Right precordial ST depression in a patient with chest pain

This case comes from Sam Ghali  (@EM_RESUS).  Thanks, Sam!


A 70-year-old man calls 911 after experiencing sudden, severe chest pain. Here is his Emergency Department 12-Lead ECG:
What do you think?
Computer read: “Non-specific ST abnormality, consider anterior subendocardial ischemia”

There is profound ST segment depression in V1-V4, which is what prompts the computer’s interpretation.

There are also very poor R-waves in V1-V4, suggesting old anterior MI

Firstly, subendocardial ischemia does not localize on 12-Lead ECG. This means that even if the right precordial ST-depression does represent subendocardial ischemia, it does not necessarily signify that the ischemia is anterior. Computer algorithms are out of date in this and many other ways.

Ischemic ST depression can be of two sorts:
1) subendocardial ischemia
2) reciprocal to ST elevation in an opposite wall


Is this precordial ST depression a result of subendocardial ischemia or is it reciprocal to posterior STEMI?


There are distinct R-waves with marked ST-depression throughout most of the precordium. Notice that the ST depression is greatest in leads V2-V4. This is a subtle, but crucial point. Precordial ST-depression is very common with subendocardial ischemia, but in those cases the vector of maximal depression is typically towards V4-V6.


The precordial ST-depressions on this ECG in this clinical setting should immediately raise suspicion for Posterior STEMI.

Posterior STEMI occurs in approximately 15-20% of AMI, but the majority of the time it is seen in conjunction with Inferior (Infero-Posterior) or Lateral (Postero-Lateral) STEMI (1). Therefore, when there is precordial ST depression, scrutinize inferior (II, III, aVF) and high lateral (I and aVL, and even leads V5 and V6) leads for any subtle evidence of concomitant STEMI. This can help in confirmation. But if there is none, then in a patient with maximal ST depression in V2-V4 (not V3-V6), the diagnosis is Isolated Posterior STEMI until proven otherwise.
In typical Posterior STEMI cases (in association with inferior or lateral wall), the accompanying posterior ECG changes may be quite subtle and since they don’t change the reperfusion decision, you may not notice them.  But if the MI is isolated to the posterior wall (about 8% of STEMI cases), identifying these precordial changes is critical in making the diagnosis (2)

Furthermore, there is also a hint of ST elevation in V6.  What is the significance?  
Such STE is frequently seen in posterior STEMI because even isolated posterior STEMI often involves the posterior aspect of the lateral wall. 

If you “flip” the ECG, 180 degrees vertically, then it is as if recorded from the opposite (posterior) wall.   You can do this with a paper ECG and hold it up to a light as you will be looking through the back on the paper.  


This is what this patient’s ECG looks like “flipped,” as if you are recording the posterior wall:

 That “ST-depression” is actually due to posterior ST-Elevation. 

In reality, you did not need to flip it: if there is ST depression in V1-V3, there will necessarily be ST elevation on the flipped ECG. 
Flipping does not help to diagnose the cause of the ST depression!!



Another diagnostic adjunct is to record posterior leadsThese leads are placed on the patients back underneath the left scapula and look directly at the posterior wall. Swing leads V4-V6 around to the back so that all 3 are at the level of the tip of the scapula, with lead V7 at the posterior axillary line, V8 at the scapula tip, and V9 at the paraspinal line.  

This is what you get:

Notice V4-V6 are now labeled V7-V9 respectively. Since these leads are further from the heart and must penetrate through the electrically insulating air of the lungs, only 0.5 mm of ST Elevation in just one lead of leads V7-V9 is both sensitive and specific for the diagnosis of posterior STEMI (4, 5).   


Case continued


The patient was given aspirin, loaded with ticagrelor and the cath lab was activated.  He was found to have a 100% acute, thrombotic Mid-Circumflex lesion.





Conclusion:
Nobody would miss the precordial ST-depressions in this case. The problem is not in identifying these abnormalities, but rather in identifying their etiology.  Patients with Isolated Posterior STEMI often do not receive appropriate reperfusion therapy simply because infarction of this anatomical area of the myocardium may manifests without ST Elevation on standard 12-Lead ECG. 


Tips for recognizing Acute Posterior STEMI:

1. Pattern recognition is one of the most powerful – and often subconscious – mechanisms by which we read ECGs. Remember this classic pattern of Posterior STEMI of Standard 12-Lead ECG.
2. Remember the trick of “Flipping” the ECG
3. You can always record a Posterior ECG. Elevation of 0.5 mm in any of leads V7-V9 appear to be most sensitive and specific. (Note: while the sensitivity of this criterion is good, it is not 100%. There may be cases of acute Posterior STEMI that simply will not meet this).
4. Realize that ultimately none of the above will make the diagnosis of Posterior STEMI often enough. Therein lies the limitation of electrocardiography in diagnosing acute coronary occlusion. The most important concept to remember is that if you clinically feel your patient is experiencing ischemic chest pain and you cannot control the symptoms with medical therapy, you must strongly consider that you’re dealing with an acute coronary occlusion that will benefit from emergent reperfusion. 
5. Echocardiography is always helpful.  An inferobasal wall motion abnormality (formerly called posterior, and correlates with posterior MI) confirms posterior MI.
6. The American College of Cardiology and American Heart Association Guidelines for the Treatment of STEMI (2013) state that thrombolytics are indicated for posterior STEMI (STE V1-V4) and even for ST depression from subendocardial ischemia with ST elevation in aVR.   So treating these as STEMI is well within the bounds of standards.  (Antman 2004)
7. You really don’t have to distinguish Posterior MI from subendocardial ischemia: any ST depression that is refractory to medical management should go emergently to the cath lab, whether it is reciprocal ST depression (precordial ST depression of posterior STEMI is reciprocal to the posterior wall) or due to subendocardial ischemia.

References:
1. Brady WJ, Erling B, Pollack M, Chan TC. Electrocardiographic Manifestations:
Acute posterior wall myocardial infarction. J Emerg Med 2001; 20:391-401.
2. Smith  SW, Zvosec Deborah, Sharkey Scott. The ECG in Acute MI – An Evidence Based Manual of Reperfusion Therapy 2002.
3. Van Gorselen EO, Verheugt FW, Meursing BT, Oude Ophuis AJ. Posterior myocardial infarction: the dark side of the moon. Neth Heart J. 2007; 15: 16-21.
4. Wung SF, Drew BJ. New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction. Am J Cardiol 2001; 87:970-4; A4.
5. Matetzky S, Friemark D, Feinberg MS, et al. 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 Card 1999; 34:748-753. 

More comments by Smith

Isolated precordial ST depression (without ST elevation) in ACS  

Isolated precordial ST depression (STD) may be due to either subendocardial ischemia (usually V4-V6) or be reciprocal to posterior ST Elevation (maximal STD in V1-V4).  There are several studies that indirectly reveal the proportion of STEMIs that are isolated to the posterior wall, and they range from 3% to 11%.(1, 2) 

A large substudy of the TRITON-TIMI 38 trial (ref. 2.5), which included 3534 true STEMI, showed that 1/3 of the acute MI that had presented with “isolated precordial ST depression” (no STE elsewhere) in leads V1-V4 who had a non-urgent angiogram (mean time, 29 hours) turned out to have acute coronary occlusion (n = 314).  These patients had worse outcomes than patients with ST depression without occlusion; half of these were circumflex.  As approximately 25% of occluded arteries will autolyse within 24 hours, many of those with open arteries would have been occluded at the time of ECG recording, so it is estimated that half of patients with STD in V1-V4 have acute occlusion.  Only a handful of these 314 patients got the benefit of emergent reperfusion therapy. 


If maximal in V1-V4, then it is due to occlusion affecting the posterior (now often called lateral, or inferobasal) wall.(3) Another slightly smaller study of NSTEMIs had nearly identical results.(4)  


Acute Posterior STEMI: Upright or inverted T-waves?  It is a misconception that acute posterior MI presenting with precordial STD must have upright T-waves; in reality, they may be either inverted or upright. The classic criteria for a posterior MI, with ST depression, a prominent R wave, and an upright T wave in the right precordial leads likely represents a subacute, evolved MI.(5)   Emphasis on these criteria could potentially delay recognition of truly acute posterior pattern: ST depression in the right-precordial leads, without significant R waves, and often with a fully inverted T wave  (6).  


Mechanism of T-wave orientation: Anterior leads represent summation of electrical activity from both the closer anterior wall, and the more distant posterior wall. In acute posterior MI, the posterior wall has hyperacute T-waves with a posterior vector (negative in anterior leads).  The summation of the positive vector from anterior leads and negative vector from posterior leads may result in either a positive or negative T-wave in anterior leads.  


With evolution, or especially after reperfusion, T-waves in posterior STEMI are always upright in precordial leads, and enlargethe posterior wall T-wave vector turns anterior, and combined with positive anterior wall T-waves consistently results in an upright T-wave in anterior leads. Thus, reperfusion especially produces tall, peaked, anterior T waves, which we call “posterior reperfusion T-waves” or Wellens’ syndrome of the posterior wall.(7)  Authors in the past have confused acutely occluded posterior MI (which may have either upright or inverted T-waves) with, on the other hand, prolonged or reperfused posterior MI (both of which do indeed have upright T-waves).  


Is there a tall R-wave in right precordial leads in acute posterior STEMI?  Similarly, a tall R-wave in V1 or V2 is not a feature of acute posterior STEMI, but of evolving MI and represents myocardial necrosis, analogous to Q-waves. 

Posterior leads: Posterior leads V7-V9 are valuable for diagnosing posterior MI. About half of patients receiving elective balloon angioplasty of the circumflex will show posterior STE ≥ 1mm.(8-12)   Because of low voltages in posterior leads, the STE threshold for diagnosis is only ≥  0.5 mm in ≥ 1 posterior lead and has few false positives.(6)  Use of posterior leads in ED patients without a high suspicion of ischemia does not show advantages beyond a standard 12-lead, but it does improve sensitivity in patients with high suspicion of ACS. (13, 14).  When the standard 12-lead is diagnostic of posterior MI, posterior leads may be falsely negative!  
This is especially true if the posterior ECG is done much later than the initial ECG; by this time, the artery may have spontaneously reperfused, and the right precordial ST depression may have also resolved.  In any case, ST depression in V2 should always show up as ST elevation in lead V8: they are opposite!  The magnitude may be different, but the direction should be opposite.  If it is not, then the state of the artery may have changed.


References

1.  Wang T, Zhang M, Fu Y, et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non–ST-elevation acute coronary syndromes undergoing diagnostic angiography Am Heart J 2009;157:716-23

2.    Matetzky S, Friemark D, Feinberg MS, et al. 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 Card 1999;34(3):748-53.


2.5  Pride YB, Tung P, Mohanavelu S, et al. Angiographic and Clinical Outcomes Among Patients With Acute Coronary Syndromes Presenting With Isolated Anterior ST-Segment Depression: A TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) Substudy Journal of the American College of Cardiology: Cardiovascular Interventions 2010;3:806-11.

3.    Matetzky S, Freimark D, Chouraqui P, et al. 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 Card 1998;31(3):506-11.

4.  Wung SF, Drew BJ. New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction. Am J Cardiol 2001;87(8):970-4

5.  Birnbaum Y, Baves de Luna A, Fiol M. Common pitfalls in the interpretation of electrocardiograms from patients with acute coronary syndromes with narrow QRS: a consensus report. J Electrocardiol. 2012 Sep;45(5):463-75.

6.    Boden WE, Kleiger RE, Gibson RS. Electrocardiographic evolution of posterior acute myocardial infarction: importance of early precordial ST-segment depression.Am J Cardiol 1987 Apr 1;59(8):782-7.

7.  Driver BE. Shroff G. Smith SW.  Posterior reperfusion T-waves: Wellens’ syndrome of the posterior wall. Emergency Medicine Journal 34(2):119.  July 2016.
8.    Goldwasser D, Senthlikumar A, Bayes de Luna A. Lateral MI Explains the Presence of Prominent R Wave (R ≥ S) in V1. Ann Noninvasive Electrocardiol. 2015 Nov;20(6):570-7. 

9.    Anand U, Kulkarni MD, Renee B. Clinical use of posterior electrocardiographic leads: A prospective electrocardiographic analysis during coronary occlusion. April 1996 Volume 131, Issue 4, Pages 736-741

10.    Chia BL, Tan HC, Yip JW. Electrocardiographic patterns in posterior chest leads (V7, V8, V9) in normal subjects. Am J Cardiol. 2000 Apr 1;85(7):911-2, A10.

11. Rosengarten P, Kelly AM, Dixon D. Does routine use of the 15-lead ECG improve the diagnosis of acute myocardial infarction in patients with chest pain? Emerg Med (Fremantle).2001 Jun;13(2):190-3.

12. Trägårdh E, Claesson M, Wagner GS. Detection of acute myocardial infarction using the 12-lead ECG plus inverted leads versus the 16-lead ECG (with additional posterior and right-sided chest electrodes). Clin Physiol Funct Imaging. 2007 Nov;27(6):368-74.


13. Langer A, Goodman SG, Topol EJ, et al. Late assessment of thrombolytic efficacy (LATE) study: prognosis in patients with non-Q wave myocardial infarction. J Am Coll Cardiol 1996;27:1327-32.

Annotated Bibliography of Langer et al.:


Langer A et al., Late Assessment of Thrombolytic Efficacy (LATE) Study: Prognosis in patients with non-Q wave myocardial infarction, 1996 and Braunwald E et al, Non-Q-wave and ST segment depression myocardial infarction: Is there a role for thrombolytic therapy? 1996.  

Methods:  Langer et al. (167), with Braunwald et al. (168), performed a post-hoc analysis of data from the LATE trial (169) (see Appendix).

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Findings:  Of 5711 patients, 1480 patients presented with ST depression without elevation; 4759 of 5711 patients (83%) ruled in for AMI by a CK enzyme level twice normal.  Of these 4759, 1309 (28%) had non-Q-wave AMI, of whom 528 (40%) had isolated ST depression of at least 2 mm.  Thirty-five day mortality in this group was 8.6% (tPA) vs. 16.6% (placebo).  One-year mortality was 20.1% (tPA) vs.31.9% (placebo).  In fact, this analysis indicated that ALL of the benefit of tPA demonstrated in the LATE study was in this subgroup of isolated ST depression of at least 2mm. Patients with ST elevation who were treated at least 6 hours post-symptom onset appeared not to benefit.


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