Friday, November 4, 2022

90 year old with acute chest and epigastric pain, and diffuse ST depression with reciprocal STE in aVR: activate the cath lab?

Case submitted and written by Mazen El-Baba MD, with edits from Jesse McLaren and edits/comments by Smith and Grauer


A 90-year old with a past medical history of atrial fibrillation, type-2 diabetes, hypertension, dyslipidemia, presented with acute onset chest/epigastric pain, nausea, and vomiting. BP was 110 and oxygen saturation was normal. What is your ECG interpretation and what would you do next?






This ECG shows a normal sinus rhythm with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, late R wave progression (and misplaced V2), normal voltages, ST-elevation in aVR and global ST-depressions. This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available.

Smith: If this is ACS (a big if), this is just the time when one should NOT use "upstream" dual anti-platelet therapy ("upstream" means in the ED before angiography). This is because, if there is an ACS etiology, the patient is at high risk of needing CABG, which would need to be delayed if a P2Y12 inhibitor is given due to surgical bleeding risks. The best course is to wait until the anatomy is defined by angio, then if proceeding to PCI, add Cangrelor (an IV P2Y12 inhibitor)


I sent the ECG and clinical information of a 90-year old with chest pain to Dr. McLaren. His response: “subendocardial ischemia. History sounds concerning for ACS (could be critical stenosis, triple vessel), but differential also includes dissection, GI bleed, etc. Anything more on history? POCUS will be helpful.”

In other words, instead of thinking about ST-elevation in aVR, it would be important to think about what could be causing widespread ST-depressions with reciprocal ST-elevation in aVR. Asking the question: “what causes widespread ST-depressions?” can prompt the clinician to consider a wide differential diagnosis that befits the clinical presentation.

Widespread ST-depression with reciprocal aVR ST-elevation can be cause by: 

  1. Heart rate related: tachyarrhythmia (e.g., SVT, rapid atrial fibrillation) 

  2. Abnormal electrical conduction 

    1. Short QT: digoxin 

    2. Long QU: hypokalemia 

  3. Tall voltages: LVH with secondary ST-depression

  4. Primary ST changes: Diffuse subendocardial ischemia

    1. Demand ischemia, from shock-like state, eg sepsis, haemorrhage, PE, aortic dissection

    2. Primary coronary plaque rupture/thrombosis etiology resulting in critical stenosis of left main or LAD, or in the presence of multi-vessel disease

If global ST-depression is thought to be due to subendocardial ischemia, then a thorough history, physical exam, and a bedside ultrasound are crucial to make the next decision point--searching for the cause of subendocardial ischemia. A emergent cardiology consult can be helpful for equivocal cases. 

Case Continued: 

The decision was made to wait for initial blood-work results to return as the clinician completed a bedside POCUS assessment and finish the physical exam. POCUS showed good LV-function and no pericardial effusion.  


Smith: It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. 

See this case: what do you think the echocardiogram shows in this case?


The patient had mild but diffuse abdominal tenderness. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. The patient was placed on telemetry. 

Initial blood work showed the following: metabolic acidosis on VBG with a lactate of 7.1; Hgb 11g/dL (110g/L) and leukocytosis, and a mildly elevated troponin (36 ng/L, with normal <26). The patient then had a bloody bowel movement, which the nurses described as the colour resembling that of an ECG paper, and BP dropped to 8.8g/dL (88g/L).  

A call was made to the radiologist to prioritize the CT/CTA. The patient was resuscitated with fluids and General Surgery was consulted on an emergency basis to a presumed diagnosis of mesenteric ischemia. CTA was not conducted by the radiologist due to concerns of an elevated creatinine, but a plain CT abd/pelvis was completed that showed evidence of pneumatosis intestinalis. The patient was taken to the operating room and a large portion of the small bowel was resected due to mesenteric ischemia. 

After resuscitation and surgery, a follow-up ECG showed improvement of subendocardial ischemia, with a peak trop of 85 ng/L: 


But the following day the patient developed STE-aVR again (and now V2 is correctly recorded)? What happened?





Now the patient is in AF with rapid ventricular response. There's wandering baseline but appears to have mild diffuse STD and reciprocal STE-aVR. Again, they do not need code STEMI but an assessment of the etiology of Afib and the STD--which could just be rate related, vs subendocardial ischemia. This revealed the development of septic shock–which requires resuscitation, antibiotics and source control, not the cath lab. Unfortunately despite maximum treatment the patient decompensated from septic shock and expired. 

Diffuse STD with reciprocal STE-aVR: high-risk but nonspecific

STE-aVR with diffuse STD has been called a "STEMI equivalent" and equated with left main coronary occlusion. But an analysis of patients presenting with such a pattern found only 28% were from ACS of any vessel and only 14% had a left main. In far more cases it was simply a baseline pattern from LVH. As they concluded, "the AHA/ACCF/HRS recommendations for interpreting this ECG pattern as representing 'ischemic due to multivessel or left main coronary artery obstruction,' implying that these patients should be referred for urgent coronary angiography based on the ECG pattern alone may not be supported by our findings the the term 'circumferential subendocardial ischemia' is probably more accurate."[1]


This is important both to avoid unnecessary cath lab activation, and to consider the other deadly differentials. In a study of patients who had the cath lab activated based on this pattern, only 10% had acute coronary occlusion of which none were left main. But a third were ACS (of which most had multi-vessel disease), a third were tach-arrythmias, and a third were non-coronary shock states (sepsis, hemorrhage, dissection, PE, hypertensive emergency, SAH). In addition, 36% of the whole group presented in cardiac arrest and in-hospital mortality rate was 31%.[2] So diffuse STD with reciprocal STE-aVR is high-risk but non-specific, so it's important to recognize the pattern and then rapidly identify and treat the underlying cause.

As a review summarized, “although nearly half of patients with >1mm STE in aVR due to ACS will require coronary artery bypass surgery for revascularization, the infarct artery is often not the LM, but rather the LAD or severe 3-vessel disease. More importantly, such ECG findings are frequently due to nonocclusive etiologies (eg, baseline LVH, demand ischemia secondary to respiratory failure, aortic stenosis, hemorrhagic shock)…thus, a number of expert reviews emphasize the low specificity of the aVR STE pattern, preferring to label it as circumferential subendocardial ischemia; in this syndrome, STE in aVR is reciprocal STE, reciprocal to an STD vector toward leads II and V5…some patients whose ECGs already meet conventional STEMI criteria might also have STE in lead aVR. This finding does not alter the need to pursue emergent reperfusion, although it might suggest a poorer prognosis.”[3]

Take home

  • STE-aVR is reciprocal to widespread ST depression, which has a wide differential

  • This may be a high risk but non-specific pattern including tachy-arrhythmias, non-coronary shock states, and ACS including both OMI and multivessel disease requiring CABG

  • A thorough history, physical and POCUS - with a focus on resuscitation of reversible causes - can help identify non-cardiac causes, and differentiate from ACS requiring angiography


1. 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. Harhash AA, Huang JJ, Reddy S, et al. aVR ST segment elevation: acute STEMI or not? Incidence of an acute coronary occlusion. Am J Med 2019, 132(5):622-630.

3. Miranda DF, Lobo AS, Walsh B, et al. New insights into the use of the 12-lead electrocardiogram for diagnosing acute myocardial infarction in the emergency department. Can J of Cardiol 2018, 34: 132-145 

Here are some other cases:

LVH, LBBB, RBBB, and RVH may manifest ST depression without any ischemia!

2 cases of Aortic Stenosis:

An elderly man with sudden cardiogenic shock, diffuse ST depressions, and STE in aVR


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.
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:

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.


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.


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).  
CommentAgain, 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.


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.


MY Comment, by KEN GRAUER, MD (11/4/2022):


Our thanks to Drs. El-Baba and McLaren — for their presentation in today’s post about an important topic worthy of our periodic reminders. We’ve presented many variations on this theme on Dr. Smith’s Blog — with today’s case being distinguished by its discovery on abdominal exam

  • Rather than reflexive assumption that diffuse ST depression with ST elevation in lead aVR invariably means acute coronary disease — complete examination of today’s patient revealed abdominal tenderness — that led to the diagnosis of mesenteric ischemia with associated septic shock. 

One More CASE:
As reinforcement of the concepts brought out by Drs. El-Baba and McLaren in today’s case — Consider the ECG in Figure-1, obtained from an older adult.

  • In view of this ECG — Should the cath lab be activated?

Figure-1: ECG obtained from an older adult. Should the cath lab be activated?

MY Approach to the ECG in Figure-1:
I routinely favor a 2-step approach to ECG interpretation:
  • Step #1 ( = Descriptive Analysis) — in which the 6 parameters of Rate — Rhythm — Intervals (PR, QRS, QTc) — Axis — Chamber Enlargement — and Q-R-S-T Changes — are systematically assessed.
  • Step #2 ( = Clinical Impression) — in which findings from Step #1 are clinically correlated and interpreted in light of the patient’s history and exam.

  • KEY Point: In my experience — clinicians all-too-often fail to appreciate that the systematic process and the findings detected from Step #1 are the same regardless of the patient’s circumstances. For example — the presence of Q waves, the size of R waves and S waves, and the number of millimeters of ST elevation or depression does not change based on the history. What does change — is how you clinically correlate these ECG findings depending on the patient’s age, their symptoms — and considering what the patient’s baseline tracing looked like (if a prior ECG is available for comparison).

  • For more on “My Take” for a systematic approach to ECG interpretation — Please check out My Comment at the bottom of the page in the October 17, 2022 post in Dr. Smith’s ECG Blog.

Systematic Assessment of the ECG in Figure-1:
My Descriptive Analysis of ECG findings in Figure-1 is as follows:
  • Sinus tachycardia at ~110/minute.
  • A normal PR interval.
  • A QRS duration that appears to be borderline prolonged — and which looks consistent with incomplete RBBB (albeit slight widening in the descent of the r’ in lead V1 almost suggests Brugada phenocopy).
  • A slightly prolonged QTc (although this is difficult to assess given the tachycardia).
  • No chamber enlargement.
  • And the most remarkable finding — which is diffuse ST depression (in at least 7 leads) — with ST elevation that is most marked in lead aVR, but which is also seen in leads aVL and V1.

MY Clinical Impression:
The ECG in Figure-1 — shows sinus tachycardia — incomplete RBBB — with marked ST depression in multiple leads (with ST elevation in lead aVR, as well as in leads V1 and aVL). These ECG findings should immediately suggest the following Differential Diagnosis:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock/profound hypotension; GI bleeding; anemia; "sick patient"; etc.).

  • To Emphasize: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion (ie, it is not the pattern of an acute MI) — but rather ischemia due to the above differential diagnosis! Practically speaking — No more than this can be said until we know the clinical circumstances of the patient in front of us.
  • IF the history for the patient whose ECG is shown in Figure-1 was new, worrisome chest pain — then the diffuse ST depression with ST elevation in lead aVR would suggest severe coronary disease that would merit prompt cath to define the anatomy.
  • It turns out that this ECG in Figure-1 is from a patient with depressed mental function as a result of a CNS bleed! As a result — cardiac cath was not performed — since results of a cath would not have altered the unfortunate outcome. Statistically — the chances are better than not that the diffuse ST depression in this ECG was not the result of severe coronary disease.

  • BOTTOM Line from Today’s Case: As per Drs. El-Baba and McLaren — it’s important to: i) Promptly recognize the ECG pattern of diffuse subendocardial ischemia; andii) Realize that the causes of this pattern are many — and not always the result of severe coronary disease!

No comments:

Post a Comment

DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

Recommended Resources