When there is less than 1 mm of ST depression, can you make the diagnosis of posterior OMI?

 Submitted and written by Alex Bracey MD, edits by Smith and Meyers

I went to see the next patient who had presented to the Emergency Department for chest pain. Before walking into the room I reviewed the triage ECG taken moments before.

What do you think?

Sinus rhythm with ST depression (STD) in V2-V5, with maximal STD of less than 1mm in lead V3-V4.

Close-up of the STD with red lines overlain. Compare the top of the line at the QRS onset to the top of the line at the J-point.

When there is less than 1 mm of ST depression, can you make the diagnosis of posterior OMI?

While subtle, the STD is certainly present and highly suggestive of posterior OMI. Because there is no clear evidence of concomitant OMI in the other three walls of the LV (inferior, lateral, or anterior), this could be called "isolated" posterior OMI.

In speaking with the patient, she was a woman in her 60s who had experienced 3 days of stuttering chest discomfort that radiated to her neck, described as a heaviness. She had experienced an episode that was more profound than the preceding days which prompted her presentation to the ED.

A bedside echo was performed which showed a posterior wall motion abnormality.

She was given aspirin and heparin while I discussed the case with the cardiology attending, who ultimately agreed to activate the cath lab despite the late hour. 

After the conversation concluded, the initial troponin I resulted at 4.00 ng/mL.

Angiogram:

Coronary angiogram demonstrating 100% thrombosis of the LCX with TIMI 0 flow.

 Coronary angiogram post-DES deployment to the proximal LCX with TIMI flow 3 restored.

The patient had an uncomplicated post-catheterization course, during which troponin I peaked at 32 ng/mL (large infarct -- but it could have been much larger. She was discharged home after several days without apparent limitations.

Formal echocardiogram (without contrast) was performed approximately 48 hours after arrival and did not show any wall motion abnormalities.

Discussion

Approximately 10% of OMIs will involve the posterior wall, most of which also have concomitant involvement of the lateral and/or inferior walls (though usually not meeting STEMI criteria). Isolated posterior OMI, however, manifests as STD without associated STE since the subepicardial myocardial ischemia that would normally generate STE on overlying leads is occurring in the opposing or negative vector compared to the recording ECG leads. The majority of isolated posterior OMIs will be due to occlusion of the LCX, RCA, or a variety of their posterior branches.

The 4th Universal Definition of Myocardial Infarction defines posterior OMI as STE greater than or equal to 0.5 mm in leads V7-V9 (posterior leads) and only mentions STD in V1-V3 as potentially indicating LCX OMI, though it refers to these findings as "nonspecific." Posterior leads, however, will not always demonstrate STE of even 0.5 mm even with clear evidence of OMI in standard ECG configuration, since more lung tissue separates the heart from the posterior ECG leads and air is a poor conductor of electricity. It is not surprising, then, that isolated posterior OMIs are often missed and associated with worse outcomes.

Teaching Points

 - Isolated posterior OMI may manifest as STD maximal in leads V1-V4. That STD may be less than 1 mm. Remember that the vast majority of individuals have normal, baseline, non-ischemic STE in V2 and V3 (hence the STEMI "criteria" require 1.5 - 2.5 mm for diagnosis). Thus, even an isoelectric J-point could be relative ST depression, and any ST depression in these leads is abnormal. 

 - Bedside echo with clear regional wall motion abnormality may help to confirm subtle but concerning ECG findings of OMI

 - Posterior leads may be helpful in the diagnosis of posterior OMI with STE thresholds of 0.5mm in any of leads V7-V9; however, since air is a poor conductor of electricity, even this small amount of STE may not manifest despite OMI. Our opinion is that posterior leads very rarely add information to careful inspection of the standard 12 leads for the presence of STD maximal in V1-V4, as long as one does not require a full millimeter of STD in those anterior leads.  The one exception is this: one study (Poh et al.) shows that diffuse subendocardial ischemia manifests ST depression, not ST elevation, in posterior leads, and this is consistent with electrophysiology. 

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