- David Didlake
Critical Left Main
David Didlake
Acute Care Nurse Practitioner
Firefighter / Paramedic (ret)
@DidlakeDW
Expert commentary and peer review by
Dr. Steve Smith
@smithECGBlog
A 57 y/o Female with PMHx HTN, HLD, DM, and current use of tobacco products, presented to the ED with chest discomfort. She described it as tightness, centralized, and associated with both dyspnea and diaphoresis. She experienced the symptoms while helping a friend carry a rather cumbersome item up a flight of stairs at an apartment complex.
She was forced to take pause and collect herself. The symptoms subsequently subsided. Then, she attempted to reengage the activities at hand, and initially tolerated this well. But the symptoms returned with similar pattern – provoked by exertion, and alleviated with rest; except that on each occasion the chest pain was a little more intense, and the needed recovery period was longer in duration.
The recurrent, and equally persistent, nature of this compelled ED evaluation. A 12 Lead ECG was captured on her arrival.
There is Sinus Rhythm with broad, near global ST-depression in most leads with ST-elevation in aVR (slightly extended out to V1) with ST-depression appears maximal in Leads II and V5.
Given the consistency of the clinical profile with typical angina, associated risk factors, and abnormal ECG findings, a cardiology consult was promptly requested. It just so happened that I was already down in the ED (attending to a separate consult) when my supervising cardiologist texted me about this case and to check it out.
By the time I made it to bedside she expressed much improvement, did not appear uncomfortable, and was able to freely engage in conversation. Prior to this current circumstance, over the past 6 months, she had felt a very pernicious, progressively worsening, exertional dyspnea requiring longer periods of rest before the symptoms resolved. Today was the first time she had experienced chest discomfort.
As an aside – in hindsight – I should have recorded another ECG at the time of bedside encounter. The overall time difference between initial evaluation by ED physician and my subsequent arrival for specialty consult was minimal, for all intents and purposes. However, a secondary ECG (specifically amidst verbalized resolution of symptoms) would have assisted in more appropriately triaging her unique circumstance while incorporating the thought process detailed below.
Whenever I encounter an ECG like this I tend to immediately consider the possible etiologies in 1 of 2 possible categories. It should be known that each category can easily manifest the generic subendocardial ischemia pattern. In general, subendocardial ischemia is a consequence of global supply-demand mismatch that usually ameliorates upon addressing, and mitigating, the underlying cause.
Category 1: Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates. This results in Type I MI.
Category 2: An increase in myocardial oxygen demand due to tachycardia, elevated ventricular afterload (BP or aortic stenosis), or increased wall stretch (admittedly this latter is more complicated) or a decrease in oxygen supply due to hypotension, anemia, hypoxia, or a combination of all of the above. This results in Type II MI.
What’s interesting is that the ECG can only detect ischemia. It cannot, however, differentiate the cause. Only the clinical scenario can do this.
Subendocardial ischemia pattern on the ECG:
STE aVR with, or without, STE V1
Global STD that is maximal in Leads II / V5
Strategies and tactics include serial ECG’s with emphasis on re-evaluation after one, or multiple, factors (delineated below) have been addressed accordingly. Does the ECG normalize? Or, is there persistent ischemic presentation, especially with unremitting symptoms? It’s judicious, then, to arrange for coronary angiogram.
Coronary occlusion, however, might be present concurrently with subendocardial ischemia on the time-zero ECG, or evolve into such. In this case, the problem is not purely a consequence of external factors (e.g. elevated BP), but rather directly correlated with coronary obstruction (due to plaque rupture and thrombosis) and, potentially, stymied TIMI flow.
Supply-demand mismatch (non-occlusive coronary disease, or exacerbation of preexisting flow insufficiency)
a. Severe Hypoxia
b. Advanced LVH
c. Severe HTN
d. Severe Hypotension
e. Aortic Stenosis
f. Anemia
g. Severe Tachycardia
Acute Coronary Syndrome (obstructive coronary disease)
a. 3-vessel disease with a culprit lesion in one or more of the arteries
b. Left Main stenosis (not thrombosed)
c. Proximal LAD disease with/without a) and b)
Let’s predict which category this ECG is most likely to be affiliated with based on physical exam and vital signs assessment:
Supply-demand mismatching (non-occlusive coronary disease)
a. Severe Hypoxia [99% Room Air saturation]
b. Advanced LVH [Possible, but doesn’t necessarily meet ECG criteria]
c. Severe HTN [NIBP 142/88]
d. Severe Hypotension [see above]
e. Aortic Stenosis [No Hx syncope, and no systolic murmur]
f. Anemia [Normal Hgb]
g. Severe Tachycardia [HR 75 bpm]
Acute Coronary Syndrome (occlusive coronary disease)
a. 3-vessel disease with a culprit lesion [Typical angina, multiple risk factors]
b. Left Main stenosis (not thrombosed)
c. Proximal LAD disease with/without a) and b)
It seemed quite apparent that this was an Acute Coronary Syndrome. The Troponin I (ng/mL) had not yet returned, but I felt comfortable, no less, sounding the alarm for urgent coronary angiogram.
Smith: This is ACS even if the troponin returns normal, and the first troponin especially might return normal. If they all return normal, then this is unstable angina. And UA still exists, even in the age of high sensitivity Troponin, which is not in use in this case.
Let’s revisit the time-zero ECG and dissect a few peculiarities that stood out to me upon initial inspection.
Notice how there is not necessarily global ST-depression. My thought process in the moment was that leads aVL and V2 display an ST-segment that is “inappropriately baseline” – not elevated, by definition, but may very well be an equivalent of such as the ischemic zone is actively “pushing” them in an upward manner. This is based on the assumption that aVL and V2 should be following suit, otherwise, with their neighbors in a depressed manner.
Smith: The typical axis for subendocardial ischemia is towards II and V5. This would mean that aVL is typically isoelectric in subendocardial ischemia. The same is true for V2. V1 and aVR are often elevated in subendocardial ischemia. And V2 is between V1 and V3 and is often isoelectric.
It has been my experience that when the ST-segment of subendocardial ischemia is elevated beyond aVR/V1 and “spread” into aVL and V2 (assuming proper lead placement) one should take pause as this implies a more directly superior ST axis and is worrisome for high proximal LAD (even ostial) occlusion. I assumed that this was actively taking place, the full extend of aVL / V2 ST-elevation simply hadn’t yet been captured. A quick way to validate this conjecture is to simply acquire a secondary ECG, but I failed to do this in the moment.
These concerns were readily conveyed to my supervising cardiologist with particular emphasis on high pretest probability for baseline advanced CAD (3-vessel disease, specifically) with a critically stenosed proximal LAD.
She was urgently taken to the Cath Lab.
Coronary Angiogram
1. Distal LM stenosis (80%), not acutely thrombosed
b. The angiographer noted “marked ST depressions on telemetry with injection of contrast”
2. Tortuous LAD consistent with hypertensive cardiac disease and luminal irregularities, but free of stenosis
3. LCx and RCA with luminal irregularities, but free of stenosis
She was referred to cardiothoracic surgery, and underwent CABG x3 the following day.
Echocardiogram findings (pre-procedure)
1. Normal LV/RV systolic function, EF 60-65
2. Stage II diastolic dysfunction
3. Mitral valve calcification with mild regurgitation
Laboratory data (pre-procedure)
1. Troponin I <0.012 ng/mL (undetectable serial, up to the point of surgery)
2. Creatnine 0.70 mg/dL, eGFR >60.0, K 4.3 mmol/L
3. Hgb 13.1 g/dL, WBC 7.4
Here is the ECG after CABG (LIMA-LAD, GSV-Ramus, GSV-OM1).
The bedside ECG is a phenomenal tool to ascertain objective evidence of ischemia. Clinical context paired with ancillary data (eg: NIBP, SpO2, etc) are helpful when categorizing subendocardial ischemia as either a result of supply-demand mismatching, or Acute Coronary Syndrome.
Careful study of what constitutes a typical pattern of subendocardial ischemia on the ECG can quickly isolate atypical and unexpected features. To review, the time-zero ECG in this case displayed broad ST-depression appropriately maximal in Leads II and V5 with corresponding ST-elevation in aVR and (minimally) V1. I suspected an active superiorly directed ST-elevation injury pattern (of proximal LAD occlusion) due to “inappropriately baseline” aVL / V2 ST-segments, which could have easily been ruled-in/ruled-out with a secondary ECG. As Dr. Smith previously remarked, aVL and V2 ST-segments are often isoelectric.
Ultimately, this was not acute coronary occlusion of the Left Main. Had such been the case, this patient would likely have been a prehospital cardiac arrest, or have been in profound cardiogenic shock at the time of ED arrival. Was there a culprit lesion that may have undergone spontaneous autolysis pre-angiogram? See Dr. Smith’s comments below.
The formal diagnosis codes were populated to the chart by the primary hospitalization teams.
Interventional Cardiology: Acute Coronary Syndrome
Cardiothoracic Surgery: Stable Angina
Smith: This is by no means stable angina! It is accelerated angina, which is by definition not stable. Stable angina means that there is chronic exertional angina without a change in pattern. It was still present at rest, when she underwent that firs ECG, so it is not even limited to exertional angina. Whether they found it or not on angiogram, there was a culprit somewhere. Angiography is not perfect at finding culprits. She had a ruptured plaque somewhere among her lesions, such that it resulted in accelerated exertional angina AND some rest angina.
