H/o MI and stents with brief angina has this ED ECG. And what is Fractional Flow Reserve?

A middle-aged man complained of 15 minutes of classic angina that resolved upon arrival to the ED.

Here is his initial ECG:

What do you think?

There is sinus rhythm with RBBB and possible LPFB (see Dr. Grauer's detail below).  There is ST elevation in II, III, and aVF, and reciprocal ST depression in aVL.  And there are Q-waves in both inferior and lateral leads.   So this is indeed diagnostic of myocardial infarction.

Should we activate the cath lab?

No! Not immediately, at least, because this is NOT diagnostic of ACUTE (occlusion) myocardial infarction (Acute OMI).  We need to do some more investigation.

Although diagnostic of MI, it is highly suspicious for "Old inferior MI with persistent ST Elevation" or "inferior aneurysm morphology" because of the well-formed Q-waves and the flat T-waves.

Inferior aneurysm can look a lot like ACUTE inferior MI because it does not usually have QS-waves (as anterior LV aneurysm usually does); instead, inferior aneurysm usually has QR-waves, which in inferior MI are often seen in BOTH acute and old MI.   QS-waves imply no remaining deplorizing forces toward the overlying lead.  To repeat: in contrast, anterior aneurysm is much more easily distinguished from acute MI due to the QS-waves.

I immediately looked for old charts, which were only available from another hospital, and an old echo confirmed inferior "akinesis" (which may also have persistent ST elevation).  A true anatomic aneurysm has "dyskinesis" (systolic outpouching of the ventricular wall) or "diastolic distortion" (diastolic outpouching of the ventricular wall).

See any of these posts for more on anterior LV aneurysm.

Here are other cases of inferior LV aneurysm.

How did I strongly suspect that this was NOT acute?

1.  The patient's chest pain had resolved by the time of the ECG
2.  There are well-formed Q-waves
3.  The T-waves are flat.  Acute T-waves are large, even if not necessarily hyperacute.


Although this ECG does not demand immediate cath lab activation, it is very worrisome.  It could be acute, though probably is not.  But it does prove that the patient has coronary disease and makes the probability that his chest pain is due to ACS very very high.

In fact, his first troponin I returned at 0.128 ng/mL, with a subsequent falling value, diagnostic of MI.

So I made an ED diagnosis of Non-Occlusion Myocardial Infarction (NOMI), and his next day angiogram confirmed NOMI.  He was treated with aspirin and heparin.

Angiogram:

Widely patent RCA and LAD stents.

Culprit Lesion: Angiographically indeterminate 50% stenosis in the proximal OM2 was assessed further with instantaneous wave free ratio (iFR) of 0.96, which is normal (see below for description of iFR*).

"After normalization in the left main, the pressure wire was advanced to the distal OM2, and iFR was 0.96, suggesting no hemodynamic significance, and no significant drift on pull back."

Therefore, no stent was placed.  (No culprit could be identified, and FFR was negative)

Impression and Recommendations:

Widely patient RCA and LAD stents

No evidence for hemodynamic significance of 50% proximal OM2 stenosis

Diffuse mild to moderate CAD without evidence for severe epicardial stenosis
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A bit about fractional flow reserve (FFR) (with my limited understanding of this, and I put a link in to an excellent article on this below): This is an angiographic technique to assess the pressure gradient across coronary lesions.  It is proven better than angiography alone in stable angina, and also has been shown to improve decisions on stenting non-culprit lesions in ACS.  However, if a culprit lesion is identified in ACS, and has low pressure gradient ("negative" FFR assessment), this does NOT mean it should not be stented -- FFR is not a good assessment for culprit lesions.

*Instantaneous wave-free ratio is performed using high fidelity pressure wires that are passed distal to the coronary stenosis. iFR isolates a specific period in diastole, called the wave-free period, and uses the ratio of distal coronary pressure (Pd) to the pressure observed in the aorta (Pa) over this period. During this wave-free period, the competing forces (waves) that affect coronary flow are quiescent meaning pressure and flow are linearly related as compared to the rest of the cardiac cycle.

Very good summary of the data on Fractional Flow Reserve and Instantaneous Wave Free Ratio:  https://www.acc.org/latest-in-cardiology/articles/2017/05/25/08/34/ffr-in-2017-current-status-in-pci-management

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MY Comment by KEN GRAUER, MD (1/31/2020):

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Interesting case to review! We are told that this middle-aged male patient has a history of prior MI with stents. He presents with an episode of brief, new-onset chest pain that had resolved by the time ECG #1 was obtained.

• For clarity — I’ve reproduced and labeled the ECG shown in this case (Figure-1).

Figure-1: The initial ECG that was done in the ED (See text).

I’d add the following thoughts to the comments by Dr. Smith. 

• Although there is resemblance to an rsR’ pattern in lead V1 — this ECG does not represent a “typical" RBBB. YES, there is a RBBB — because there is a predominant positive triphasic complex in lead V1 that occurs in association with wide terminal S waves in lateral leads I and V6. But a closer look at lead V1 reveals marked fragmentation of the QRS complex in both the small S wave downward deflection, as well as in the bifid terminal R’ (Be sure to look at the magnified view of ECG #1, by clicking on the Figure!).
• Fragmentation of the QRS complex is marked, and present in numerous leads in ECG #1 (ie, in each of the inferior leads — and, dramatically so in the upslope of the S wave in lead V2, and to a lesser extent in the S wave of lead V3). The phenomenon of fragmentation has been discussed and illustrated numerous times on Dr. Smith’s ECG Blog (I’ll add reference to THIS CASE of mine). The importance of recognizing fragmentation (especially when it is as marked as it is in ECG #1) — is that it tells us there has been scarring, which may be the result of prior infarction, cardiomyopathy, or some other form of structural heart disease. Such fragmentation does not tell us whether heart disease is acute or has been present long-term — but even IF we had not been told that the patient in this case had prior MI with stents — it would be very clear from the fragmentation we see in ECG #1, that this patient has severe underlying structural heart disease!
• There are 2 clues that scarring in ECG #1 is the result of prior MI: i) There is even fragmentation within 2 of the 3 inferior Q waves (RED arrows); and, ii) Q waves are not only present in the chest leads, but these Q waves begin as early as lead V3 (BLUE arrows) — and extend through to lead V6 (with the Q in V6 being deeper-than-is-likely-to-be-seen with a normal septal q wave). It is uncommon that you will see septal q waves as far over as lead V4. Septal q waves should simply not occur as early as lead V3. And — the presence of RBBB does not account for Q waves in these 4 chest leads. BOTTOM Line: The presence of inferior and antero-lateral Q waves in ECG #1 is diagnostic of inferior and anterolateral MI that must have occurred at some point in time.

Otherwise — I would not diagnose LPHB (Left Posterior HemiBlock) on this tracing ( = my opinion). Instead — I would describe the conduction defection as RBBB alone.

• It is well to keep in mind that among the bifascicular blocks (ie, RBBB/LAHB and RBBB/LPHB) — RBBB/LAHB is far more common (ie, more than 90-95% of the bifascicular blocks in my experience manifest Left Anterior HemiBlock instead of LPHB). The reasons for this are simple: i) The left posterior hemifascicle is much thicker anatomically than the left anterior hemifascicle; and, ii) The posterior hemifascicle has a dual blood supply. As a result of these 2 factors — much more extensive damage is needed to produce true RBBB/LPHB.
• NOTE — It is rare to see a true isolated LPHB. Instead, when LPHB does occur — it is almost always seen in association with RBBB, as a form of bifascicular block. In contrast — isolated LAHB is extremely common, especially in older individuals. And as just mentioned — RBBB/LAHB is by far the most common form of bifascicular block.
• Terminology — While I have seen significant variation among cardiologists regarding the criteria they use for diagnosing LPHB — the criteria I have always used require clear predominant negativity for the QRS complex in lead I. When assessing a tracing for possible LPHB in a patient who also has RBBB — it is the straight downward portion of R wave descent into the S wave in lead I that should be assessed (ie, the portion of the QRS before the terminal delay produced by the RBBB). Predominant negativity of the QRS complex in lead I is not present in ECG #1. Note the positive portion of this straight-line descent (ie, the vertical RED line in lead I) equals the negative portion (ie, the vertical GREEN line in lead I) — so predominant negativity is lacking.

Finally — As per Dr. Smith, the ST-T wave changes we see in ECG #1 do not look acute. Instead, T waves in multiple leads (ie, leads I, aVL, V2-thru-V6) look flat. In addition, ST segments in these leads lack the gentle upsloping that is usually seen in a normal tracing.

• Typically, with simple RBBB — there is slight ST depression with more marked T wave inversion in lead V1 than we see in ECG #1.
• There is ~1 mm of ST elevation in each of the inferior leads. That said — the shape of the ST segment in these inferior leads manifests gentle upsloping (ie, it just doesn’t look acute).
• Although there is some scooping to the ST segment in lead aVL — the J-point in lead aVL is not depressed. Therefore, the “magical” reciprocal relationship seen between leads III and aVL with acute inferior OMI is not seen in ECG #1 (See My Comment in the 1/29/2020 post, among many other references to this phenomenon in Dr. Smith’s blog).
• THE ABOVE SAID — We can not overlook the fact that: i) This middle-aged man has documented severe underlying coronary disease — and, he presents with new (albeit short-lived) chest pain; ii) There is ST elevation in each of the inferior leads in ECG #1; iii) We were not given a prior tracing for comparison (so we do not know for certain which ECG changes are old) — and, iv) It is possible that the ST-T wave flattening we see so diffusely in ECG #1 could be, at least in part, a “net effect” of prior ST-T depression + new ST elevation, in which the "net" result is some cancelling out of opposing forces (ie, "pseudo-normalization"). 
• BOTTOM LINE: I agree entirely with Dr. Smith. The ECG findings we see in ECG #1 do not look acute — BUT — it is impossible to be certain that these findings are not acute from this single ECG, which is why more investigation was indicated for final decision-making.

Our THANKS to Dr. Smith for presenting this case!