The cardiologist disagreed with cath lab activation. What do you think?

This was sent by a reader who is obviously a very astute clinician.

A middle aged male presented after 4 days of intermittent chest pressure which suddenly became worse and radiated down his left arm.  

Here was his initial ECG:

What do you think?

The emergency physician recognized that the "inferior ST depression" was reciprocal to high lateral OMI (very subtle STE in aVL).  There is some minimal downsloping ST depression in V3 and V4, further confirming the diagnosis.

She activated the cath lab at the referral institution (she is at a smaller hospital without a cath lab).

The patient suddenly had much worse pain and this ECG was recorded:

What is going on?

There are no P-waves before the QRSs.  The rate is regular and is about 100.  Complexes are wide.  So it is too slow for VT and too wide for a junctional rhythm.  

This is Accelerated Idioventricular Rhythm (AIVR).  There are retrograde P-waves after the QRS, as is virtually always the case with AIVR.  AIVR is sometimes seen during reperfusion and is usually a good sign, a sign of reperfusion.  It is often accompanied by relief of pain because the myocardium is again receiving oxygen.   

This AIVR also has superimposed high lateral OMI and inferior reciprocal ST depression that is out of proportion to the preceding R-wave.

In this context, it further confirms acute coronary syndrome. 

Clinical Course:

Immediately after the AIVR ECG, the pain became much better.  This ECG was recorded:

It is back in sinus rhythm with a normal QRS.  

There is still ischemic ST depression and ST Elevation, but it is much better, consistent with reperfusion.

The downsloping ST depression in V3 and V4 is gone.

See how V2 is also changed from the first one.

The cardiologist at the referring institution did not want to take the patient for cath and did not think this was acute MI, or at least not acute MI that needed the cath lab now.  He cancelled the cath lab activation.

The pain returned.  She gave nitroglycerine and the blood pressure dropped.  The cardiologist agreed to take the patient to cath.

The first troponin returned at 1.98 ng/mL (not a high sensitivity assay, diagnostic of acute MI).  This result was faxed to the receiving cardiologist.

The patient was transferred.

Angiogram

The angiogram showed a small 2nd diagonal with a hazy 60% proximal stenosis (which is exactly consistent with the ECG).  

Mysteriously, the angiographer wrote:

"INDICATIONS"

"--persistent bilateral arm/hand/chest pain"

"--junctional rhythm with hypotension" (Smith comment: he did not recognize AIVR)

"--troponin negative" (this is what is most mysterious -- the troponin was clearly positive)

IMPRESSION

"Unclear etiology of pain. Doubt small diagonal responsible for symptoms as he had excellent exercise capacity in between paroxysms of pain and HTN."

Smith comment: The "hazy" 60% stenosis is an acute thrombotic culprit lesion.

Learning Points

1. All of us, including cardiologists, need to learn to recognize electrocardiographically subtle OMI (Occlusion MI).

2. Learn to differentiate accelerated idioventricular rhythm (AIVR) from junctional rhythm.

3. Know the significance of AIVR.

4. Pay attention to the troponin level, especially when it is faxed to you!  A level of 1.98 ng/mL is very high and, in this clinical context (even without the ECG!), is diagnostic of acute type 1 MI.