Is this a STEMI?

This interesting case reminded me that the STEMI vs pericarditis vs other cause of chest pain never gets old. It is a topic that is discussed endlessly by everyone yet somehow is never put to rest. I think this case is exemplary.

This mid-60’s male was sent to the ED by his primary care physician because of concerning chest pain. The patient complained of retrosternal chest pain/pressure with associated shortness of breath, ongoing for about 24 hrs with peaks and valleys. His PHx included HTN. He had no previous MI’s, was a non-smoker and did not have any of the other traditional cardiac risk factors. The family physician obtained an ECG in the office, which he found concerning, although the pt had previously elevated anterior ST’s on a previous ECG.

On exam, BP is in normal range. HR about 80. RR is 24 with normal O2 sat. The patient appears uncomfortable and tachypneic. JVP is normal, no murmurs. Mild bibasilar crackles are heard. No peripheral edema. Nitro caused minimal relief.

The first ECG done in the department is shown below – very similar compared to the one sent with the patient by the family doctor. 

V1-V3 show possibly concerning ST segments – difficult to say if these are concave up or horizontal. There are some T-inversions in other leads.


 

ECG #2, done 10 minutes later, is shown below. 

V1-V3 essentially unchanged. There is, however, new changes in leads I and AVL. On initial look, there appears to be concave ST segment elevation. Further scrutiny reveals PR depression, downsloping, in these leads – this actually makes the ST segment, at least in lead I, appear elevated. There is also more dramatic ST depression and T-inversion in leads III, AVF, V5 and V6. The 15-lead ECG was unremarkable.

CXR showed bilateral infiltrates. The physician looking after this pt called a “code STEMI”, as the ECG was evolving, with ST elevations and reciprocal changes, and the pt appeared in distress. Reminder – his CP history was >24hr. He was transferred to a facility with primary PCI.

After the patient was transferred out, his troponin came back at 1.7 (our normal lab cutoff is  <0.12). Potassium was 2.8 and creatinine was about 250 (micoMol/L), suggesting some degree of acute renal failure. WBC count was 15.4.

ECG #3, after the pt was transferred back 2 days later, is shown below.

Before you read below for the case resolution and cath report, review the ECGs and ask yourself “Is this a true STEMI?”

Argument for For STEMI:

• Diffuse ST elevation? No – less likely pericarditis.
• Reciprocal ST depression and T-wave inversion? Yes.
• Unwell patient? Yes – probably favours STEMI.
• We cannot apply the ST elevation in III>II rule because these leads do not have ST elevation.

Arguments for Pericarditis:

• Is it horizonal/convex or concave upward? Concave up – supports pericarditis.
• Is there PR depression? Yes, look at lead I and II. (although PR depression can occur with atrial ischemia, generally in inferior leads)
• Are there reciprocal changes in lead AVR (ST down, PR up)? Yes.

Case resolution

The pt was transferred back to our hospital 2 days later with a cath report showing no occlusions and no more than 30% stenosis in any vessel. He was diagnosed as myopericarditis. Echo in followup showed a "low normal" LV with a 50% and no effusion.

Pre-cath report, would you have called this a STEMI?

Further reading/resources:

• Amal Mattu’s EKG of the week website. STEMI vs Pericarditis – September 2012 http://ekgumem.tumblr.com/post/30868011279/finally-the-truth-about-pr-segments-and
• Amal Mattu’s EKG of the week website. STEMI vs Pericarditis – May 2012 http://ekgumem.tumblr.com/post/22587341701/heres-some-ugly-st-elevation-but-not-a
• Life in the Fastlane - http://lifeinthefastlane.com/ecg-library/basics/pericarditis/