Thursday, December 10, 2020

"Pay me now, or pay me later"

This patient presented with acute pulmonary edema without chest pain.

A bit of history prior to showing the ECG:

The patient had been hospitalized at a different hospital for pneumonia and NonSTEMI for a week. The troponin I had peaked at 40 ng/mL, and echo showed multiple wall motion abnormalities and EF of 35%.  The patient suffered third degree heart block with bradycardia and required permanent pacemaker placement.  A troponin that high is usually associated with Occlusion.

I reviewed the ECGs from that hospital and they do not show OMI.  But many ECGs in patients with OMI do not reveal the OMI, even when I interpret them.

The patient unequivocally had myocardial infarction by very high troponin I (of 40 ng/mL!) and was diagnosed with a type 1 MI.

However, for unknown reasons, the patient did not get an angiogram. Without an angiogram there could of course also be no intervention on the ruptured plaque that would have caused this.

That is not standard practice, and I don't know why it was not done.

Then the patient presented with pulmonary edema 2 weeks later.

Here is the ECG:

What do you think?












ED physician interpretation: "Ventricular paced rhythm with ST elevation out of proportion to the preceding S-wave in both V4 and V5.  Meets Smith Modified Sgarbossa Criteria in 2 leads (only 1 is necessary), diagnostic of acute OMI."

Smith interpretation: same.

Cardiology was consulted.

Cardiologist: "Current findings and clinical presentation not a definite STEMI.  In light of multiple WMA on ECG, underlying ECG is highly likely but the anterolateral ECG findings don't guide a treatment path thus far."  --frustrating, no?  Cardiologists still do not widely accept the Modified Sgarbossa Criteria.

Case continued

Nevertheless, due to persistent pain and a very elevated initial troponin I (8256 ng/L), the patient went to the cath lab within a few hours.  

This troponin is so high at presentation probably because it had not yet normalized from the previously known MI. 

Angiogram

Culprit Lesion (s): 80% calcific stenosis in the proximal LAD with TIMI II flow in the apical vessel.

Two vessel CAD of a heavily calcified, left dominant system

Culprit for the patient's NSTEMI and pulmonary edema is uncertain, but LAD was thought to be contributing presentation and was treated percutaneously.

Successful PTCA of the ostial/proximal ramus intermediate with 2.0 x 20 mm to restore flow following plaque shift associated with ostial LAD PCI.


Post PCI ECG:

STE persists, which is a bad prognostic sign and suggests "No Reflow," which is when downstream smaller vessels are clogged with platelet fibrin aggregates.


Troponin Profile
Usually after artery opening, the troponin usually spikes to a high peak.
Perhaps it did not do so due to "No Reflow."


Formal Echo

Decreased left ventricular systolic performance severe.  Regional wall motion abnormality-distal septum anterior and apex.  Regional wall motion abnormality-anterior. Regional wall motion abnormality-inferior.

Outcome

Unfortunately, the patient developed cardiogenic shock and did not survive.


Pay me now or pay me later

One of my mentors, an interventionalist, used to say about NonSTEMI: "Pay me now or pay me later." He meant this: Patients with NonSTEMI, even if a Non Occlusion MI, have culprit lesions (except in the unusual cases of MINOCA) even if the artery is wide open, with TIMI-3 flow.  These need stenting!  The angio and stenting may be delayed up to 24-36-72 hours (no more than 24 is best), but they need it because at some time in the future, the ruptured plaque may thrombose again and the outcome could be bad.  

There are many randomized trials of intervention vs. medical therapy for NonSTEMI, and with a few exceptions they show that intervention improves outcomes, especially if certain high risk features are present.  Even in patients who don't have a bad outcome, many end up needing a stent at a later date.  

These trials are under the general category of "Invasive vs. Conservative Therapy for NonSTEMI".

So if you don't do the intervention on this admission ("pay me now"), it will need to be done at a later time ("pay me later") when the patient has another infarct of the same lesion (if the patient survives it!).

So the fact that this patient who clearly had a significant type 1 MI, with very elevated troponin, heart block, and wall motion abnormalities, did not undergo angiogram is puzzling. Perhaps because of the pneumonia.

In any case, the patient returned with a positive Modified Sgarbossa EKGs and LAD thrombosis and in spite of relatively rapid reperfusion of the artery, did not survive, probably partly due to No Reflow.  

This is very unlikely to have happened if there had been an intervention on the Non-OMI 2 weeks prior.

Learning Points:

1. In general, a type I MI, even if a Non-Occlusion MI (NOMI) should have an angiogram and if a culprit is identified, it should be stented.  There are of course countless considerations that the interventionalist needs to take into account.  That is why I say this is a "general rule."  It is approved by ACC/AHA and ESC guidelines.

2. The Modified Sgarbossa criteria work in ventricular paced rhythm.  Do not ignore them!

3. Absence of ST resolution after PCI is a bad sign and strongly correlates with absence of reperfusion to the microvasculature.  If the epicardial artery is open, this is likely due to No Reflow, or downstream small vessel obstruction. 

4. You can read all about reperfusion and reocclusion in Chapter 27 of my book

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