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.