Chest pain, and Cardiology didn't take the hint from the ICD

Submitted and written by Megan Lieb, DO with edits by Bracey, Smith, Meyers, and Grauer

A 50-ish year old man with ICD presented to the emergency department with substernal chest pain for 3 hours prior to arrival. The screening physician ordered an EKG and noted his ashen appearance and moderate distress. 

Triage EKG:

What do you think?

Triage physician interpretation: 

-sinus bradycardia

-lateral ST depressions

While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Additionally, lead V3 has ST depressions, which are always abnormal (recall that lead V3 will have ST elevation under normal circumstances!)

Smith: also VERY important is the downsloping ST segment in V3.  This is a very specific marker of posterior OMI.  Additionally, V2 has a very flattened T-wave, which is typical of posterior OMI.

Close up of V3 with baseline in red

Close up of V4 with baseline in red

This ECG alone is highly suspicious for posterior OMI! This pattern is recognizable by the ST depressions maximal in lead V4. Recall that, in the setting of ACS symptoms, ST depression that are maximal in leads V1-V4 (as opposed to V5 and V6) not attributable to an abnormal QRS complex is specific for OMI. 

Meyers HP, Bracey A, Lee D, Lichtenheld A, Li WJ, Singer DD, Rollins Z, Kane JA, Dodd KW, Meyers KE, Shroff GR, Singer AJ, Smith SW. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). J Am Heart Assoc. 2021 Dec 7;10(23):e022866. doi: 10.1161/JAHA.121.022866. Epub 2021 Nov 15. PMID: 34775811; PMCID: PMC9075358

A bedside ultrasound was performed, shown here:

Parasternal short axis view demonstrating inferior LV wall motion akinesis

Apical 2 chamber view again demonstrating inferior LV wall akinesis

The cath lab was not activated based on the ECG and bedside echo.

Back to the case:

After the patient was roomed, he revealed that he had undergone several episodes of syncope in the last 24 hours with each event resulting in a shock during which his wife reported that he would immediately awaken. The most recent event had occurred just before being triaged.

At this time he reported ongoing chest pain and was given aspirin and nitroglycerin. Labs were drawn and a repeat ECG was performed:

ST depression markedly worse in V3 and V4 

Comparison of leads V3 and V4

While the ICD was preparing to be interrogated, the interventional cardiologist was consulted for evaluation for emergency catheterization. After reviewing the available information, cardiology did not feel that the patient warranted emergent PCI and recommended heparin infusion and cardiac catheterization the following morning. 

Around this time the troponin I resulted at 0.05 ng/mL (ULN 0.04). 

A second ECG was performed this time:

Resolution of ST depression in the anterolateral leads

A posterior ECG  was also performed at this time:

Posterior orientation ECG (leads V4, V5, and V6 are actually V7, V8, and V9 respectively)
There is no ST elevation in the posterior leads (V7-V9) 
But one would not expect STE in V7-V9 because the STD in V3, V4 has resolved.

Cardiology reviewed the posterior ECG and once again concluded that as there was no ST elevation in the posterior leads, there was no need for emergent PCI. It is important to note, however, that there should have been no expectation for ST elevation in the posterior on this ECG as the ST depression in the anterior leads had resolved! The vessel was likely patent or nearly patent at the time of this ECG.

When the ICD was finally interrogated, the syncopal events and shocks correlated with two VF events that were defibrillated successfully. 

Smith: This is a failure of the cardiologists to comply with their own guidelines, which state that ACS with electrical instability needs the cath lab emergently

The cardiology service was alerted to the finding of episodes of VF and obvious dynamic ECG changes and did not feel immediate cath was indicated, and instead deferred cardiac cath until the next morning.

A repeat troponin I was elevated at 0.07 ng/mL and 7.59 ng/mL at hours 4 and 7 from arrival respectively. Serum troponin I level just before the cardiac catheterization procedure was 16.69 ng/mL.  

90% stenosis of the proximal ramus intermedius, pre procedure TIMI II flow

The ramus intermedius is a normal variant on coronary anatomy that arises between the LAD and LCX. Its course is variable, often supplying the lateral wall of the LV. In this case, the vessel supplied a portion of the posterior LV circulation.

Post procedure 0% stenosis, TIMI III flow

A post procedure ECG was performed 24 hours after PCI:

Standard orientation 12-lead ECG demonstrating reperfusion of infarcted territory

Note that leads V2-4 show posterior reperfusion T waves (now more upright in these leads, as they are reciprocal to negative, reperfusion T waves inversions on posterior leads). Lead aVL also demonstrates typical reperfusion pattern, indicating high lateral wall reperfusion.

The patient was started on dual antiplatelet therapy and discharged from the hospital on day 3 without further event.

Take home points:

ST depressions maximal in leads V1-V4 (not otherwise attributable to an abnormal QRS complex) are highly specific for posterior OMI in a patient with new ischemic symptoms.

Serial ECGs are often helpful in identifying more subtle ECG manifestations of OMI

Posterior leads will often have little to no ST elevation even in the setting of posterior OMI owing to lung tissue being in between the posterior LV wall and the posterior chest wall. However, when the ST depressions resolve, there will be no ST elevations in posterior leads either, as this case highlights. Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5 mm in any posterior lead to be considered positive). Thus, it is essential for you to be able to recognize posterior OMI in the standard orientation 12-lead ECG!

Ventricular fibrillation is a common outcome in OMI and should greatly heighten the suspicion for ischemic heart disease even in the absence of profound ST elevation.

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My Comment by KEN GRAUER, MD (1/23/2023):

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The importance of today's case by Drs. Lieb, Bracey, Meyers & Smith — relates to how often similar situations occur. The cath lab was not activated after review of the initial ECG. For clarity in Figure-1 — I've reproduced this initial tracing.

• Given the history of new-onset chest pain and this patient's initial appearance described as "ashen and in moderate distress" — the cath lab should have been activated immediately on seeing ECG #1.

Figure-1: The initial ECG in today's case. I've added a magnified view of the mirror-image of the 1st complex in lead V3 (within the RED-border insert).

WHY the Cath Lab Should Be Immediately Activated:

As per the above case discussion by Drs. Lieb and Bracey — ECG #1 is highly suspicious for acute posterior OMI (Occlusion-based MI) because of the chest lead ST depression that is maximal in lead V4 — and because of the ST depression in lead V3 that has replaced the slight upsloping ST elevation that is normally seen in this lead.

• The "similar situations" I was referring to in my opening sentence — relates to 3 Oversights made by all-too-many clinicians. These oversights are: i) Failure to appreciate the characteristic "shape" of ST-T wave depression in the anterior chest leads, that when seen in a patient with new chest pain is indicative of acute posterior OMI; ii) Failure to appreciate that the "culprit" artery in many acute occlusion MIs will spontaneously reopen (thereby reperfusing) even without treatment — sometimes opening, then reclosing, then reopening again a number of times until eventually the vessel's final state is reached; and, iii) Even without ST elevation — a patient with new-onset and persistent cardiac chest pain that occurs in association with ischemic ST depression is indication for prompt cath.

The Positive "Mirror" Test in Figure-1:

Much more than just the amount of ST depression in leads V3 and V4 of ECG #1 — it is the shape of the ST-T wave in lead V3 that instantly told me the 50-ish year old man in today's case was having an acute posterior OMI. 

• I don't know why the pattern of ST-T wave abnormality seen in lead V3 of ECG #1 continues to go unrecognized by all-too-many clinicians. I've found the easiest way to convey appreciation for this important ECG sign — is with the Mirror Test. As I've illustrated multiple times in Dr. Smith's ECG Blog, the Mirror Test is simply a visual aid that facilitates recognition of acute posterior OMI from the standard 12-lead ECG without need to apply posterior leads (See My Comment at the bottom of the page in the September 21, 2022 post).

• The rationale for the Mirror Test is based on the premise that anterior leads provide a mirror image of electrical activity in the posterior wall of the left ventricle. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the "mirror-image" of leads V1-thru-V4.
• 
  
• In Figure-1 — the principal lead showing a positive Mirror Test is lead V3 (Seen within the magnified, RED-border mirror-image insert of lead V3). QUESTION: Doesn't the shape of the slightly elevated ST segment, in association with deep, symmetric T wave inversion in this lead suggest acute infarction?

Failure to Appreciate Spontaneous Reperfusion

Although the shelf-like straightened ST segment in lead V3 of Figure-1 is typical of acute posterior OMI — the amount of ST depression in this lead is modest. Instead — the T wave in lead V3 is distinctly peaked and taller than the R wave in this same lead.

• As suggested in Figure-1 by the deep T wave inversion within the RED-border insert — the peaked T wave in lead V3 strongly suggests that there has been at least some reperfusion of the "culprit" artery. That this might happen should not be surprising — since the patient's chest pain was already ongoing for 3 hours prior to arrival in the ED.
• Additional evidence in support of spontaneous "culprit" artery reperfusion in ECG #1 — is suggested by the flat ST segment in neighboring lead V2. With acute posterior OMI — ST depression is typically most marked in leads V2,V3,V4 — such that the flat ST segment in lead V2 presumably reflects some return-to-the-baseline of the ST depression that most probably had been present earlier in lead V2.
• Final evidence in strong support of recurrent spontaneous opening and reclosure of the "culprit" artery — was forthcoming when the patient revealed having several syncopal episodes while at home during the previous 24 hours, with each episode culminating in a shock from his implanted ICD.

BOTTOM Line in Today's Case:

As we have shown numerous times on Dr. Smith's ECG Blog — a "culprit" artery that spontaneously opens — may at any time spontaneously reclose. This most probably happened multiple times in today's case. Optimal treatment for today's patient would have been prompt cath with PCI to the "culprit" artery with the goal of maintaining coronary perfusion.  

• The patient's "ashen appearance" with ongoing chest pain at the time he arrived in the ED — in association with the diffuse ST segment changes on the initial ECG — should have been enough to indicate prompt cath, even without recognizing that the ST-T wave appearance in lead V3 of ECG #1 was diagnostic of acute posterior OMI.
• If doubt remained about the need for cath after reviewing the initial ECG — the recent history of 2 syncopal epsiodes that were both terminated by ICD shock — and/or — the subsequent dynamic ST-T wave changes on serial ECGs would have more than satisfied criteria for prompt cath.