Saw this ECG while reading through a stack. Lots here: myocardial stunning, MRI viability, P2Y12 inhibitors and CABG.

I had just finished passing the shift off to my partner and the next shift of residents.  It was 11:30 PM.  I turned to the computer system to finish reading any EKGs from the shift and I saw this one, which had been recorded after the end of my shift at 11:11.

Usually these are brought immediately by the tech to the faculty physician.  I'm not certain whether another faculty had seen this or not.

What do you think?

I immediately saw the ST depression in V3 and V4 of at least 1.5 mm.  There is also minimal STD in II, III, aVF.  

When you see this inferior STD, you should not think "inferior ischemia" because ischemic ST depression does not localize to a myocardial territory (it usually manifests with an STD vector towards leads II and V5, with reciprocal ST elevation in aVR).

Instead, when you see this, you should be thinking that it is reciprocal (opposite) ST Elevation in the opposite lead (aVL).  So I looked at aVL and of course there is ST Elevation there; it is miniscule, but so is the QRS!

The STD in V3, V4 is diagnostic of posterior OMI, and this would usually be due to the circumflex or a branch thereof.  And when the circumflex is involved, it is likely that the high lateral wall (aVL) will also be involved.

Therefore, the entire picture presented by this ECG is a circumflex (or branch) OMI.

But it must be in the context of a clinical presentation consistent with ACS.

So I looked at the chief complaint on the computer: "lightheaded".  Hmmm.....

So I went to see the patient.  He stated that he had come in tonight because "felt something right here" and pointed to his chest.  After coaxing, he did admit that the discomfort was still going on.

So we activated the cath lab and obtained another ECG, recorded 33 minutes after the first: 

Yikes

Translation: looks very worrisome!

We did an bedside echo while waiting for the cath team in the middle of the night:

Here you can see that the wall closest to the transducer is contracting and thickening vigorously.  The wall opposite (posterior/lateral wall) is barely moving.

The patient received aspirin, heparin, and ticagrelor.

The first high sensitivity troponin I returned at 22 ng/L (URL = 34 ng/L, so it was normal)

The patient went to the cath lab.

Angiogram (detailed results at the bottom):

Severe 3 vessel disease, with very severe stenoses throughout the circumflex and its branches.  They did not find a specific culprit, and the patient’s pain was gone by the time of the angiogram, so I suspect one of those severe stenoses had a transient thrombosis that autolysed before the angiogram.

There was also distal left main disease.

Due to all this coronary disease, it was determined that bypass surgery (CABG) would be required.

Here is the post angiogram ECG:

Much better than the 2nd ECG; it looks like the first one

The 2nd troponin was over 1000 ng/L, and no more troponins were measured after that.

Formal echocardiogram with contrast:

Normal LV size & wall thickness w severely decreased systolic fct: 

Ejection Fraction = 33%.

Wall motion abnormalities involving basal-mid segments of the inferior, inferoseptum, inferolateral, anterior, and anterolateral walls. The apex is relatively spared.

 

Regional wall motion abnormalities in multiple vascular territories with relative sparing of the apex suggestive of multivessel coronary disease, predominantly involving the RCA and Left circumflex.

Case continued

The patient was considered for Coronary bypass surgery, and so an MRI viability study was done which showed preserved viability and normal ejection fraction.

In other words, the wall motion abnormalities and the low ejection fraction on the day after admission were "myocardial stunning," and NOT due to completed infarction.  It often takes days to weeks for ischemic myocardium that is NOT infarcted to regain function.  One can assess the amount of completed infarction from: Peak troponin (estimate), ECG findings of completed infarction (estimate), or viability studies such as MRI (more exact).  Also, one can do a "convalescent" echocardiogram at 6 weeks after the event, at which time the stunning should be resolved.

A subsequent echo showed EF of 78%.

He underwent Coronary Artery Bypass Surgery 5 days after admission.  The delay was a result of having received ticagrelor in the ED, which makes for bleeding complications.  There is some controversy over the use of P2Y12 inhibitors in ACS.  They are generally recommended for STEMI, but with poor evidence (I would consider this OMI to be analogous to STEMI).  They are discouraged for Non-STEMI.  See below for a brief discussion of P2Y12 inhibitors. 

Learning Points:

1. In the right clinical setting (chest discomfort), ST depression maximal in V1-V4 is posterior OMI until proven otherwise.  STD in V5 and V6 is usually due to non-occlusive etiologies (subendocardial ischemia, including ACS with partial coronary obstruction)

2. Inferior ST depression is reciprocal to high lateral ST Elevation

3. High lateral ST elevation may be minimal, especially when the QRS is small

4. Triple vessel disease without an identified culprit does not mean there was no culprit and no OMI.  It means that the culprit could not be identified and that the artery was open by the time of the angiogram.

5. P2Y12 inhibitors can delay CABG surgery

6. Wall motion abnormalities and poor ejection fraction can reverse if the myocardium is not infarcted.  This is called "myocardial stunning."

Full angiogram results 

Three vessel CAD including distal left main disease and CTO of RCA with left to right and right to right collaterals.

 

Disposition

 

CV surgery consult for CABG due to three vessel CAD and diabetes.  

Potential targets include LIMA-LAD, SVG to OM1, OM2 and dRCA.

No evidence of plaque rupture in any of the large epicardial vessels.

Heparin gtt ACS protocol overnight after removal of TR band.

Nitro gtt in case of chest pain.

Echocardiogram tomorrow am.

 

Coronary Angiography (Note: All Coronary Angiograms were done in the usual views)

 

LMCA: Moderate to large caliber vessel with moderate diffuse disease distally with calcification extending into LAD.

 

LAD: Moderate caliber vessel with severe diffuse disease with calcification in the proximal to mid LAD. The rest of the LAD has diffuse disease without focal stenosis. There are multiple small diagonal branches with diffuse disease. There are septal collaterals supplying RPDA.

 

LCx: Large caliber vessel. There is severe serial stenosis in the proximal to mid segment with calcification. There is moderate caliber bifurcating OM1 with severe ostial stenosis. OM2 is moderate caliber vessel and has moderate to severe proximal stenosis. OM3 is small caliber with diffuse disease.

There are epicardial collaterals supplying the RPLAs.

 

RCA: Large caliber vessel with severe diffuse calcification. It is chronically occluded in the proximal segment. The distal RCA, RPDA and RPLA are filled by right (conus, SA nodal and RV marginal branch) collaterals and also septal collaterals from LAD and epicardial collaterals from LCx.

P2Y12 inhibitors, brief discussion.  

This is copied from a section I (Smith) wrote in the EmRap CorePendium (Dr. Meyers and I wrote the section on Acute Coronary Syndromes)

Here is the section on "Upstream" use of P2Y12 inhibitors, upstream meaning in the ED or ambulance, prior to angiogram "defining" the coronary anatomy: if the anatomy mandates CABG, then they will not be given.  On the other hand, if there will be PCI, a P2Y12 inhibitor must be given.

“Upstream” (pretreatment, in the ED or prehospital) administration of P2Y12 inhibitors and of glycoprotein IIb-IIIa inhibitors.※

• Should dual antiplatelet therapy be given in the ambulance or ED prior to the angiogram? Or should the practitioner wait until the angiogram “defines” the coronary anatomy and the choice of therapy (PCI, CABG, or neither)?
• American College of Emergency Physicians clinical guideline: “P2Y12 inhibitors and glycoprotein IIb/IIIa inhibitors may be given in the ED or delayed until cardiac catheterization” (Level C recommendation).※
• Only prasugrel (NSTEMI with PCI only) and ticagrelor (STEMI with PCI only) have been studied in dedicated trials comparing pretreatment vs. no pretreatment.
  • For patients who are sent immediately for an angiogram (eg, STEMI/occlusion MI):
    • ATLANTIC trial: Ticagrelor
      • Prehospital (31 min earlier than the controls) treatment resulted in 5% more patients (47.5% vs. 42.5%) with ST resolution after PCI (P = .05), a secondary outcome. The outcomes of this trial were considered negative.※
  • For patients undergoing delayed angiogram/PCI (eg, for NSTEMI):
    • For NSTEMI with PCI, P2Y12 inhibitors are typically not given “upstream” (in ED) unless by interventionalist or per interdisciplinary protocol.
    • ACCOAST trial: Prasugrel
      • 30 mg upstream followed by 30 mg at angiography as compared with 60 mg at angiography, had more bleeding with the same ischemic outcomes.※
      • The median was 19 h from symptom onset to angiography.
    • Unstudied problem: Patients who must wait over the weekend, up to 72 h, for an angiogram. Does upstream dual antiplatelet therapy, along with anticoagulants, decrease preprocedure re-infarction?

Here is the section on CABG and P2Y12 inhibitors in Unstable angina/NSTEMI with PCI:

• Only give before PCI with institutional approval due to CABG bleeding risk. CABG is required in up to 16% of NSTEMI cases.※
• However, good evidence of safety and efficacy has been documented even in the CABG group:
  • ACUITY (non-randomized).※
    • Editorial※
  • 1,539 of 13,800 had CABG, with a 5-d washout before CABG
  • A longer length of stay by 3 d was recorded
  • 30-d death/MI/revasc: 17.3% vs. 12.7%, favoring clopidogrel pretreatment
  • No CABG bleeding difference