Severe Chest Pain on ED Arrival, after Wellens' waves Seen on Prehospital ECG

A 40-something woman called 911 in the middle of the night for Chest pain that was intermittent.   

On arrival, she complained of severe pain.

The medics had recorded this ECG and were uncertain whether it was recorded during chest pain:

Let's get a better image with use of the PM Cardio app:

What do you think?

There is deep T-wave inversion in proximal LAD territory (V2-V4, I, aVL) that is all but diagnostic of Wellens'. This is acute ACS, but it almost always seen in a pain free state.  Since the patient has active pain now, if this is indeed Wellens,' she must be re-occluded at this moment.  

An ED ECG, if recorded with pain, should show LAD OMI.

So this ECG was immediately recorded: 

Indeed, as predicted, a patient with previous Wellens' waves who now definitely has chest pain has acute Occlusion, with new ST elevation in I, aVL, V2-V5.

The Cath lab was activated.

Repeat ECG while waiting for cath team, t = 56 min after arrival:

It is getting worse

Angiogram showed 99% acute proximal LAD thrombosis.  It was opened and stented.

Initial hs troponin I returned at 48 ng/L

Post PCI ECG:

This shows huge persistent ST Elevation and suggests that there is "No Reflow", meaning that there is so much downstream platelet-fibrin aggregates obstructing small vessel flow, that there is poor tissue reperfusion.  This may be seen on angiogram as poor "blush" or a low "TIMI Myocardial Perfusion (TMP) Grade."  

Low TMP grade correlates very well with resolution of ST Elevation.  

Relationship of TIMI Myocardial Perfusion Grade to Mortality After Administration of Thrombolytic Drugs

Time-to-treatment significantly affects the extent of ST-segment resolution and myocardial blush in patients with acute myocardial infarction treated by primary angioplasty

6 hour post PCI ECG:

The ST Elevation has mostly resolved, but there are deep QS-waves, another sign of significant myocardial loss.

Peak trop ＞ 50,000 ng/L

Formal Bubble contrast echo

Severe LV systolic dysfunction.

The estimated left ventricular ejection fraction is 33 %.

Regional wall motion abnormality-mid and apical segments of the septum, anterior, anterolateral and apex, large and akinetic.

Regional wall motion abnormality-apical inferior, akinetic .

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My Comment by KEN GRAUER, MD (3/13/2023):

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Today's case illustrates optimal clinical use of a pre-hospital Wellens' pattern for understanding the evolution of acute OMI. KEY Point: Correlation by Dr. Smith of the pre-hospital ECG with patient symptoms shows how optimal care can be expedited in practice.

• For ease of comparison in Figure-1 — I've put together 3 of the serial ECGs in today's case.

Figure-1: Comparison between selective ECGs from today's case. (To improve visualization — I've digitized the top tracing using PMcardio).

MY Thoughts on the ECGs in Figure-1:

As per Dr. Smith — in the setting of a patient with new chest pain — the initial ECG in today's case ( = ECG #1 — obtained by the EMS team prior to ED arrival) — is diagnostic of ACS (Acute Coronary Syndrome) until proven otherwise.

• Unfortunately — the paramedics did not write down whether today's patient was (or was not) having chest pain at the time they recorded ECG #1. To qualify as "Wellens' Syndrome" — the period of total coronary occlusion should be brief, with the deep T wave inversion on ECG reflecting a now pain-free state following spontaneous reperfusion of the "culprit" artery.
• That said — severe chest pain was present at the time the patient arrived in the ED (corresponding to the time ECG #2 was recorded).
• 
  
• KEY Point (that I'll again cite Dr. Smith on from his above discussion) — If ECG #1 indeed reflects Wellens' Syndrome — then the fact that the patient was having severe chest pain at the moment she arrived in the ED must mean that the "culprit" vessel has reoccluded. This presumed change in chest pain severity on ED arrival is indication to immediately repeat the ECG.
• Confirmation of "culprit" vessel reocclusion was forthcoming on this repeat ECG (ie, marked new ST elevation now seen in leads I,aVL; and V2,V3,V4 — with increased reciprocal inferior lead ST depression — as seen in ECG #2 in Figure-1). Thus, correlation of the presence and severity of chest pain with ECG findings prompted immediate repeat of the ECG — which indisputably established the need for immediate cath lab activation.

Reflections on the 3 ECGs in Figure-1:

The final ECG in today's case was ECG #5 — obtained ~6 hours following successful PCI. The patient was pain-free at this time — and the "culprit" vessel was at least partially perfusing.

• Note that once again — there is deep, symmetric T wave inversion in multiple leads. This appearance is consistent with reperfusion T waves. This supports our presumption that at some point in time during the evolutionary process in today's case — the similar-looking deep, symmetric T wave inversion in multiple leads from ECG #1 did reflect at least some component of spontaneous reperfusion. Unfortunately — the "culprit" vessel reoccluded.
• 
  
• Unfortunately — there remains 1-2 mm of residual ST elevation in multiple leads in ECG #5 (ie, in leads I,aVL; and in V2-thru-V6). In addition — large Q waves have developed in multiple leads, including fragmented QS complexes in leads V4,V5. Thus, despite prompt activation of the cath lab in today's case — the myocardial damage evident on ECG #5 is extensive (ie, the R wave in lead I has now been lost — and a tiny R wave in lead V6 is all that remains of positive precordial forces).

KEY "Take-Home" Point: 

• Correlation of the presence and severity of chest pain correlated to the timing of each serial ECG — is KEY for appreciating the status (open or closed) of the "culprit" vessel.