Atrial Fibrillation w Rapid Ventricular Response and ST Depression Maximal V1-V4: Not always subendocardial.

A patient presented a few years ago with chest pain, but also cough, low grade fever, and malaise.  She had one prehospital saturation at 88%, but otherwise all vital signs and labs were normal, without tachycardia, elevated BP or anemia.  She was never in any distress.

She had this prehospital ECG:

What do you think?

There is diffuse ST depression, in I, II, III, aVF and V3-V6.  It is diagnostic of ischemia.  It is maximal in V5 and II, with reciprocal STE in aVR, and is thus most consistent with subnendocardial ischemia (Posterior OMI would have maximal STD in V1-V4, and Posterolateral OMI would have STD in lead III but without STD in lead I).  So this is not typical of OMI.  Most likely, this patient does not have OMI.

By the time of arrival in the ED, the ECG had normalized.  It is not clear that any physician ever saw that prehospital ECG.

She was admitted, not given aspirin in the ED, and here are the serial troponins:  the first 6 are from a previous visit, showing that she does not have chronic myocardial injury (chronically elevated troponins).  The last 5 are from a subsequent visit showing she does not have chronic injury afterwards either. 

This is a rise and fall of troponin diagnostic of acute myocardial injury.  When there is proven ischemia, as there is by the ECG, then acute injury is acute MI. Then you must decide if it is type I or type II.  

She was diagnosed with "Type II MI" (due to supply demand mismatch).  However, there were no recorded supply/demand mismatch (no persistent hypoxia, tachycardia, anemia, hypertension, or hypotension) that could have cause type II MI, so I think this was a case of "Nah, couldn't be," and probably was a type 1 MI, though not OMI (type I Non-OMI, or NOMI).  

When a patient has not only chest pain, but also some other symptoms (cough, low grade fever, malaise), it is easy to explain away ischemia as NOT being due to ACS.  

She had an echo the next day: Moderate concentric left ventricular hypertrophy.  Normal left ventricular size and systolic function with an estimated EF of 66%.  But diffuse subendocardial ischemia often has no acute wall motion abnormality.  Same for NOMI.  And this is also sometimes true for OMI that has rapid reperfusion.

She did not have an ACS workup (no stress test, CT coronary angiogram (CTCA), nor angiogram)

I believe this was her first episode of ACS and a CTCA or angiogram would have significant coronary disease.  A stress test is much less sensitive, but might have revealed it.

________________

A few years later, she presented with CP and tachycardia, and was found to be in new Atrial Fibrillation with RVR.  The previous visit was apparently not noticed.

Here is her ED ECG:

There is profound ST depression, maximal in V3. 

Normally, STD maximal in V1-V4 is all but diagnostic of posterior OMI (we have submitted a paper showing this).  

However, when a patient has tachycardia, especially due to atrial fibrillation with RVR, it is not uncommon for subendocardial ischemia to present with maximal STD in V1-V4. 

 

Before concluding that it is posterior OMI, one should slow the heart rate and re-assess.  

Case Progression

She was electrically cardioverted, and this was her ECG 1 minute after cardioversion:

The heart rate is normal in sinus.  The ischemia is resolved.

This suggests that all that ischemia on the first ECG was really demand ischemia.  It makes it likely that she has coronary disease, with stenoses, but much less likely that there is ACS.

ACS is due to ruptured plaque, as opposed to stable plaque.

  

Stable plaque with significant stenosis limits coronary flow when more flow is required to supply the tachycardic myocardium. and such plaque is contributory to a type II MI)

First hs troponin I = 15 ng/L (URL = 16)

Peak hs trop = 749 ng/L (this is typical of a type II MI, but suggests that she at least has coronary stenoses that make her vulnerable to tachycardia)

The patient was admitted.  Unfortunately, she had no cardiology consult.  She was discharged soon thereafter.

5 days later she had sudden severe crushing chest pain and called 911.

Medics again found her in atrial fib with RVR.  They attempted cardioversion twice without success.

Here is her ED ECG:

Again, atrial fibrillation with RVR and ST depression maximal in V3.

Cardioversion was attempted twice in the ED without success.

She was given 1 mg of ibutilide over 10 minutes and cardioverted again.  After this "facilitation" with ibutilide, cardioversion was successful.

See this for more information on ibutilide: What to do when Atrial Fib with RVR will not Electrically Cardiovert. And how do you measure the QT in Atrial Fib?

Here is her ECG 30 minutes after cardioversion:

There is persistent ST depression maximal in V3.

The patient still had chest pain.

This should be considered diagnostic of posterior OMI until proven otherwise.

Cardiology was consulted, but because it was "not a STEMI" and was due to "subendocardial ischemia," the patient was not taken to the cath lab.

The patient continued to have chest discomfort, but it was explained away by the admitting physician as "chest wall pain."

Troponins overnight:

First hs trop = 76 ng/L

Next is 4 hours later = 27,600 ng/L

Next is 2 hours after (t = 6 hours) = 43,300 ng/L

Next is 3 hours after that (t = 9 hours) = over 50,000 ng/L (too high to measure)

After many hours, the ECG normalized.

Angiogram the next day showed BOTH 3 vessel disease and a culprit in the obtuse marginal (off the circumflex) with thrombus and 95% open.

Echo showed a new lateral (posterior) wall motion abnormality.

This is not a STEMI, but is an OMI of the obtuse marginal that led to a lot of myocardial loss.

Learning Points:

1. Do not diagnose Type II MI unless there are definite causes of increase oxygen demand or decreased supply.

2. ST depression in leads I, II, III, aVF and V4-V6 is usually subendocardial ischemia.  The ST vector is towards leads II and V5, with reciprocal ST elevation in aVR

3. ST depression maximal in V1-V4 in usually due to posterior OMI, but can be due to atrial fibrillation with RVR or other stresses; in the latter situations, it should resolve after resolution of tachycardia.

4. Patients with 3 vessel disease who have sudden chest pain and EKG abnormalities must have some culprit for their acute presentation, even if it isn't seen (in this case it was seen).  Just because there is 3 vessel disease does not mean there is not also an OMI.

5. Many, or even most, OMI will be open by the time of angiogram, but not before they have done a lot of damage.  This artery was 95% open, but it had been closed long enough that the peak troponin was over 50,000, with a wall motion abnormality.

6. Whether it is OMI or not, and whether you believe the ECG or not, if the patient has chest discomfort uncontrolled by aspirin, heparin (or LMWH), and Nitroglycerine, then such refractory chest discomfort is an indication for emergent angiogram by ACC/AHA guidelines. 

Do not call it "chest wall pain."  "Control" of pain does NOT include using opiates or analgesics; you should commit the patient to the cath lab if such medications are required to control pain.