Monday, November 10, 2008

Classic LV aneurysm (persistent ST elevation after previous MI)

70 yo with h/o MI, recent CABG, has acute onset of chest pain.

What are the worrisome EKG findings, and what is the differential diagnosis? What is the most likely diagnosis? What info would you like to have to make a decision?

There are deep QS waves in V1 and V2, and tiny R-waves in V3 and V4. With ST elevation in V1-V3, one must always entertain the possibility of acute MI in this patient with CP. The differential is wider, however, and mostly includes "old MI with persistent ST elevation," otherwise known as "left ventricular aneurysm morphology". This morphology is very common after an old and completed or nearly completed anterior MI. By complete, that is to say that there was no early reperfusion (spontaneous or therapy related). It was, in the old terminology, a "transmural" infarction. More accurately, there was a substantial mass of myocardium that died (infarcted, meaning irreversibly). Very often, such large anterior MI result in persistent ST elevation and they may or may not have a demonstrable "LV aneurysm" by echo. Echocardiographically, this is called "diastolic dyskinesia", meaning that the infarcted territory is thinned out and bulges even in diastole. Much of the time, there is only "akinesis", meaning no contraction of that territory. The important point is that old MI frequently has persistent ST elevation.
This is an example of "old MI with persistent ST elevation". So how do you differentiate old MI from acute MI? First, there are deep QS waves. Although anterior MI may have Q waves very early after onset, these are always QR waves (Q waves followed by an R-wave). The fact that there are zero anterior forces should lead you to think that there is no remaining anterior wall left to infarct. Second, in acute MI, as long as there is significant viable myocardium, the T wave is usually upright; remember that acute MI has large T waves. Lastly, acute infarction should have not only an upright T wave, but a prominent one. The "hyperacute T wave" is not simply a phenomenon of early infarction; it is simply more visible early on.
If you want a rule, I derived one a few years ago (AJEM 23(3):279-287; May 2005). Comparing proven acute LAD occlusion to patients with proven old MI and diastolic dysfunction and ST elevation, I found that the T/QRS ratio in any one of leads V1-V4 was almost always higher than 0.36 in acute MI, and almost always lower in LV aneurysm. Better was a T amplitude (V1+V2+V3+V4) / QRS amplitude (V1+V2+V3+V4) <> 0.22. The only acute MI's missed by this rule had at least 6 hours since symptoms onset.
I cannot tell from this ECG if it is 12 hours or 12 years since the MI. But looking through the records, I found that he had an old anterior MI with anterior apical akinesis.
He did have improvement of pain on a nitro drip, so we admitted to the CCU. He ruled out for MI.


  1. Interesting...thanks Sir !

  2. First of all, thank you for this wonderful blog. I've been going through all the posts and learned a lot. And that's exactly why I have to correct a statement in the post above: diastolic dysfunction refers to the inability of the LV to relax and fill in diastole, and the dyskinetic area bulges out in systole, when the rest of the ventricle contracts.
    Looking forward to new cases!

    1. Thank you for pointing that out, it was a typo: I meant to write "diastolic dyskinesia" and will shortly correct that.

  3. do u manage such patients as unstable angina with LMWH? whats the role of heparin in such situations?

    1. I would prefer LMWH if our interventionalists would also prefer it. But if they do not, one should not use it. For management of ACS, including anticoagulants, see my lectures here:

  4. Very interesting! Thank you!
    How do you calculate the amplitude of the QRS complex when you have R and S waves? Do you sum them or count only the S wave?


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