, Worrall C, Thompson P, Marti D, Smith SW. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med 2016;34(2):149–54. Available from: http://dx.doi.org/10.1016/j.ajem.2015.09.035

This study showed that ANY ST depression in lead aVL is highly sensitive for inferior OMI, and that zero patients with pericarditis had this feature.

Of the 154 patients with catheterization laboratory diagnosis of inferior STEMI, 154 patients (sensitivity, 100%; CI, 98%-100%) had some degree of ST depression in lead aVL (at least 0.25mm).  In addition, all 154 patients demonstrated T-wave inversion in lead aVL (sensitivity, 100%; CI, 98%-100%).  Of the 49 pericarditis patients, zero (0%) had any ST-segment depression in lead aVL (CI, 0%-7%), and 7 (14%) of 49 (CI, 7%-27%) had T-wave inversion in aVL.  ------Of an additional 272 inferior OMI from a different cohort, 267 (98%) had STD in aVL.   

2) Witting MD, Hu KM, Westreich AA, Tewelde S, Farzad A, Mattu A. Evaluation of Spodick’s Sign and Other Electrocardiographic Findings as Indicators of STEMI and Pericarditis. J Emerg Med 58(4):562-569; April 2020;Available from: http://dx.doi.org/10.1016/j.jemermed.2020.01.017

Note that, in the Witting study, 3/42 pericarditis patients had ST depression.  It is not specified in what lead the ST depression was found.  Bischof et al. found zero STD in aVL.  

3) Lee DH, Walsh B, Smith SW. Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization. Am J Emerg Med 34(11):2182-2185; November 2016; Available from: http://dx.doi.org/10.1016/j.ajem.2016.08.053

A man in his early 40s with chest pain: STD in V1-V4, but posterior lead are negative

Written by Pendell Meyers

A man in his early 40s with hyperlipidemia and family history of MI presented at 545 AM with acute onset substernal chest pain with nausea and diaphoresis. He reported that the pain began at 8pm last night, and was unclear whether it was constant or intermittent overnight, but his wife convinced him to present to the ED.

His triage ECG was performed at 0550 (no prior for comparison):

What do you think?

There is STD in precordial leads, maximal in V2-V4.  There is zero STE anywhere on the ECG.

It is yet another ECG diagnostic of posterior OMI, with STD present from V1-V5 and maximal in V2-V4. If you have been reading this blog for any length of time, you will have seen countless cases just like this one, and you will see the pattern over and over that these patients are very unlikely to be recognized as OMI and receive emergent reperfusion.

Smith comment on terminology of posterior MI: The posterior wall has been reclassified as part of the lateral wall, but we continue to refer to the portion of the lateral myocardium which which does not face any overlying leads of the standard 12-lead ECG as the posterior wall.(Bayes de Luna)

----Bayes de Luna A, Zareba W. New terminology of the cardiac walls and new classification of Q-wave M infarction based on cardiac magnetic resonance correlations. Ann Noninvasive Electrocardiol [Internet] 2007;12(1):1–4. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17286644

Case continued

This ECG was not recognized as OMI, but rather interpreted as "ST depression." Generalized chest pain workup was ordered.

At around 0730 the initial high sensitivity troponin I returned at >25,000 ng/L (the lab's upper limit of reporting, and consistent with a very large OMI).

The documentation is unclear as to whether the patient was having ongoing pain since triage. In response to the troponin another ECG was obtained at 0744, this time with posterior leads (unclear which leads are intended to be posterior, or where they were placed, but it appears that V4-V6 are likely V7-V9):

Posterior leads.
Ongoing active posterior OMI is evident by persistent STD in V1-V2. There is a hint of STE in V4-V6, but most cardiologists would say that it does not meet posterior leads criteria (0.5mm in just one lead).
Smith comment: Notice also that the ST Depression in V2 is still present. This is important in verifying the validity of the posterior leads.  Sometimes, posterior leads are recorded later after there has been spontaneous reperfusion (not simultaneously).  In order to assess posterior leads in relation to anterior STD, one much ascertain that the STD which prompted the recording of posterior leads is still present.

This is exactly the problem with posterior leads. Those who can see posterior OMI on the standard 12 lead ECG don't need the posterior leads, and those who can't see posterior OMI on the standard 12-leads may be misled by posterior leads because of their very low voltage. In the end, neither provider has their decision making improved by posterior leads. 

We have no cases on this blog in which posterior leads truly helped when the standard 12 leads did not have STD maximal in V1-V4. Even when they do show very small STE in posterior leads that agrees with STD maximal in V1-V4, the smaller voltage on the posterior leads causes the amount of STE to be very very small, so small that humans report that there is no STE at all.

Smith comment: Posterior leads may be beneficial if the standard 12-lead is non-diagnostic.  There is literature to support this (see below literature on posterior leads).  However, that literature always requires at least 1 mm of ST Depression in 2 consecutive precordial leads for the diagnosis of Posterior MI. If that amount does not exist, the ECG is considered nondiagnostic. But in fact many ECGs with minimal ST Depression in V2 and V3 are diagnostic.  This is because V2 and V3 normally have baseline ST Elevation. ANY AMOUNT of ST depression is abnormal in these 2 leads.  Thus many "non-diagnostic" 12-lead ECGs really are diagnostic.  (I often say that "It is not the ECG that is not diagnostic; it is the interpreter.) See example ECG of tiny STD, at the bottom.

Case continued

ED bedside US: "inferolateral wall motion abnormality."

The patient was taken for cath at around 0900 (more than 3 hours after ED arrival). A proximal LCX occlusion (100%, TIMI 0) was found and stented.

The second troponin also resulted at >25,000 ng/L, and no further troponins were ordered.

Here is the ECG after cath:

Resolving STD,  posterior reperfusion T waves, and developing R waves (like posterior Q waves). 

2 days later:

Similar to prior, increasing R waves, and persistent STD (this is consistent with developing posterior aneurysm, or at least "persistent ST deviation after old MI").


See this ECG of a patient with proven inferior-posterior aneurysm, from Smith's book:

Learning Points:

The most important and reproducible finding for posterior OMI on the standard 12-lead ECG is ST depression maximal in V1-V4. We are studying this now, have published this in abstract form, and are currently writing a full manuscript.  We did not record posterior leads for the study, but we did find that ST depression maximal in V1-V4 had 88% specificity for OMI.

See these other cases of posterior OMI, many of which were missed, and some of which died:

Cardiologist declines taking patient to the cath lab. Patient dies.

Interventionalist at the Receiving Hospital: "No STEMI, no cath. I do not accept the transfer."

"It isn't a STEMI," so cath lab refusal (again). Were they right?

A middle aged man with ST depression and a narrow window of opportunity

A man in his 50s with 2 hours of chest pressure

A woman in her 70s with bradycardia and hypotension

You have two hours to save this patient's life

A man in his early sixties with palpitations

A female in her 60s with sudden chest pressure

How much time are you willing to wait for OMI to become STEMI (if it ever does)?

Chest pain and Concordant ST Depression in a patient with aortic valve and previously normal angiogram

Right Bundle Branch Block and ST Depression in V1-V3. Is that normal? And a complication.

See this case of posterior MI with tiny ST depression:

This was texted to Dr. Smith with "46 year old with chest pain".  

He texted back: "Posterolateral OMI, activate the cath lab".  

This is diagnostic because V2 and V3 have a tiny amount of ST depression which should not be there, AND also a tiny amount of STD in III and aVF, which is reciprocal to a tiny amount of STE in aVL.  And it all fits together as a posterolateral OMI. Cath showed 100% obtuse marginal occlusion and peak troponin I was 85 ng/mL, a very large OMI.

More Discussion by Smith on Posterior Leads

This is a letter to the editor that is a great review: Wong C-K. Usefulness of leads V7, V8, and V9 ST elevation to diagnose isolated posterior myocardial infarction. Int J Cardiol [Internet] 2011;146(3):467–9. Available from: http://dx.doi.org/10.1016/j.ijcard.2010.10.137

The below 2 studies by Matetzky are the best prior evidence on posterior leads vs. ST Depression in V1-V4.  Studies comparing the 2 lead locations compare 1 mm ST depression in V1-V4 with 0.5 mm STE in posterior leads (actually, only one of the 2 studies specified the amount of ST depression and number of leads).  This ignores the fact that most people have at least 1 mm of STE at baseline in leads V2 and V3.  Thus, ANY ST depression in V2 or V3 is abnormal: to require 1 mm STD in these leads will result in poor sensitivity.

Thus, my practice is the following: if there is STD of any amount that is maximal in V1-V4, especially V2 and V3, I will not let absence of STE in posterior leads dissuade me from the diagnosis of posterior OMI.  One might use posterior leads to detect ST depression in those leads, which will support the unlikely possibility that the ST depression in V1-V4 is due to subendocardial ischemia.(Wong)

Baseline ECG has STE in V2, V3 (Surawicz, Macfarlane):

Surawicz B, Parikh SR. Prevalence of male and female patterns of early ventricular repolarization in the normal ECG of males and females from childhood to old age. J Am Coll Cardiol [Internet] 2002;40(10):1870–6. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12446073.

Macfarlane PW, Browne D, Devine B, et al. Modification of ACC/ESC criteria for acute myocardial infarction. J Electrocardiol [Internet] 2004;37 Suppl:98–103. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15534817

This study by Shah et al. shows that the STD of subendocardial ischemia (in contrast to posterior OMI) is maximal in V5 and V6.

Shah A, Wagner GS, Green CL, et al. Electrocardiographic differentiation of the ST-segment depression of acute myocardial injury due to the left circumflex artery occlusion from that of myocardial ischemia of nonocclusive etiologies. Am J Cardiol [Internet] 1997;80(4):512–3. Available from: https://europepmc.org/article/med/9285669

However, STD in V1-V4 can occasionally be due to subendocardial ischemia.  

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.  These authors studied 35 patients with ST depression on exercise test. None had posterior ST Elevation and many had posterior ST depression.

Thus, if posterior leads also show ST depression, then subendocardial ischemia is probable!!  This review supports that, if it is subendocardial ischemia, it should manifest as STD in posterior leads in addition to anterior leads.  The subendocardial ischemia is diffuse, with ST depression pointing outward from all walls except for the "base" of the heart, which has no wall, and therefore the combined ST depression vector is towards the apex (V5, V6)

Matetzky-1:

Matetzky S, Friemark D, Feinberg MS. Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-V9: “hidden” ST-segment elevations revealing acute posterior infarction. J Am Coll Cardiol 1999;34(3):748–53.

33 patients with proven posterior OMI.  Admission ECG. ST-segment elevation was present in leads V7 and V9 in 30 patients (91%) and in all 33 patients in lead V8. ST-segment depression (ST2) was noted in leads V1 through V3 in 20 patients (61%), and in 22 patients (67%) in at least two consecutive leads of the anterior chest leads V1 through V6 (Figs. 1A and 2). Prominent R-waves appeared in lead V1 in 3 patients (9%) and in lead V2 in 14 (44%). The method of measurement of STD was not specified.

Matetzky-2:

Matetzky S, Freimark D, Chouraqui P. Significance of ST segment elevations in posterior chest leads (V7-V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J Am Coll Cardiol 1998;31(3):506–11.

46 of 87 inferior MIs with posterior leads had posterior ST elevation of at least 0.5 mm in 2 consecutive leads of V7-V9.  

Results:

Comparison of ST segment elevation in leads V7 to V9 and ST segment depression in leads V1 to V3. Significant ST segment depression in leads V1 to V3 was noted in 52 patients (60%). The occurrence of ST segment depression in the precordial leads agreed only partially with the occurrence of ST segment elevation in the posterior chest leads. In 10 Group A patients (22%), ST segment depression was not present on the admission ECG, and 16 patients (31%) with ST segment depression in leads V1 to V3 had no ST segment elevation in leads V7 to V9 (Fig. 1).

When ST segment elevation in leads V7 to V9 and ST segment depression in leads V1 to V3 at hospital admission were compared with respect to diagnostic accuracy of posterior involvement (at least severe hypokinesia), ST segment elevation in leads V7 to V9 had a similar sensitivity (80% vs. 72%, p 5 0.34) but a higher specificity (84% vs. 57%, p 5 0.02) and test accuracy (82% vs. 66%, p 5 0.01).

In this study, they required at least 1 mm STD in 2 consecutive leads.

Matetzky-2 makes the following claim (with the references below):

During the acute phase of inferior infarction, ECG detection of posterior infarction rested on the appearance of concomitant ST segment depression in leads V1 to V3  (2–7). However, these changes are relatively insensitive and not specific (3,7,9,10) and may represent inferoseptal infarction (11) or, as suggested earlier by a number of other investigators (12–16), anterior ischemia or non–Q wave MI.

Here are the references:

3. Croft CH, Woodward W, Nicod BP, et al. Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction. Am J Cardiol 1982;50:428 –30.

7. Lew AS, Weiss AT, Shah PK, et al. Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphy evidence of adjacent posterolateral or inferoseptal involvement. J Am Coll Cardiol 1985;5:203–9.

9. Mukharji J, Murray S, Lewis SE, et al. Is anterior ST depression with acute transmural inferior infarction due to posterior infarction? A vectorcardiographic and scintigraphic study. J Am Coll Cardiol 1984;4:28 –34.

10. Cohen M, Blanke H, Karsh KR, Holt J, Rentrop P. Implications of precordial ST segment depression during acute inferior myocardial infarction: arteriographic and ventriculographic correlations during the acute phase. Br Heart J 1984;52:497–501.