A 70-year-old man calls 911 after experiencing sudden, severe chest pain. This is his 12-Lead ECG:
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| What do you think? Computer read: "Non-specific ST abnormality, consider anterior subendocardial ischemia" |
There are very poor R-waves in V1-V4 suggesting old anterior MI. Notably there is profound ST-depression in V1-V4 which prompts the computer's interpretation. Firstly, subendocardial ischemia does not localize on 12-Lead ECG. This means that even if these right precordial ST-depressions do represent subendocardial ischemia, they do not necessarily signify that the ischemia is anterior. Computer algorithms have remained behind the times in this regard.
But the real question at hand is: Are these precordial ST-depressions a result of subendocardial ischemia?
There are two main etiologies of ischemic ST-depression:
1) subendocardial ischemia
2) reciprocal to ST-elevation in an opposite wall
Here there are distinct R-waves with marked ST-depression throughout most of the precordium. Notice that the magnitude of 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-depression pattern on this ECG (and in this clinical setting) should immediately raise suspicion of Posterior STEMI!
Posterior STEMI occurs in approximately 15-20% of acute MI, but the vast majority of the time it is seen in conjunction with inferior (Infero-Posterior) or lateral (Postero-Lateral) STEMI (1). So the next thing I would do is scrutinize the inferior (II, III, aVF) and high lateral (I & aVL) leads for any subtle evidence of concomitant STEMI. This can help in confirmation. But if there is none - then you are looking at least at an Isolated Posterior STEMI until proven otherwise.
In typical Posterior STEMI cases (in association with inferior or lateral wall), the accompanying posterior ECG changes do not change the reperfusion decision and so you may not even notice them at all. But if the MI is isolated to the posterior wall [3-11% of cases (2)], identifying these precordial changes is critical for making the diagnosis!
What's also interesting to note is that there is ST-elevation in V6 on the ECG. What's the significance of this? You often see this in Posterior STEMI (even isolated Posterior STEMI) and it is the result of involvement of the posterior aspect of the lateral wall.
If you "flip" the ECG 180 degrees horizontally and 180 degrees vertically then it is as if recorded from the opposite (posterior) aspect of the heart. You can do this with paper ECG and hold it up to light as you will be looking through the back of the paper.
This is what our patient's ECG looks like flipped:
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| Those "ST-depressions" are actually very concerning ST-elevations. While you don't need to do this (because if there is ST-depression in V1-V3 there will necessarily be ST-elevation on the flipped ECG and it does not help to diagnose the cause of the ST-depression), it may give you a better intuitive sense of what is really happening to the posterior wall! |
Another diagnostic adjunct is to record posterior leads. These are leads placed on the patient's back underneath the left scapula and look directly at the posterior wall. You can move any three leads. I usually use V4-V6 so that they become leads V7-V9 as seen below:
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| 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 0.5mm of ST-elevation in just one lead (of leads V7-V9) is both sensitive and specific for the diagnosis of Posterior STEMI (4,5). Furthermore although there is no literature on morphology of ST-elevation in posterior leads, it is interesting to note that the morphologies of these elevations are in and of themselves concerning as well. |
Case Resolution:
The patient was given aspirin, loaded with ticagrelor and the cath lab was activated. He was found to a have 100% acute, thrombotic Mid-Circumflex lesion.
Conclusion:
Nobody would miss the precordial ST-depressions in this case. The problem is often not in identifying these abnormalities but rather in identifying their etiology. Unfortunately, patients with Isolated Posterior STEMI often do not receive appropriate reperfusion therapy simply because infarction of this anatomical area of the myocardium manifests differently on standard 12-Lead ECG. It is our job to identify this entity and ensure these patients receive the same care they would for a STEMI in any other coronary artery territory.
Tips for recognizing Acute Posterior STEMI:
1. Pattern recognition is one of the most powerful - and often subconscious - mechanism by which we read ECGs. Remember this classic pattern of Posterior STEMI on standard 12-Lead ECG.
2. Remember the trick of "flipping" the ECG. Although it doesn't really add any additional diagnostic value it may help give you a better intuitive sense of what is actually happening to the posterior wall.
3. If you have concern for Posterior STEMI you can always record a Posterior ECG. Elevation of just 0.5 mm in any of leads V7-V9 appears to be most sensitive and specific. Just realize that 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 criterion.
4. Don't forget about Echocardiography. A posterior (inferobasal) wall motion abnormality would confirm Posterior MI. While it was not needed to make the diagnosis in this case it can be quite a powerful diagnostic adjunct.
5. Realize that ultimately none of the above ECG findings 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 can not get their symptoms under control with medical therapy, you must strongly consider that you are dealing with an acute coronary occlusion that will benefit from emergent reperfusion!
Note that the American College of Cardiology and American Heart Association Guidelines for the Treatment of STEMI state that thrombolytics are indeed indicated in this scenario when a true posterior (inferobasal) MI is suspected. So treating these as STEMI is well within the bounds of guideline recommendations (6).
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 S, 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 myocardial ischemia validated by 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-elevations revealing acute posterior infarction. J Am Coll Card 1999; 34:748-753.
6. O'Gara et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. Dec. 2012.
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 enlarge: the 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).
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 enlarge: the 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.
ReferencesPosterior 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.
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.
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.:
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).
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.
thank you both for the true explanation !
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thanks for the feedback!
DeleteGreat case and your entire explain~~
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