Precordial ST depression. What is the diagnosis?

A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG:

Here is the patient's previous ECG:

Here is the patient's presenting ED ECG:

There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6.  There is no ST elevation.  Precordial ST depression may be subendocardial ischemia or posterior STEMI.  How can we tell the difference?  See the list below.



If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)].  This was indeed done:

Notice the limb leads have been reversed (axes of every lead are inverted!).  But we are now concerned with the precordial leads.  V7-V9 (labelled V4-V6) have no ST elevation. 

Notice there is tachycardia.  I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia.  In this case, the patient had failed to take his atenolol in the AM and was having reflex tachycardia in addition to ACS.  BP was 160/100.  He was given metoprolol IV which succuessfully brought his heart rate and BP down.  His chest pain resolved completely, but his ECG continued to show profound ST depression.  We performed a bedside echo and found a posterior wall motion abnormality.

The cath lab was activated and the patient went for immediate angiography, which showed a 95% hazy thrombotic lesion with TIMI III flow in a large first obtuse marginal (OM-1) off the circumflex.  Therefore, the angiographer had time to visualized the other arteries.  The RCA was chronically occluded but supplied a small area.  The LAD had a 75% proximal lesion that by fractional flow reserve was hemodynamically significant.  So there was 3-vessel disease, but with an acute posterior STEMI.  The OM-1 was opened and stented, then the LAD was stented 3 days later.

The acute infarct-related artery was off the circumflex and the affected wall was posterior (STEMI).  The posterior leads were falsely negative.  See far below for data on posterior leads.

Does this matter that the posterior ECG was a false negative?  If there is ST depression (as there is here), it is ACS.  Whether it is subendocardial ischemia or posterior STEMI, if you cannot get it to resolve, you must activate the cath lab.  And even if it is STEMI, if you get it to resolved with medical therapy, then you have opened the artery without intervention and a delay is acceptable.


This is very popular post from almost 4 years ago on posterior MI.  At the bottom are 7 ways to help differentiate the ST depression of posterior STEMI from subendocardial ischemia.  I have copied them here:

Some ways to differentiate subendocardial ischemia from posterior STEMI

First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved.
Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia.
Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs. younger smoker).
Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs.
Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations).
Sixth, placement of posterior leads (take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in just one lead is very sensitive and specific for posterior MI.
Seventh, an immediate echocardiogram can make the distinction.  These are very difficult and it is very hard to detect a posterior wall motion abnormality unless you are very experienced.  I recommend a formal study with Definity before concluding there is no posterior wall motion abnormality.
Eighth, see above.  Whether or not it is STEMI, the cath lab should be activated if the ischemia cannot be controlled medically: aspirin, nitro, beta blockers, clopidogrel, heparin/enoxaparin, GP IIb/IIIa inhibitor. 


Here is a short summary of data on posterior leads, from: 

Critical Decisions in Emergency and Acute Care Electrocardiography.  William Brady and JD Truwit, editors.  Blackwell Publishing 2009. (Smith SW as editor of section on Acute Coronary Syndromes).  This is a quoted excerpt from a chapter that was written by Daniel T. O’laughlin, MD, and edited by me.

Posterior Lead Orientation and Diagnostic Criterion

The posterior precordial leads are positioned in the 5^th intercostal space at the same horizontal line as V6.  Lead V7 is placed at the posterior axillary line, V8 just below the tip of the scapula and V9 at the paravertebral border.¹  STE up to 0.5mm measured at the J point relative to the PR segment in all three leads can be normal.²  Wung and Drew evaluated the posterior ST segment changes during PTCA of the LCX and determined that utilizing a criterion of STE of greater than or equal to 0.5mm, rather than greater than or equal to 1mm, demonstrated a sensitivity of 94% for detecting LCX occlusion related STE.³  This is compared to a sensitivity of 49% when the criterion was greater than or equal to 1mm STE.  Conversely, Matetzky et al. showed 100% specificity for posterior MI of STE greater than or equal to 0.5mm in at least one posterior lead.  In Wung’s study, 81% of patients with greater than or equal to 1mm STE in posterior leads also had other significant STE on the 12-lead ECG, and 96% had some ST deviation.³ However, 22-39% of patients experiencing posterior MI who have greater than or equal to 0.5mm STE in the posterior leads do not demonstrate STD in V1-V3.^3-5

1.         Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the Standardization and Interpretation of the Electrocardiogram: Part I: The Electrocardiogram and Its Technology: A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology. Circulation 2007;115(10):1306-24.

2.         Taha B, Reddy S, Agarwal J, Khaw K. Normal limits of ST segment measurements in posterior ECG leads. J Electrocardiol 1998;31 Suppl:178-9.

3.         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.

4.         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.

5.         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.