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Inferior-posterior Wall M.I.

Dawn's picture
Sat, 06/15/2013 - 21:40 -- Dawn

This 66-year-old man presented with a complaint of chest pain.  His ECG shows a "classic" inferior wall ST-elevation M.I. (STEMI).  The ST elevation is apparent in Leads II, III, and aVF, which are the leads that reflect the inferior wall of the left ventricle.  In addition, this ECG shows ST elevation in Leads V5 and V6, the low lateral wall.  The ST depression in V1 and V2 are reciprocal changes caused by acute injury in the posterior wall. In the majority, the RCA supplies the inferior-posterior wall, the right ventricle, the right atrium (including the SA node and the AV node), and in some, the low lateral wall.  The proximal location of this man's occlusive lesion has caused damage in all these areas.  The relatively slow rate is common in IWMI and can be caused by SA node injury, vagal stimulation, or medications.  Clinical data is not available for this patient.  

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CardioLimassol's picture

Nice example of a proximal RCA occlussion. For confirmation of RV involvement you can consider right sided leads. These proximal RCA infarcts are often complicated by rhythm disturbances, most commonly AV block of varying degrees. For this reason during the setting of primary PCI you have to be prepared for temporary pacing which can be discontinued once the restored flow down the RCA has corrected the arrhythmia.

Dr Stasinos Theodorou


Interventional Cardiologist

Dave Richley's picture

Just a question: how can we tell from this ECG that there is RV invlovement? To me, it just looks like an inferolateral MI.

Dave R's picture

My guess would be that there is no RV involvement in this patient - given the lack of any hint of ST elevation in lead V1 with an ECG picture otherwise totally consistent with acute infero-posterior STEMI. As per Dr. Theodorou - confirmation would be forthcoming with use of right-sided leads (esp. lead V4R).

Ken Grauer, MD   [email protected] 

Dawn's picture
Submitted by Dawn on

Generally accepted "clues" for RV injury are ST segment elevation greater in III than in II, and ST elevation in V1.  Of course, in the setting of POSTERIOR MI, the ST depression in V1 can "cancel out" the elevation caused by RVMI.  I have seen many ECGs in patients with RVMI and PWMI where V1 had a "flat" ST, or slightly coved, as it tried to show both the elevation and depression.  Of course, right sided leads, such as V3R and V4R, are the gold standard.  The are lateral enough to avoid the influence of the posterior wall.

Dawn Altman, Admin's picture


Highly interesting ECG by Dawn on many levels:
On the most Basic Level - there is sinus rhythm with obvious acute infero-postero-lateral STEMI:

  • There is marked inferior ST elevation (in II,III,aVF) - with reciprocal ST depression in leads I, aVL, and V2.
  • Note that small-but-real Q waves have already formed in leads II, III, aVF - plus in V5, V6. Although not very deep - these Q waves are clearly wider-than-would-be-expected for normal sepatal q waves. In the context of this tracing - they clearly indicate infarction that is presumably acutely ongoing.
  • Acute posterior involvement is suggested by the positive "mirror test" in leads V1,V2 (Click HERE for Review of the "Mirror" Test).
  • Acute lateral involvement is suggested by the hyperacute T wave in leads V4,V5,V6 - with frank ST elevation in lateral precordial lead V6.

On a More Advanced Level:

  • This ECG suggests acute RCA (Right Coronary Artery) occlusion - because the amount of ST elevation in lead III > II - and - the amount of reciprocal ST depression in lead aVL > I (Click HERE for Review).
  • In the setting of acute Inferior MI - the anterior ST depression that we see here in leads V1,V2 may be due to one or more of 3 causes: i) Reciprocal changes due to the Inf. MI; ii) Concomitant anterior ischemia (if in addition to RCA occlusion there is also LAD narrowing); and/or iii) Posterior Infarction. These 3 entities comprise our LIST #5 (Click HERE for Review).

On an Even More Advanced Level:

  • The ST-T wave changes in leads V5,V6 probably do not reflect "lateral" infarction in this case - but rather acute "posterior" infarction. There are many who advocate use of a 15-lead ECG for assessment of patients with acute inferior MI - in which the 3 additional leads obtained are V8, V9 and V4R. The thought is that since none of the usual 12 leads on a standard ECG directly assess the posterior wall of the LV - that obtaining Lead V8 (at the tip of the left scapula at the same horizontal level of lead V6) - and Lead V9 (in the left paraspinal area in between the scapula and posterior spine, level with V6) - would show ST elevation with acute posterior MI. That said, in our experience - careful attention to anterior leads with use of the "mirror test" provides equal yield for suggesting acute posterior MI. Lead V6 may provide additional input - since it does provide some posterior perspective (albeit not nearly as sensitive as V8,V9). BUT - if in fact you do see either hyperacute T waves and/or ST elevation in lead V6 in a patient with acute inferior MI suspected to be the result of acute RCA occlusion (because of ST elev in III > II and ST dep in aVL > I ) - this strongly supports acute posterior involvement (See Vince DiGiulio's Medial Approach post on Use of Lead V6 in Posterior MI). This is precisely what we see in this case!
  • In about 15% of patients - it is the LCx (Left Circumflex coronary artery) that is "dominant". In this case - the LCx supplies not only the lateral wall of the LV, but also the inferior and posterior LV walls (Click HERE for Review)
  • As a result - Patients with a left dominant circulation may present with acute infero-postero-lateral MI. That said - We strongly suspect acute RCA occlusion in this case, because ST elevation in lead III > II - and ST depression in lead aVL > I.
  • We also strongly suspect that the ST-T wave changes we see here in leads V1,V2 are predominantly due to acute posterior involvement. Lead V2 is the "perfect reciprocal" of the QRST complex we see in each of the inferior leads. In addition - there is NO ST depression in lead V3, as we would expect to see if anterior changes were due to concomitant LAD narrowing.
  • This patient is in process of an extremely large acute infarction - given infero-posterior involvement and marked ST elevation and depression. Although details of the history are not specified - the patient has potentially much to gain from acute evaluation for possible reperfusion.

Ken Grauer, MD   [email protected] 

Indeed, a nice example of RV-involvement in a proximal occlusion of the right coronary artery. Of course, as Stasinos Theodorou suggests, a right sided ECG, i.e. lead V4R, helps to differentiate whether there is RV-involvement. Another hint here should be the relative big difference in ST-deviation between V1 and V2. Involvement of the posterior wall in a proximal RCA-occlusion would render ST-depression, both in V1 and V2. Here, ST-depression in V1 is relatively masked by ST-elevation of an RV-infarction. This should trigger to consider RV-involvement in a proximal RCA-occlusion.

Dr. Mohamed Boulaksil, MD PhD
Resident in Cardiology's picture

I agree with Dr. Boulaksil that the "setting is right" for acute RV involvement (ie, strong suggestion on ECG of acute proximal RCA occlusion). That said - to my eye, the amount of ST depression that we do see in lead V1 is not all that "masked" given relative size of QRS amplitude in V1 and V2. I'd be more inclined to agree with you if the ST-T wave in V1 was more isoelectric - but it's not. So I think it remains open to debate as to whether this ECG does or does not suggest acute RV involvement. Unfortunately - there is no V4R, and no clinical information. Too bad we'll never know for sure ...

Ken Grauer, MD   [email protected] 

Dave Richley's picture

Good question from aaa! Although AHA have said that they are sticking with the term 'posterior MI' for now, I personally have been impressed by the evidence of Bayes de Luna and others and believe that the characteristic ECG changes of 'posterior' infaction are actually due to lateral wall damage. I suspect that it's just a matter of time before AHA is persuaded by the evidence  from MRI and changes its guidance but the current terminology has been in place for decades so it's perhaps understandable that things don't change overnight.

Dave R

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