Ischemic ST depression maximal in V1-V4 (vs. V5-V6), even if less than 0.1 millivolt, is specific for Occlusion Myocardial Infarction (vs. subendocardial non-occlusive ischemia)

This is a case from many years ago that I discovered recently.  The patient has heart failure as a result of this event.

A 50-something man with history only of alcohol abuse and hypertension (not on meds) presented with sudden left chest pain, sharp, radiating down left arm, cramping, that waxes and wanes but never goes completely away.  There was SOB at the start and increased work of breathing.  He had been drinking 5 beers.  He does not seek medical attention often.  He called 911.  

Medics recorded this ECG:

There is a lot of artifact, but you can clearly see ST depression in V2 and V3.

There is no significant ST Elevation.

In this setting, this is diagnostic of Posterior OMI.

They gave him 2 nitroglycerine and transported to the ED.

In the ED, the patient was "moaning, writhing in bed, and clutching his chest."

Here is the first ED ECG (there was no previous ECG on file for comparison):

Sinus rhythm and LVH

There is some (less than 1 mm) of STD in V3 and V4.

If this STD were due to LVH or to subendocardial ischemia, rather than posterior OMI, it would be maximal in V5 and V6.

Since V3 usually has non-ischemic ST elevation at baseline, ANY ST depression is abnormal and should be considered to be ischemic.

Exceptions are when STD is expected: in RBBB, hypokalemia, seen on previous ECGs.

  

If it is maximal in V1-V4, and the patient's presentation in consistent with ACS (as this certainly is), then it is DIAGNOSTIC of Occlusion with 90% specificity 

(We have an upcoming article that proves this).

This was not recognized.  The patient was started on a nitro drip.  The initial troponin I returned at 0.67 ng/mL (URL = 0.030 ng/mL).  

A chest X-ray was obtained:

This was read by radiology as "Bilateral lower lobe interstitial opacities. Differential favors aspiration/developing pneumonia and follow to resolution recommended."

To me, this looks like pulmonary edema.

The patient did not have a cough or fever.

A bedside ultrasound was done, with dozens of clips, and was even done with Speckle Tracking.  Here are a few clips.  (Sorry for the sound effects -- explanation is complicated)

Parasternal Short Axis:

This clearly shows a posterior wall motion abnormality

Apical 4-chamber

Poor LV function. Several walls are not contracting and thickening normally.

Speckle Tracking Apical 4-chamber

Very poor LV function

Lung (this is only one side, but both sides looked the same)

B Lines typical of pulmonary edema, and not typical of pneumonia

This ultrasound was formally interpreted later as showing exactly what it shows:

Window: Subxiphoid, Parasternal Short Axis, Parasternal Long Axis and
Apical 4-Chamber

Findings: Poor LV systolic function with lateral wall motion abnormality.  
No pericardial effusion.  B-line predominance bilateral lungs indicates
pulmonary edema.

Impression: Poor LV systolic function with lateral wall motion
abnormality.  No pericardial effusion.  B-line predominance bilateral
lungs indicates pulmonary edema.

A 2nd ED ECG was done at 3 hours after chest pain onset:

ST depression maximal in V2-V4 persists, and is actually a bit more profound.

There is also some minimal STE in aVL, with slight, possible, STD in inferior leads.  By itself these would not be diagnostic as they do not have typical morphology (flat T-waves, possible atrial repolarization wave to account for ST depression).  If I saw this without the STD V2-V4, I would not make anything of it, and even with that precordial STD, I am not convinced that it is a manifestation of ischemia.

At 5 hours after onset, the 2nd troponin returned at 1.33 ng/mL, and another ECG was recorded and was identical.

This was recorded at 6 hours after onset:

The ST depression is resolved.  The normal amount of expected STE is now present in V2-V4.  The T-waves are taller.  This all appears to represent reperfusion of the posterior wall.

Symptoms persisted however.

Cardiology was not consulted in a timely manner, but they were consulted at some point.  The cath lab was not activated emergently.

8 hours after pain onset, the patient went for angiogram.

Clinical course:

Patient was treated with antibiotics for "pneumonia," aspirin, heparin, zyprexa and morphine for pain, and set up for an angiogram at a convenient time.

Angiogram: 

"ACS - Non ST Elevation Myocardial Infarction. persistent pain despite medical Rx brought emergently to Cath lab."

Meyers note: notice in their documentation many of the classic mistakes of the STEMI generation: "Non ST Elevation MI" as their reasoning for why the patient did not merit emergent reperfusion, while simultaneously calling it "emergently" (after 8 hours!!!) All guidelines in the world suggest that ACS patients with ongoing pain despite medical management require emergent cath within 2 hours, yet in our USA experience this does not usually happen. Also there is the problem that they used opioids and other adjuncts to mask pain, prolonging the time until realized as "persistent pain despite medical Rx", further preventing the patient from receiving timely reperfusion therapy.

Culprit is 100% occlusion in the proximal LCX.

Here are the serial troponins:

Peak Troponin I of 196 ng/mL (=196,000) ng/L).  This is a HUGE myocardial infarction.  And it barely shows on the ECG.  This is one of the highest troponins I have ever seen, and there are many studies using MRI that show that peak troponin is a reasonably good marker of infarct size.

Formal echo:

The estimated left ventricular ejection fraction is 39 %

 

Regional wall motion abnormality-inferolateral .

Left ventricular hypertrophy concentric .

Regional wall motion abnormality-posterior .

Regional wall motion abnormality-lateral .

Decreased left ventricular systolic performance moderate .

2 months later, he presented in pulmonary edema with atrial flutter and formal echo had EF 20%

Why did this happen?  How could an occlusion (Occlusion MI, OMI) that results in the loss of a massive amount of myocardium and results in Heart Failure be missed?

Because we are hypnotized the STEMI paradigm.  "If there is no STEMI, there is no emergent problem and the patient can wait."

Why should we have recognized this was an Occlusion MI (OMI)? (It was not a STEMI)

1. Patient had no prior cardiac history except for hypertension.

2. Symptoms were classic for MI

3. ECG showed ST depression maximal in V2-V4, which is diagnostic of posterior OMI.

4. We should not have been fooled by the radiology reading of "pneumonia". There was no cough or fever, the CXR looks like pulmonary edema, the ultrasound showed classic pulmonary edema B lines.

5. We did not pay attention to the bedside echo which, by itself, was diagnostic of OMI.

6. The patient was given morphine, which is associated with worse outcomes in NonSTEMI (probably because it fools you into thinking you have treated the ischemia).  I only give morphine after I am committed to the cath lab).

7. Alcohol intoxication?  That may have played a role in biasing the clinicians.

In this article, we showed that expert interpretation using expanded criteria for Occlusion MI (beyond ST Elevation) was more than twice as sensitive as STEMI criteria, with equal specificity, for occlusion MI.  Many of these occlusion MI were posterior:

Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction

We published this abstract for SAEM (the details in the full manuscript are fascinating; it is under review at the Journal of the American Heart Association):

Ischemic ST depression maximal in V1-V4 (vs. V5-V6), even if less than 0.1 millivolt, is specific for Occlusion Myocardial Infarction (vs. subendocardial non-occlusive ischemia)

ABSTRACT 

Background: 

Occlusion Myocardial Infarctions (OMI) of the posterior and lateral walls are the most commonly missed, with >50% of circumflex occlusions not receiving emergent reperfusion and suffering double mortality, partly because posterior OMI is not well identified by STEMI criteria. ST depression (STD) maximal in leads V1-V4 (STDmaxV1-4), in contrast to STD maximal in V5 and V6, has been suggested as a possible indicator of posterior OMI. We sought to evaluate the diagnostic accuracy of STDmaxV1-4 for OMI.

Methods:

We performed a retrospective review of a high-risk ACS population. OMI was defined from prior studies as an acute culprit lesion with either TIMI 0-2 flow, or TIMI 3 flow plus peak troponin T >1.0 ng/mL or troponin I >10 ng/mL. STEMI was defined by the 4th universal definition of MI. ECGs were interpreted for OMI, as well as various characteristics of ST depression, blinded to outcomes.

Results:

Among 808 patients, there were 265 OMIs with 108 (41%) meeting STEMI criteria. 118 (15%) patients had “suspected ischemic” STDmaxV1-4, of which 106 (90%) had an acute culprit lesion, 99 (84%) had OMI, and 95 (81%) underwent PCI. Suspected ischemic STDmaxV1-4 had 97% specificity for OMI. Of the 99 OMIs detected by STDmaxV1-4, 34% had <1mm STD, and only 47 (47%) had accompanying STEMI criteria, of which 17 (36%) were identified a median of 1.00 hour earlier by STDmaxV1-4 than by STEMI criteria. There was no association of T-wave orientation with OMI. Despite statistically identical infarct size, TIMI 0/1 flow, and coronary interventions, patients with STEMI(-) OMI and STDmaxV1-4 were significantly less likely to undergo cardiac catheterization within 90 minutes compared with STEMI(+) OMI and STDmaxV1-4 (46% vs. 68%, p=0.028).

Conclusion: 

Among high-risk ACS patients, the specificity for OMI of suspected ischemic STDmaxV1-4 was 97%. STEMI criteria missed half of OMIs detected by STDmaxV1-4. These data support that any ischemic STD maximal in V1-V4 in ACS is due to OMI until proven otherwise.