A 64 year old man with chest tightness

Submitted and written by Kaley El-Arab MD

Peer reviewed by Pendell Meyers, Alex Bracey, Stephen Smith

 

A 64-year-old male with past medical history of coronary artery disease with prior MI s/p stent to RCA (2008), hypertension, dyslipidemia, and diabetes presented with acute onset of chest pain.  Around 15:00 while at work he developed left-sided chest tightness that lasted for a few hours, then eventually went away, but returned the same evening around 22:00 when it woke him from sleep. He reportedly tried to “walk it off” which relieved the pain transiently. When the pain returned it was more severe and associated with nausea and diaphoresis, prompting him to call 911. On EMS arrival, the patient was bradycardic down to the 40s, but had a normal blood pressure. He reports that his baseline heart rate is in the 50s. He denies any lightheadedness, dizziness, abdominal pain, or back pain. His chest pain has improved slightly with the aspirin by medic, but did not resolve it.

 

Here is the patient’s initial ECG at 3:14am (time zero) in the Emergency Department:

What do you think?

 

ECG Interpretation:

Raw findings:

Sinus bradycardia

Narrow QRS with normal axis and early R wave progression in the precordial leads

Slight elevation of ST segments with convex T wave morphology in aVL.

Subtle reciprocal ST depression in inferior leads

ST depression with down-up T waves in V2-V4

 

Impression:

Findings consistent with posterolateral Occlusion MI (OMI)

 

Case Continued:

Initial high sensitivity troponin returned elevated at 48 ng/mL (Beckman coulter hs trop I, URL 12 ng/L for women, 20 ng/L for men) on presentation to the emergency department.

The patient was admitted, placed on heparin infusion, and received serial ECGs and troponins as well as a cardiology consult; however he was not understood as having acute coronary occlusion (Occlusion MI, OMI) and not given emergent reperfusion.

Repeat high sensitivity troponin was 210 ng/L.

Repeat ECGs show evolving ischemic changes of continued Occlusion: ST elevation in I and aVL, ST depressions in inferior leads, as well as depressions in V3-V5.

There is no mention of whether the patient had persistent pain.

ECG #2 at 9:02 am (about 6 hours after arrival)

ECG #3 at 10:33 am (about 7 hours after arrival)

ST depressions in inferior leads are becoming more pronounced. ST elevation is increased in I and aVL. ST depression in V3-V5 is persistent.

 

ECG #4 at 11:20 am (about 8 hours after arrival)

Now the OMI findings are resolving, indicating at least some temporary reperfusion.

Around this time, cardiology saw the patient, who had return of chest pressure associated with nausea and took the patient for emergent left heart catheterization.

The chart clearly states the preoperative diagnosis as “NSTEMI.”

A third high sensitivity troponin resulted at 226 ng/L before catheterization, but no further troponins were drawn.

 

The angiogram performed at 13:06 (about 10 hours after arrival) showed 100% occlusion of the proximal left circumflex artery with TIMI 0 flow. Of note, the angiographer described this lesion both as a “chronic total occlusion,” but also “the culprit lesion” (which is of course impossible and contradictory). A drug eluting stent was deployed resulting in TIMI 3 flow.

RCA: They found a prior mid-RCA stent. They describe a distal RCA lesion, 50% stenosis, “hazy...with filling defect consistent with thrombus,” but TIMI 3 flow. Separately from this lesion, they describe what they call “RCA posterolateral extension”, with 90% stenosis, no TIMI flow listed. The report is difficult to decipher, but 1 or perhaps 2 stents were placed in either or both of these RCA lesions. Post procedural TIMI flow was recorded as 3 in all arteries. The RCA lesions were also listed as “culprits.”

 

Meyers note: The ECG is clear that the culprit artery supplies the lateral and posterior walls. After learning this patients anatomy, it is possible that the LCX or the RCA could have been the culprit. The most specific finding on the cath report is the presence of a hazy, thrombotic culprit, leading me to believe that the RCA was the true culprit. At the same time, it is not always easy to open a “chronic total occlusion” (which is how they described the LCX), so it is not completely clear to me which lesion was the culprit.

ECG #5 at time 14:06 (11 hours after arrival), soon after left heart catheterization

According to the EMR, this ECG was obtained at 14:06, after cath. Unfortunately, it shows signs of reocclusion compared to the last ECG (#4 at 11:20 above). This can be due to in-stent immediate thrombosis, or could be caused by the stent occluding side vessels, or downstream showering of thrombus, or other causes.

 

An echocardiogram was performed on day two that demonstrated left ventricle ejection fraction of 50-55%, estimated visually, and no segmental wall motion abnormalities. The patient was discharged home later that day.

He did not have any more ECGs recorded unfortunately.

 

Learning Points:

 

ST depression maximal in V1-V4, without an alternative reason (e.g., RBBB), should be considered posterior OMI until proven otherwise.

This case demonstrates why more than half of LCX OMIs (or whichever artery supplies the high lateral and posterior walls) are missed. The high lateral wall STE is subtle and often does not meet STEMI criteria, while the focal anterior STD of posterior OMI is simply thought of as “ST depression from subendocardial demand ischemia,” or as “ACS with non-occlusive subendocardial ischemia.” 

But data shows that ST depression maximal in V1-V4, in contrast to V5-V6, is highly specific for OMI vs. subendocardial ischemia.

The ECG shows ongoing OMI even when the patient's symptoms fluctuate in intensity.

ED bedside US likely could have been an adjunct that may have helped recognize a wall motion abnormality in this case.

Recall that 25-30% of NSTEMI cases will have an acute coronary occlusion at the time of cardiac catheterization (in other words, be STEMI(-) OMI(+)). It is prudent to re-examine the case, the patient, and the ECG for subtle signs of OMI and ongoing ischemia before settling on the diagnosis of NSTEMI.