Two patients with diffuse ST depression and reciprocal ST elevation in aVR: do either/both/neither have Occlusion MI?

Written by Jesse McLaren, with additions from Smith

Two patients presented with chest pain with ST elevation in aVR, and the same final ECG interpretation: “repolarization abnormality, severe global ischemia (LM/MVD).” Do either, both, or neither require the cath lab?

Patient 1: 75 year old, history of aortic stenosis, with recent cough accompanied by shortness of breath and chest pain, then syncopal episode.

There’s sinus tachycardia, first degree AV block, borderline right axis, and normal voltages. There’s significant ischemic STD in I/II/II/aVF and V4-6 (maximal V5-6) with reciprocal STD aVR/V1.

 

This has been called a “STEMI equivalent” but is nonspecific subendocardial ischemia, with a differential that includes demand ischemia (sepsis, severe anemia, severe AS), critical stenosis of any coronary artery or triple vessel disease, and other causes (PE, dissection). So this requires resuscitation, looking for non-cardiac causes, and angiography if a coronary (ACS) cause is likely.

 

The patient presented with cough and syncope, so pretest likelihood for acute coronary occlusion was low, while severe aortic stenosis plus pneumonia could explain subendocardial ischemia. There was a consolidation on Xray and elevated white cell count. But because of STE-aVR the patient had a stat cardiology consult and then cath lab activation, which revealed normal coronaries, with minimal troponin I elevation to 60 ng/L (normal <26 in males and <16 in females). The final diagnosis was pneumonia and critical aortic stenosis. Next day ECG showed resolution of subendocardial ischemia:

Patient 2: 60 year old with two days of fluctuating chest pain, now constant

There’s normal sinus rhythm, normal intervals/axis, and low voltages. There are hyperacute T waves in V1-3 (including deWinter T wave in V3), and precordial swirl pattern (STE or hyperacute T wave in V1-2 with reciprocal STD in V5-6). There’s also straightening of ST segment in aVL, with reciprocal inferior ST depression. Because there’s ST depression in II and V5-6, there’s reciprocal STE-aVR.

 

This indicates proximal LAD occlusion, but it doesn’t meet STEMI criteria so the cath lab was not activated. The patient had serial troponin I, which were 65ng/L and then 550ng/L two hours later. Because of ongoing chest pain and an ECG that was interpreted as nonspecific, a CT chest was also done which excluded aortic dissection, and then the patient was referred to cardiology as Non-STEMI.

 

Repeat ECG done 7 hours after arrival:

Now there’s further loss of anterior R waves. The hyperacute T waves have deflated over time, and there’s a suggestion of reperfusion in aVL, but the patient had ongoing chest pain. After repeat troponin that rose from 5000 to 9000 ng/L, with ongoing chest pain refractory to nitro and morphine, the cath lab was activated. Door to cath time was 10 hours, there was a 100% proximal LAD occlusion. Peak troponin was a massive 420,000 ng/L, and echo showed EF of 30%.

 

Post-PCI ECG showed ongoing loss of R waves, and reperfusion T wave inversion:

 

 

Subendocardial ischemia vs precordial swirl

 

The first patient had unnecessary cath lab activation while the second had delayed cath lab activation. Both had initial ECGs with the same final interpretation that focused on the ST elevation in aVR reciprocal to diffuse ST depression, but there were important differences in the patients and the ECGs which could have changed management:

 

The first patient had a low pre-test likelihood of ACS, and an ECG showing non-specific subendocardial ischemia – with the main injury pattern being ST depression in the inferior and lateral precordial leads. This is nonspecific and requires resuscitation, finding the cause, and angiography if primary cardiac cause is likely. The Queen of Hearts called this “OMI high confidence” because this assumes a pre-test likelihood of ACS, but this patient’s pretest likelihood was low. Future versions may indicate "subendocardial ischemia" to alert providers to the broader differential.

 

The second patient had chest pain and an ECG showing LAD occlusion – with the main injury pattern being anterior STE/hyperacute T waves and precordial swirl. The Queen of Hearts also called this OMI high confidence, but the patient had a higher pre-test likelihood of ACS and a more specific ECG pattern. This could have saved 10 hours of reperfusion delay and prevented a massive infarct.

 Register for access to Queen of Hearts here

Take away

1.     ST elevation in aVR is reciprocal to diffuse ST depression, which has a broad differential.

2.     Subendocardial ischemia is non-specific: find and treat reversible causes, with angiography if cardiac cause is suspected

3.     Precordial swirl can help identify subtle LAD occlusion

4.     ECGs diagnostic of STEMI/OMI are unlikely to be secondary to aortic dissection

5.     ACS with refractory ischemia requires reperfusion, not morphine

6.     Queen of Hearts can help identify OMI on ECG, but needs to be applied in clinical context to the right patients

 

See these posts

-   precordial swirl – 20 cases of swirl and look-alikes

-    SW elevation in lead AVR, with diffuse ST depression, does not represent left main occlusion

Literature

1. Knotts et al. found that such ECG findings (STE in aVR) only represented left main ACS in 14% of such ECGs: 

Only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as ≥ 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).  It was a baseline finding in 62% of patients, usually due to LVH.

Reference: Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

2.  Now there is a paper published in 2019 that proves the point beyond doubt, though makes it clear that this pattern is associated with very high mortality.

https://www.sciencedirect.com/science/article/abs/pii/S000293431930049X
Harhash AA et al. aVR ST Segment Elevation: Acute STEMI or Not? Incidence of an Acute Coronary Occlusion.  American Journal of Medicine 132(5):622-630; May 2019.

Here is the abstract:

Background

Identification of ST elevation myocardial infarction (STEMI) is critical because early reperfusion can save myocardium and increase survival. ST elevation (STE) in lead augmented vector right (aVR), coexistent with multilead ST depression, was endorsed as a sign of acute occlusion of the left main or proximal left anterior descending coronary artery in the 2013 STEMI guidelines. We investigated the incidence of an acutely occluded coronary in patients presenting with STE-aVR with multi-lead ST depression.

Methods

STEMI activations between January 2014 and April 2018 at the University of Arizona Medical Center were identified. All electrocardiograms (ECGs) and coronary angiograms were blindly analyzed by experienced cardiologists. Among 847 STEMI activations, 99 patients (12%) were identified with STE-aVR with multi-lead ST depression.  

Smith comment: this is a very limited population, as it only includes those with STEMI activations.  There are likely many other patients with STE-aVR who did not get a STEMI activation as they were not suspected of having ACS.

Results

Emergent angiography was performed in 80% (79/99) of patients. Thirty-six patients (36%) presented with cardiac arrest, and 78% (28/36) underwent emergent angiography. Coronary occlusion, thought to be culprit, was identified in only 8 patients (10%), and none of those lesions were left main or left anterior descending occlusions. A total of 47 patients (59%) were found to have severe coronary disease, but most had intact distal flow. Thirty-two patients (40%) had mild to moderate or no significant disease. However, STE-aVR with multilead ST depression was associated with 31% in-hospital mortality compared with only 6.2% in a subgroup of 190 patients with STEMI without STE-aVR (p less than 0.00001).  

Comment: Again, this does not include the many STE-aVR patients who were not activated, so even fewer would have ACS, and mortality in this group is much greater than in all STE-aVR patients.

Conclusions

STE-aVR with multilead ST depression was associated with acutely thrombotic coronary occlusion in only 10% of patients. Routine STEMI activation in STE-aVR for emergent revascularization is not warranted, although urgent, rather than emergent, catheterization appears to be important.