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Written by Jesse McLaren
A 65 year old with a history of atrial flutter, CABG and end-stage renal disease on dialysis presented with 3 days of fluctuating chest pain, which was ongoing at triage. What do you think? Do you need posterior leads?
There’s atrial flutter with controlled ventricular response, a non-specific intra-ventricular conduction delay, borderline right axis, normal R wave progression and normal voltages. The abnormal depolarization from the IVCD can produce secondary repolarization abnormalities, but here there appears to be superimposed primary ST depression V2-4 indicating posterior OMI.
Here's the prior ECG:
So a patient with high pretest probability (prior CABG with new chest pain), had new ECG changes showing posterior OMI. Do you need posterior leads? If so, how will they change management?
Posterior leads are unnecessary if anterior leads are diagnostic
According to the STEMI paradigm an ECG has to have ST elevation to diagnose acute coronary occlusion, and if there’s no ST elevation on anterior leads you can look for it on posterior leads. But for decades we’ve known that you don’t have to have posterior leads to diagnose posterior MI in the setting of typical LBBB: In both the Original Sgarbossa criteria, and in the Smith Modified Sgarboss Criteria, criterion 2 only requires concordant STD in one lead of V1-V3 to diagnose posterior MI, without the need for posterior leads. In this case there was not typical LBBB, but the principles of concordant STD still apply.
In this case the IVCD complicates the ECG interpretation, but there was clearly new ischemic STDmaxV1-4, which is diagnostic of posterior OMI.
Here’s the first ECG flipped upside down, which shows concordant ST elevation in V2-4.
Why not just get posterior leads anyway, to confirm?
Posterior leads can be falsely negative
A 15 lead can be helpful if the 12 lead is non-diagnostic. But if the 12 lead is already diagnostic the 15 lead posterior leads can be falsely negative.
The emergency physician was worried about posterior MI, so recorded a 15 lead ECG:
There’s still ischemic STDmaxV1-4, but posterior leads are negative. So when the first troponin returned at 2,200 ng/L (normal <26 in males and <16 in females) the patient was referred to cardiology as a non-STEMI.
So a patient with high pretest probability and now lab confirmation of MI, had an ECG with ischemic STDmaxV1-4 that identified the MI as being occlusive (OMI) rather than non-occlusive (NOMI). But because there was no ST elevation on either anterior or posterior leads, they were diagnosed as ‘non-STEMI’ – which can produce diagnostic momentum that can be difficult to reverse.
‘Non-STEMI’ diagnostic momentum
Cardiology repeated the ECG and troponin, and did a bedside echo.
There’s still ischemic STDmaxV1-4, but now there’s subtle posterior STE (but still less obvious than the anterior STD). Cardiology noted “transient concordant ST elevation”, and echo showed posterior RWMA and CHF with MR.
So now there’s clinical, laboratory, ECG and echo findings of OMI.
But the pain had improved on nitro infusion and the repeat troponin 2 hours after the first was the same, so the patient was admitted as ‘non-STEMI’ with a focus on medical management and dialysis for fluid overload.
The next day troponin rose to 20,000 and then 50,000, with ECG showing ongoing ischemic STDmaxV1-4 – which was now interpreted as “anterior STD similar to prior ECGs”:
The following day the patient had non-urgent angiogram: 95% circumflex occlusion (not fully occluded due to some spontaneous reperfusion in those intervening 20 hours), with peak troponin ＞65,000 ng/L (this is a huge infarct).
Discharge diagnosis was still “non-STEMI” based on the initial ECGs – despite the diagnostic 12 lead, transient STE on posterior lead, echo findings and massive troponin elevation.
Discharge ECG showed normalization of anterior segments.
'Working diagnosis' vs 'final diagnosis'?
The new ESC guidelines has for the first time merged both STEMI and non-STEMI in the same guideline because they are both on the spectrum of ACS. They have also recommended differentiating between the initial “working diagnosis” of STEMI vs non-STEMI vs the “final diagnosis” based on troponin, echo and angio.
This is a helpful starting point to separate the initial tests from the actual patient outcome. But as an analysis by Dr. Robert Herman explained, “Although coronary angiography and further diagnostic testing establish the presence of an occlusive or flow-limiting lesion as a culprit for the present symptoms, the guidelines continue to give a 'final diagnosis' based on inaccurate ECG terminology (ST-elevation and Non-ST-Elevation Myocardial Infarction). This reinforces the logical fallacy of the STEMI vs. NSTEMI paradigm called the 'No False Negative Paradox,' in which no NSTEMI patient can ever be recognized as a false negative for OMI, regardless of their underlying pathology or their benefit from emergent reperfusion.”
In this case all investigations – ECG, echo, peak trop, and angio – confirmed OMI, but the ‘working diagnosis’ never changed. But the very first test could have identified OMI at triage, before the first troponin was back, and reduced reperfusion delay by two days.
I sent the first ECG to Smith and Meyers without any clinical information or comparison to prior ECG, and they both immediately identified posterior OMI.
The Queen of Hearts had the same interpretation:
Take home
1. Ischemic STDmaxV1-4 is highly specific for posterior OMI, without the need for posterior leads.
2. Posterior leads can be falsely negative and lead to missing an OMI
3. ‘NSTEMI’ triaged for non-urgent angio should be reconsidered if there is dynamic ST changes, refractory ischemic, large troponin elevation, or echo findings of RWMA
4. To differentiate between ‘working’ and ‘final
diagnosis’ of ACS we need to shift to OMI paradigm to acknowledge missed occlusions retrospectively and work to identify them prospectively
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