The forgotten lead- aVR

By Chris Paul MD, OSU EM Assistant Professor // Edited by Michael Barrie MD, OSU EM Assistant professor

54 yo F presented with chest pain and shortness of breath for two days
past medical history included prosthetic aortic valve, endocarditis, MI, DM, HTN, HLD, cough variant asthma and stroke

Vital signs -HR 130’s, bp – 110’s, spO2 – low 90s/high 80’s

initial EKG

IMG_2843 copy

What’s your interpretation? Plan for management?


A STEMI was not called on the initial read

Trop resulted at 14; BNP – 1300

Patient was aggressively managed for cardiogenic shock and taken for LHC, which discovered 90% LMCA stenosis
Also TEE showed severe AI with perivalvular abscess

Left Main Coronary Artery Disease

LMCA carries bad prognosis and is (according to some) a STEMI equivalent. Remember to look out for EKG consistent with LMCA pathology:

  • Widespread horizontal ST depression, most prominent in leads I, II and V4-6
  • ST elevation in aVR ≥ 1mm
  • ST elevation in aVR ≥ V1

Here is the link to a good review of this topic, and Summarized below

“Given the ability of STE in aVR to predict critical coronary lesions and death, this ECG pattern is increasingly being recognised as a ‘STEMI equivalent’ that requires emergent reperfusion therapy to prevent cardiogenic shock and death.”

“Furthermore, the presence or absence of STE in aVR may potentially inform the decision to give thienopyridine platelet inhibitors (e.g. clopidogrel, prasugrel) during an acute coronary syndrome:
Clopidogrel treatment ≤ 7 days before CABG is associated with an increase in major bleeding, haemorrhage-related complications, and transfusion requirements.
Prasugrel is associated with even more bleeding than clopidogrel.
If urgent CABG (within 7 days) is likely, then there is an argument for omitting thienopyridines during the initial management of an acute coronary syndrome (or at least using clopidogrel instead of prasugrel).”

“This constellation of findings can be easily missed especially on more subtle EKG’s with tachycardia where rate-related ST depressions may be seemingly explained away.”