Tuesday, December 27, 2011

Subtle Lateral ST elevation. False positive. This diagnosis is hard.

Case 1.  A middle-aged woman presented with severe substernal crushing chest pain radiating to the left shoulder.  This was her presenting ECG:
There is a Q-wave in aVL and Minimal ST elevation in I and aVL (less than 0.5 mm) in the context of a 10 mm QRS.  There is minimal reciprocal ST depression in III.  There are some features of left anterior fascicular block, but  there is not enough left axis deviation to meet criteria for this.  This could be high lateral MI with circumflex or diagonal occlusion.
Management options are to get an immediate echocardiogram, look for old EKGs (there were none), do serial ECGs, or just do an immediate angiogram.  The interventionalist was consulted and he opted to go for immediate cath.  It was negative.

Below are 3 typical cases (cases 2-4) of lateral ST elevation with inferior reciprocal ST depression that were actually circumflex or diagonal occlusions.  In these cases, the findings are not as subtle as in case 1.  But when you look at the last case (case 5), you'll see how subtle real occlusion can be.  

It is important to remember that only about 50% of lateral MI due to coronary occlusion have significant ST elevation, and for this reason the lateral wall is often called "electrocardiographically silent."  Often this is due to low QRS voltage in lateral leads, and because ST elevation is always proportional to the QRS, the ST eleavtion is low voltage.  (See Schmitt et al. Chest 2001;120(5):1540-6, free full text)

Case 2.
Acute Circumflex occlusion (also old inferior MI with Q-waves, and early repol giving anterior STE)

Case 3.
Lateral STEMI with very low voltage QRS in aVL, therefore very low voltage STE in aVL, but best seen by marked ST depression in inferior leads.  Diagonal occlusion.  Remember ST depression in inferior leads is not inferior ischemia, but rather reciprocal to lateral STEMI
Case 4.
Circumflex occlusion with hyperacute T wave in aVL and reciprocal inferior ST depression.  Notice the precordial ST depression of concomitant posterior STEMI.




Case 5a.
D2 occlusion, lateral MI

Case 5b.
After nitroglycerine, inferior ST depression and STE in aVL resolve.  D2 is open by the time of angiography.

Here is one of the most popular posts of all time, also relevant to this:  ST depression does not localize: 2 cases of "inferior" ST depression of high lateral STEMI. 

8 comments:

  1. Great cases Dr. Smith...
    one observation... the "subtle" lateral MI ECG's seem to have some left axis deviation, but not much with leads I and II being positive and III negative, while the less subtle lateral MI's have more pathological left axis deviation..
    is that just a coincidence?

    ReplyDelete
  2. Dave,

    The first one (case 2) has left axis because of the old inferior MI

    Case 3 has a left axis deviation (directly vertical), so that would not correlate with the rule you are trying to make, right?

    Case 4 has an inferior, normal, axis.

    So I'm not sure there is a rule here, but maybe

    ReplyDelete
  3. what was the eventual outcome of case 1/false positive?

    ReplyDelete
  4. what sinister medical entity did you guys decide on that was responsible for her crushing chest pain?

    ReplyDelete
  5. Good question. We see this often: serious chest pain with no apparent etiology. Much of it is probably esophageal spasm. Some small amount may be angina in which the angiographer cannot see a lesion (smooth lesion or spasm). Most of these, if they are causing ECG abnormalties, have a positive troponin also and the ECG evolves. And then there is just the mystery of unexplained chest pain!!

    ReplyDelete
  6. Dr. Smith,

    Here and in other posts I have seen you comment on the importance of interpreting ST changes in the context of the QRS amplitude. We recently had a case of an inferior STEMI that did not quite meet STE criteria (max elevation was ~ 0.8mm), but the EKG was very low voltage. I looked at the EKG and immediately said inferior STEMI, but when challenging to backup the practice of interpreting the STE in the context of the QRS size, I could not find any literature to support this. The 2001 CHEST article you cite above does not seem to address the issue of what to do with STE that is not large enough to meet STEMI criteria but is proportionally very large relative to the QRS. Is this proportional approach borne out of your experience, or is there also literature to support looking at the ratio of STE to QRS amplitude in the setting of LOW voltage? (I know you and others have looked at such ratios in LBBB, PPM, LVH, and other high voltage states).

    Many thanks for the outstanding education on your site, and any thoughts you can provide on this issue,
    Mark

    ReplyDelete
    Replies
    1. Mark,
      The only literature I know of is my own studies of early repol, LV aneurysm, LBBB.
      But there is also literature on "lead strength", especially in relation to stress tests:
      https://scholar.google.com/scholar?hl=en&q=lead+strength+electrocardiogram+ST&btnG=&as_sdt=1%2C24&as_sdtp=

      But I don't think it even requires literature. By simple electrophysiology, it is axiomatic that repolarization will be proportional to depolarization, but this is just not well appreciated and recognized. Sometimes simple truths just do not occur to people or penetrate their preconceptions, and we have been so programmed to measure millimeters of ST elevation that the obvious (which is contrary) can seem revolutionary.

      Physicians are a very conservative group and new ideas, even though obviously true, are hard for them to accept, especially when they contradict textbooks, statements of professional societies, etc.

      New paradigms to not readily enter the lexicon.

      Here T/R ratio and ST/R ratio was far better than ST elevation. The formula was immeasurably better than any ST elevation criteria: http://www.annemergmed.com/article/S0196-0644(12)00160-6/pdf

      Steve

      Delete

Recommended Resources