Saturday, December 5, 2009

Posterior ST Elevation MI in the Setting of Right Bundle Branch Block, with Posterior Leads V7-V9

This is a 68 year old man who had a resuscitated cardiac arrest. His prehospital ECG looks identical to this one which was recorded upon arrival to the ED:

There is sinus rhythm with a wide QRS, with rSR' in V1 and a wide S-wave in lateral leads, consistent with right bundle branch block (RBBB). ST elevation or depression in RBBB is not difficult to find if you identify the end of the QRS. In this case, the QRS duration is about 135 ms, and in V2 and V3 there are 2 small S-waves; only after these S-waves does the ST segment begin. There is also almost 4 mm of ST depression in right precordial lead V3. Some ST depression (up to 1 mm) in the opposite direction (discordant) to the positive QRS is normal in RBBB, as in V1 here. This much ST depression (V2 and V3) is always abnormal (ischemia).

Most posterior STEMI is in conjunction with either inferior STEMI, lateral STEMI, or both. Only 3-11% of all MI are isolated posterior. In this case, there is no ST elevation elsewhere on the ECG. Marked isolated ST depression in the right precordial leads in a clinical scenario consistent with STEMI is usually posterior STEMI. Such ST depression can also (much less likely) be due to subendocardial ischemia. Two modalities that can help are: 1) recording posterior leads V7-V9 and 2) echocardiography with a posterior wall motion abnormality. In this case, both were done. The posterior ECG is shown here and was done 31 minutes later. Leads labelled V4-V6 were actually recorded on the back as leads V7-V9 (V7 at posterior axillary line, even with tip of scapula; V9 paraspinal at same level; V8 between them).

There is only one lead with ST elevation, lead V9 (labelled V6). There is approx 0.75 mm of ST elevation. Up to 0.5 mm is within normal limits, but any amount in even one lead >/= 0.5 is abnormal and very sensitive and specific for posterior STEMI (Matetzky S. et al. JACC 1998;31:506-511. Matetzky S et al. JACC 1999;34:748-753. Taha B et al. J Electrocardiol 1998;31(Suppl):178-9. Wung SF et al. Am J Cardiol 2001;87:970-974;A4.) Moreover, the QRS amplitude in V9 is tiny, and the ST elevation is very high in proportion. Similarly, there is also now a small amount of ST Elevation (< 1 mm in context of very small QRS) in aVL, suggestive of lateral STEMI.

Emergency physician performed bedside echocardiogram showed evidence of posterior wall motion abnormality and no anterior WMA. Immediate angiography showed a thrombotic occlusion of the mid circumflex, as well as disease in the RCA and LAD. Formal Echo the next day confirmed posteriorlateral WMA. Max troponin I was 12 ng/ml.

Approximately 75% of posterior STEMI will manifest at least 1 mm of anterior ST depression. (Matetzky S et al. JACC 1999;34:748-753. Wung SF et al. Am J Cardiol 2001;87:970-974;A4.)


  1. Dr. Smith -

    It's a fascinating case, no doubt, and I see how the ST-elevation in lead V9 is supportive (along with the bedside echo). I also know from personal experience that isolated posterior STEMI is sometimes diagnosed as NSTEMI (which is doubly bad because in addition to the patient not being emergenty cathed it's not recognized as a STEMI fallout). So I can see why modified leads V7-V9 are utilized.

    Here's my question.

    Are you familiar with any cases of isolated posterior STEMI where the right precordial leads looked perfectly normal? Also, would you have felt comfortable calling in the cath team based on the first ECG in this case? How often do guys get a quick bedside echo for marginal cases and what has this done for your percentage of false positives?



  2. Tom,

    Right precordial leads do not help with this diagnosis. Only leads V1R and V2R are likely to be abnormal, and that is because they correspond to leads V2 and V1, respectively.

    I would feel comfortable activating the cath lab in this case without echo.

    TRITON-TIMI 38 showed that 26% of patients with "anterior" ST depression have an occluded artery (Gibson CM et al. Abstract 1999: Angiographic and Clinical Outcomes Among Patients with Acute Coronary Syndrome Presenting with Isolated Anterior ST-Segment Depressions. Circulation. 2008;118:S_654.). Unfornutately, the study has not been published and the details are most important.

    Previous studies suggest that ST depression of > 2mm in V1-V3 is 90% specific for posterior MI. Posterior ST elevation clinches the diagnosis

  3. Dr. Smith -

    Thanks for the reply.

    Perhaps you addressed this in the first paragraph of your reply, but to your knowledge have any studies measured the sensitivity of ST-depression in leads V1-V3 for acute posterior STEMI?

    Best regards,


  4. Tom,

    This has not been studied directly, but from two of the studies listed above, one can indirectly say that approximatey 75% of posterior STEMI manifest at least 1 mm of ST depression in anterior leads. (Matetzky S et al. JACC 1999;34:748-753. Wung SF et al. Am J Cardiol 2001;87:970-974;A4.)


  5. Wt about ST depression in V4,5

  6. As ST depression gets out to V4-V6, it becomes more likely that it is a result of subendocardial ischemia. But it still can be posterior STEMI.

  7. re: Posterior MI

    vs Septal Ischemia (Chan TC, et al. ECG in EM and Acute care):
    1. R/S ratio <1
    2. R wave width <0.03 sec

    vs Subendocardial Ischemia (Emerg MEd Clin N Am 24 (2006) 53-89):
    1. STD is transient and downsloping (post MI is usually upsloping)
    2. STD extends up to V6

    But I think the algorithm should be, if you see STD on anterior leads, just do posterior leads which the nurses on my place don't do.

    This particular case is very tough, by looking at the ECG alone, I thought it's a classic RBBB.

    This is a real great site, btw.

    Dr Smith, do you have any data on incidence of isolated RV infarct?

  8. This is a reply to JD's comment on downsloping and upsloping and R/S ratio's.

    I, in fact, wrote both sections that you are referring to (Chan TC et al. and Em Clin N Am), and was using the best evidence available (opinion, mostly), but it is not good evidence. These are ideas that have survived from the pre-angiographic era, but have little evidence to support them, and many counterexamples. This is one area that needs a lot of data, and even angiographic data must be critically appraised.

    One of the problems with the data is that the ECG is recorded at a different time from the angiogram. For instance, it is my belief, which I have yet to prove, that posterior STEMI that has a persistently occluded artery has an inverted T wave. The idea that posterior STEMI has an upright T wave comes from posterior STEMIs that have spontaneously reperfused. When they reperfuse, that inverted T wave becomes upright. The angiogram shows a culprit in a posterior artery, and the echo shows posterior wall motion abnormality, so the erroneous conclusion is that posterior MI may have an upright T. But I believe only reperfused posterior STEMI has an upright T.

    As for isolated RV infarct, it is very uncommon. I do have one case in my book (Case 15-3 in "The ECG in Acute MI"), but it is a case in which there was an old inferior MI from distal RCA occlusion, with resulting Q waves, and then a new, superimposed, proximal occlusion with ST elevation in V1-V3.

    Thanks for the nice comment!