Written by Jesse McLaren, with edits from Smith and Grauer
A 60 year old with no past medical history presented with two hours of chest pain radiating to the left arm, with normal vitals. What do you think?
I sent this to Dr. Meyers without any other information, and he responded, “do you have a prior to make sure that it is all just because of the delta wave? Would be careful to make sure it’s not inferoposterior OMI superimposed on baseline WPW.”
In other words, when there are ST/T wave changes the first question is whether there’s abnormal depolarization, because this will be followed by abnormal repolarization. Here there is WPW with pre-excitation (short PR and delta wave that widens the QRS). In this case there are tall R waves in precordial leads (from a left sided accessory pathway), which are followed by discordant ST depression and T wave inversion.
But the second question is whether or not there is superimposed signs of Occlusion MI. WPW causes appropriately discordant ST/T wave changes, so superimposed OMI can be identified by inappropriately concordant or excessively discordant ST/T changes. Here, there could be subtle inferior concordant ST elevation from inferior OMI, and the precordial ST depression could be exaggerated by superimposed posterior OMI.
There were no prior ECGs, the first ECG was signed off as unremarkable, and the patient waited to be seen. An hour later the first troponin returned at 49 ng/L (normal <16 in females and <26 in males), so the patient was brought into an acute bed and the ECG was repeated, with ongoing symptoms. What do you think?
The WPW pattern has disappeared (all conduction via the AV node, not the accessory pathway). But there is still precordial tall R waves with ST depression, along with inferior ST elevation and hyperacute T wave with reciprocal STD/TWI in aVL. Now, none of this can be attributed to secondary repolarization abnormalities: it is all primary ischemic changes, which are diagnostic of inferoposterior OMI. But it doesn’t meet STEMI criteria, and was not identified by the computer or the over-reading cardiologist.
The emergency physician wasn’t sure what to make of the changes from one ECG to the next but was concerned about ACS. So they gave the patient aspirin and plavix, repeated the ECG and trop, and called for a stat cardiology consult. Here’s the third ECG, 30 minutes after the second. What do you think?
Still no WPW pattern, and more obvious inferoposterior OMI, but still STEMI negative. A second trop 90 minutes after the first had doubled to 97. The cardiologist then assessed the patient, and a fourth ECG was done 2 hours after the third. What do you think?
The WPW pattern has returned, but with intermittent normal conduction in beats 2-3, which have less STE and normal T waves. So there’s an element of reperfusion, and now inferior leads with accessory pathway conduction have lost their initial concordant elevation and developed appropriate discordance.
A 15 lead ECG was done 7 minutes later – with V5-6 as V8-9:
Now every beat has accessory pathway conduction, without any sign of occlusion.
Compare this with the first ECG:
Both have similar degrees of pre-excitation. But compared with the recent ECG (bottom), the first ECG (top) had inferior concordant ST elevation with subtle reciprocal STD in aVL from superimposed inferior OMI, and excessively discordant STD in V2 from superimposed posterior OMI--confirming Dr. Meyers' initial warning.
But despite the transient reperfusion on the ECG the patient continued to have pain, with a rising trop, and inferobasal (formerly called "posterior") wall motion abnormality on bedside echo. So the cardiologist activated the cath lab: 100% proximal RCA occlusion, ECG-to-Activation time of 4 hours, and peak troponin 24,000 ng/L.
On discharge the WPW pattern was gone again, revealing inferior Q waves and reperfusion T wave inversion, and tall anterior T waves from posterior reperfusion.
WPW, previous Q wave MI, and acute coronary occlusion
Depending on the location of the accessory pathway, WPW pattern can mimic ventricular hypertrophy (including RVH or LVH) or myocardial infarction (including anterior, inferior, lateral or posterior MI) [1]. So the first step is identifying WPW: short PR, delta wave with slurred QRS, and discordant ST/T changes. WPW can mimic old MI with persisting Q wave. But as a study of pseudo-Q waves in WPW found, "In the case of WPW, Q wave-T wave vector discordance results from secondary T wave changes. As a result, depolarization and repolarization vectors are oriented in opposite directions," while T wave inversion concordant with Q waves would suggest myocardial infarction.[2]
Conduction through the accessory pathway can be intermittent (with different degrees of pre-excitation), and affected by ischemia. As a review explained, “some pathways may only carry impulses in the retrograde manner and thus are ‘concealed’ conduction pathways; these pathways are ‘silent’—normal PR interval and QRS complex and the absence of the Delta wave—on the resting 12-lead ECG. In other cases, the bypass tracts conduct intermittently, depending upon other factors such as cardioactive medication use, physiological stressors with catecholamine release, the development of coronary ischemia, and normal aging.”[3] So a patient with WPW can have the pattern induced by ischemia, and there is also a report of a patient with pre-existing WPW which was “ablated” by myocardial infarction after an LAD occlusion.[4]
The sequence of ECGs above shows the pitfalls and pearls of identifying OMI in the presence of WPW:
- ECG #1: WPW with pre-excitation + superimposed OMI (concordant and excessively discordant ST changes)
- ECG #2-3: WPW with normal conduction, and obvious OMI
- ECG #4: intermittent WPW with subtle OMI during normal conduction
- ECG #5: WPW with pre-excitation and without sign of OMI, from transient reperfusion
- discharge ECG: WPW with normal conduction, and reperfusion
So the easiest way to identify OMI in the presence of WPW is if there are periods of normal conduction. But if there is pre-excitation, we can draw from the principle of appropriate discordance: as with other causes of abnormal depolarization (hypertrophy or bundle branch block), WPW causes discordant ST/T wave changes, so acute coronary occlusion can be identified by inappropriate concordant or excessively discordant changes--for example this case of WPW with LAD occlusion causing concordant T waves[5].
On the other hand, STEMI criteria failed on every ECG: not only did it fail to identify infero-posterior OMI during normal conduction, but it can't identify OMI in the presence of abnormal conduction (whether LVH, LBBB or WPW).
See these 5 cases of WPW mimicking and/or obscuring acute OMI
Take home
1. WPW can mimic hypertrophy or old infarct, so the first step is identifying the presence of the accessory pathway: short PR, delta wave which widens the QRS, and discordant ST/T changes
2.
WPW causes discordant ST/T changes, so OMI can
be identified by concordant or excessively discordant changes – and comparing
to baseline (if available) can be helpful if there are similar degrees of pre-excitation
3. Serial ECGs can also be helpful, especially if there are periods of normal conduction that can reveal primary ischemic changes without secondary repolarization abnormalities, or periods of reperfusion showing return of appropriate discordance
References
(first 2 are for WPW with pseudo-Q mimicking old MI, last 2 are WPW + LAD OMI)
1. Khan and Shaw. Pseudo ventricular hypertrophy and pseudo myocardial infarction in Wolff-Parkinson-White syndrome. Am J Emerg Med 2000.
2.
Goldberger. Pseudo-infarct patterns in
Wolff-Parkinson-White syndrome: importance of Q wave-T wave vector discordance.
3. Rosner et al. Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues. Am J Emerg Med 1999.
4. Chang and Liu. Wolff-Parkinson-White syndrome ‘cured’ by myocardial infarction? CMAJ 2014.
5. Chang and Liu. Wolf-Parkinson-White syndrome influenced by myocardial infarction. Int J Cardiol 2014.
- WPW is not a common in adults. It definitely occurs — and all emergency providers who have practiced for any length of time have seen a series of patients with WPW on ECG. That said — the estimated prevalence of WPW on ECG in the general adult population is ~2/1000 (and many of those individuals with WPW only manifest preexcitation on ECG intermittently).
- Emergency providers may have a "sense" of a more frequent occurrence — but that is because many (most) of the patients with WPW who are seen in emergency care present with problematic tachyarrhythmias. As a result — the diagnostic dilemma of trying to identify acute OMI in a patient with overt preexcitation (ie, WPW) on ECG is not a common problem. Our accuracy for the interpretation of any particular ECG entity is likely to be significantly reduced when we only encounter that entity on a infrequent basis.
- There is no "Gold Standard" for the ECG diagnosis of acute OMI that occurs in association with WPW. That's because WPW is "the Great Mimic" — in that this ECG entity may manifest any of a multitude of QRS morphologies (depending on the origin and path of the AP [accessory pathway] ). As a result — WPW on ECG may mimic LVH, RVH, LBBB, RBBB and/or any unusual type of IVCD.
- As per Dr. McLaren — conditions that alter ventricular depolarization also alter ventricular repolarization. With WPW — this alteration occurs in an unpredictable way. In short — it is exceedingly difficult in many cases to tell if ST-T wave appearance in the various ECG leads is a result of AP conduction — or — AP conduction plus ST-T wave changes from superimposed OMI. Therein lies the dilemma!
- It is because of how uncommon it is to be able to confidently identify acute OMI on the ECG of a patient with WPW — that we need to remain vigilant to this possibility.
- The beauty of today's case by Dr. McLaren — is that preexcitation was intermittent. This allowed confirmation during periods of normal conduction that acute OMI was occurring! It also provided us with invaluable insight — by illustrating via direct comparison (during periods of normal conduction) the alterations in ST-T wave morphology that WPW may produce.
- Unfortunately, the reality is — that many (most) WPW patients who present with chest pain do not manifest intermittent preexcitation. In such cases — recognition of acute OMI will be especially challenging!
- The rhythm in ECG #1 — is sinus bradycardia and arrhythmia. Delta waves are seen in 11/12 leads. In most of these leads — the PR interval is clearly shortened, with resultant QRS widening.
- NOTE #1: Depending on the relative amount of "preexcitation" (ie, what percentage of conduction passes over the normal AV nodal pathway vs over the AP) — you may see delta waves in more (or fewer) leads — and the QRS complex may be more or less widened. In Figure-1 — it appears that the degree of preexcitation must at the least, be nearly complete.
- NOTE #2: I see no suggestion of WPW in lead I. The P wave in this lead looks normal — it is not followed by a delta wave — and the QRS does not look widened. It is easy to imagine that IF there was a lesser degree of preexcitation — that more leads might look "normal" (as does lead I) — in which case it may not always be obvious (or at all evident) that a given patient has WPW from a single ECG.
- While true that there is subtle unexpected ST segment coving in the inferior leads in ECG #1 (which we saw when compared with the 2nd and 3rd ECGs during normal conduction in this case — corresponded to inferior lead ST elevation) — this inferior lead ST-T wave appearance in Figure-1 was not diagnostic to me. I was not at all confident that this appearance represented inferior OMI.
- In contrast — I'm simply not used to seeing the J-point ST depression in the leads that I've marked with RED arrows in Figure-1 as representing a simple repolarization change from WPW. Although I was not confident about the ST depression in these leads (that I thought could reflect WPW-related changes) — it was the unexpected amount of J-point depression in this patient with WPW and new-onset chest pain that prompted me to conclude — "Assume acute OMI until proven otherwise".
- CLICK HERE — for a similar case of a patient with WPW and new-onset chest pain. Would you have recognized the acute posterior OMI?
- CLICK HERE — for an example of acute OMI in a patient with intermittent preexcitation (occurring every-other-beat)!
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| Figure-1: I've labeled the J-point depression in the initial ECG of today's case. |
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