Posterior Leads Fail to Diagnose Posterior STEMI

For more cases of posterior MI:

http://hqmeded-ecg.blogspot.com/search/label/posterior%20STEMI

A 54 year old male with recent angiogram that showed only scattered coronary lesions of less than 50% developed chest pain at 11:30 AM.  It became progressively worse, so he decided to drive to the ER.  The pain became so intense that he flagged a passing fire truck. They called the medics.  En route to the hospital, the patient went into ventricular fibrillation.  He was defribillated.  It happened again and he was shocked again.

In the ED, here was his first ECG:

Sinus rhythm with a slightly prolonged QRS, but not bundle branch block.  There is ST depression in V2-V4, maximal in V3.  There is also ST depression in II, III, and aVF.   This should always alert to ST elevation in aVL, and, sure enough, aVL has minimal ST elevation. 

This is diagnostic of posterolateral STEMI.  When precordial ST depression is maximal in V1-V3, in contrast to V4-V6, then posterior infarct is the usual etiology.

As stated many times in this blog, high lateral STEMI may show itself primarily through "inferior" reciprocal ST depression.

On the contrary, with ST depression in II, III, aVF and also in precordial leads but maximal in V4-V6, then subendocardial ischemia is fairly certain, often accompanied by ST elevation in aVR.  In such cases (not this one!), the "inferior" ST depression is not reciprocal to ST elevation.

A consulting cardiologist requested posterior leads, but these showed no ST elevation (not shown).  Nevertheless, the patient was taken to the cath lab and found to have a 100% acutely occluded obtuse marginal off the circumflex supplying the posterior and lateral walls.


Why were posterior leads negative?  One must remember that it is a long way from the heart to the back, with a lot of air (lung) interposed.  So the voltage is far less.  A lot of indirect evidence suggests that 0.5 mm of ST elevation in just one of leads V7-V9 is quite sensitive and specific for posterior STEMI, but even 90% sensitivity misses 1 in 10.

Here is a case in which absence of ST elevation in posterior leads helped to diagnose subendocardial ischimia:  http://hqmeded-ecg.blogspot.com/2010/12/st-depression-v2-v4-posterior-leads.html


Here is a worthwhile paper: 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; April 15 2001..

The 12-lead ECG, without the posterior leads, is so clearly due to posterior STEMI that in spite of negative posterior leads, I was certain that this was posterolateral STEMI because:

1) nothing else causes ST depression in II, III, aVF and in right precordial leads greater than left precordial leads
2) high pretest probability for STEMI (chest pain followed by cardiac arrest)

Pretest probability:
--Nearly half of all ventricular fib arrests are due to STEMI
--MI is nearly certain if arrest preceded by chest pain
--Non STEMI can of course also cause ventricular fibrillation, but not nearly as commonly.

An academic note on terminology of posterior MI: Bayes de Luna determined by MRI that what was thought to be posterior MI as manifested by enlarged R-waves in V1-V3 is really "lateral."  One Society changed the terminology; here is the article:
http://circ.ahajournals.org/cgi/content/extract/114/16/1755

The committee on standardization of electrocardiography prefers to keep the term "posterior" for acute MI (I think appropriately):
http://content.onlinejacc.org/cgi/reprint/53/11/1003.pdf  page 1007