Left Circumflex MI - Rhythm Nation - ECG

Remember where we left off: you just spoke to a fifty-year-old woman describing severe, intermittent chest pain radiating to the back and left arm. You order aspirin and nitroglycerin, along with a troponin and you are now looking at her ECG:

Left Circumflex MI

You note the rate is about 75 per minute, the rhythm is sinus, and the axis is normal. The PR, QRS, and QT intervals appear unremarkable. Then you note an approximately 1 mm ST-elevation in aVR along with subtle (<1 mm) ST-elevation in V1 and V2. A depressed – upsloping – ST-segment can be seen in lead I along with depression in lead II and, arguably, subtle depression in lead V6. T wave inversions can be seen in leads II, III, and aVF. You look in the chart for prior ECGs, but no luck.

What do you make of this?

The patient is presenting with chest pain so let’s first ask: Is this a STEMI? Based on the 2018 AHA criteria, this ECG would not qualify. It does not have 1 mm of ST-elevation in two contiguous leads or greater than 1.5 mm elevation in V2 and V3 (men < 40 would need 2.5 mm elevation in these leads; 2 mm is needed for men > 40) [1]. This means our patient is not having a heart attack – or at least not having one that would benefit from prompt reperfusion. Right? Not exactly (as you likely guessed, since I’m writing about this).

The problem with STEMIs is that not all heart attacks are STEMIs (and as previously reported in County EM – here, here and here – not all ST-elevation is an MI). More importantly, not all heart attacks with occluded coronary arteries that may benefit from emergent reperfusion are STEMIs. Studies have consistently shown that a sizable portion of patients with NSTEMI – patients that get treated with dual antiplatelets and delayed catheterization per guidelines [2] – actually have acute coronary occlusion. For example, in 2008, Wang et al published a study in which 528 of 1957 (27%) patients with NSTEMI had complete occlusion on angiography [3].

Whether or not we are aware, we already know this. We know that patients may need reperfusion even without a STEMI. This is why we look for STEMI equivalents like hyperacute T waves and De Winter’s T Waves. But I am guessing that many of us – myself included – were not aware of just how many patients with occluded vessels don’t have ‘STEMI” on their ECG. Studies have shown that nearly a quarter of patients with acute coronary occlusions do not meet STEMI criteria [4,5]. Knowing this, some have suggested that we abandon the STEMI criteria completely [6,7]. At the very least, this knowledge ought to push us to closely study the ECGs we’re given at work and then study up on ECGs at home.

. . . Which is what you and your team do for this patient. Recognizing ST-elevation in lead aVR with multi-lead ST-depression (lateral leads I and V6, inferior lead II) in this patient with typical ACS symptoms, you and the team decide to activate the cath team. At first, cardiology defers catheterization. Given the pattern of pain, you order a CTA to rule out acute dissection which is negative. You’ve already started the patient on aspirin and nitroglycerin but her discomfort persists, and troponin comes back ~4.5 ng/ml. A repeat ECG is unchanged but now, in the setting of persistent pain, cardiology takes the patient to the cath lab. There, she is found to have triple vessel disease with 100% occlusion of the proximal left circumflex (deemed the culprit lesion) along with occlusions of the left anterior descending and right coronary artery. Three drug-eluting stents are placed and she is discharged a few days later. Notably, the second troponin had increased to 7 ng/ml meeting criteria for acute MI [1]. Despite having no risk factors and “non-specific” ST changes on ECG, this patient had severe multivessel disease with acute occlusion myocardial infarction (“OMI” [6]).

What can we learn from this case?

Along with highlighting the limitations of the STEMI criteria, this case nicely illustrates several important learning points in ECG interpretation and the management of acute MI.

Lesson One: aVR ST-elevation with diffuse ST-depressions may be indicative of left main coronary artery insufficiency or severe triple vessel disease.

ST-elevation in aVR with multi-lead ST-depression is a STEMI equivalent that has been officially recognized by the AHA/ACC since 2013 [8] (and previously described in County EM here and here). There is a growing body of literature investigating this ECG finding. For example, ST-elevation in lead aVR in patients with NSTEMI has been linked to increased in-hospital mortality: Barrabés et al found that among 525 patients with NSTEMI, 1.3% with no aVR ST-elevation died in the hospital compared to 8.6% with 0.05 mV (0.5 mm) elevation and 19.4% with ≥ 0.1 mV (1 mm) elevation [9]. Historically, this finding has been linked to occlusion of the left main coronary artery, the proximal left anterior descending, or severe multivessel disease (as seen in our patient) [10,11].

Before jumping to reperfuse every patient with aVR ST-elevation, however, it is important to understand some important context. First, studies have shown that aVR ST-elevation and diffuse ST-depression is not specific for left main coronary artery disease, despite this historical association. For example, a study by Knotts et al [12] found that 26% of the patients with this ECG pattern were found to have no significant angiographic coronary artery disease whereas only 23% had left main or left main equivalent disease.

(We recently had a case of a patient with a history of CAD who presented with severe exertional chest pain and ECG showing aVR ST-elevation and diffuse ST-depression. Some of the team insisted on calling a cardiologist, but upon further questioning, they reported recent, black stools. Their ECG abnormalities resolved with transfusion, and the patient had multiple normal troponin levels.)

Furthermore, Miranda et al in the Canadian Journal of Cardiology [13] explain that the studies linking aVR ST-elevation to “occlusion” of the left main define “occlusive” based on interventional standards of 50% fractional flow reserve or 75% stenosis (i.e. NOT actually complete occlusion). In the EMCrit blog [14], Dr. Stephen Smith explains that aVR ST-elevation with diffuse ST-depression often represents left main or left anterior descending insufficiency, not necessarily total occlusion. So if the patient’s anginal symptoms are controlled medically, he argues, they can wait for urgent – as opposed to emergent – coronary intervention.

Nonetheless, this is an important ECG finding to be aware of and look out for. And in the patient whose anginal pain persists despite initial therapy, this ECG finding may be a reason to activate the cath lab.

Lesson Two: Left circumflex artery occlusion is among the most common occlusive myocardial infarctions that does not meet “STEMI” criteria.

Earlier, I cited a study published by Schmitt et al [4]. This study looked at 418 patients with acute coronary occlusion. Of these, 29% percent did not meet STEMI criteria. When breaking down this data by coronary artery, they showed that nearly 50% of Left Circumflex occlusions will be missed by STEMI criteria. Other studies have shown similar trends; Stribling et al found that 33% of 27,711 Left Circumflex occlusions presented as NSTEMI [15]. So, perhaps it is not surprising that our patient’s Left Circumflex occlusion was not an obvious STEMI.

Unfortunately, Left Circumflex artery occlusions account for an estimated 20% of MI [16]. These patients likely need reperfusion, but if they aren’t showing ST-elevations, how are we going to convince a cardiologist to cath? Dr. Smith walks us through a few cases on his blog here [17]. His suggestions? First, look for subtle signs of ischemia such as T wave inversions and ST-depression to guide us. Second, use other tools like serial ECG, biomarkers, and POCUS looking for wall motion abnormalities. Finally (and most importantly), he urges us to remember that patients with uncontrollable anginal pain and no ST-elevations on ECG warrant an emergent trip to the cath lab. This brings us to our third and final takeaway.

Lesson Three: Even without ST-elevation, patients with persistent anginal pain despite maximum medical management should be taken to the cath lab immediately.

The 2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes states: “An urgent/immediate invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients . . . with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures)”. Citing Level A evidence, they recommend invasive management within two hours [16]. The European Society of Cardiology recommends an immediate invasive strategy within two hours in patients with at least one “very-high-risk criterion” that includes “recurrent or ongoing chest pain refractory to medical treatment [17].”

Ultimately, the ECG is not the only reason to activate the cath lab. And as we saw with this case, not all heart attacks meet established STEMI criteria. For this patient, the ED team noticed subtle ECG findings, recognized a potential acute coronary occlusion, and notified the cath lab right away. And when medical management wasn’t resolving her pain, the ED team convinced the cardiologists to do a catheterization, diagnose triple vessel disease, and stent open her blocked arteries.