Tuesday, October 10, 2017

Chest pain and Concordant ST Depression in a patient with aortic valve and previously normal angiogram


60-something presents with acute onset of chest pain.

His pain was accompanied by shortness of breath.  It awoke him from sleep.

Here is the prehospital ECG:
What do you think?








The rhythm appears to be atrial fibrillation.  There are no pacing spikes and the morphology is not right for a paced rhythm.  There is a wide complex that appears to be RBBB + LAFB.  There is excessive ST depression in V1 and V2.  Where normally RBBB would manifest a large R'-wave in V3, the lead may have been placed to far lateral and, instead, there is an S-wave.   In RBBB, a lead with a prominent S-wave, as is normal in V5 and V6, should not have ST Elevation or Depression.  This is all but diagnostic of posterior STEMI.

Then we see V4-V6 which have very broad, wide, "bulky" T-waves.  These by themselves are all but diagnostic for lateral hyperacute T-waves.

When you put the posterior and lateral together, it spells an occlusion of the circumflex territory.

The medics were concerned for STEMI but not certain enough to activate the cath lab, but did give ASA and NTG x 3, and the pain diminshed from 10/10 to 6/10.

On arrival, this ECG was recorded:
What do you think?









The same thoughts apply here.  The concordant ST depression in V3 is all but diagnostic of posterior STEMI.

There was a previous ECG available from one week prior:
This one is paced, with appropriate ST segments, though the concordant T-waves are slightly unusual



So what is going on?


The patient had a normal angiogram 1.5 years ago.  Could he have an acute STEMI now?

The cardiologist on call did not think so.  He suggested looking for other etiologies of chest pain.


The INR returned at 1.8.

The initial troponin I returned at 0.011 ng/L (normal: LoD = 0.010, 99% = 0.030).  This "negative troponin" seems to support the cardiologist, no?


A nitroglycerine drip was started but had to be stopped for hypotension.

Another ECG was recorded 30 minutes later:

Now there is the typical R'-wave in V3 and the concordant ST depression is in V4.
It still looks like a STEMI.


The pain pretty much fully dissipated.

The patient was treated medically, and a 2 hour troponin returned positive at 0.30 ng/mL.  4 hours into his stay, a third troponin returned at 23.5 ng/mL (quite high, and typical of a STEMI), at which time this ECG was recorded:
ST changes are much less pronounced.
This suggests reperfusion, either by lysis of thrombus or through collaterals.



Angiogram showed a lesion in the 2nd obtuse marginal off the circumflex.  Interestingly, at this point it was only 90% occlusive with TIMI-2 flow (this explains the relief of pain).  It could not be aspirated.  Presumably, it was 100% occlusive during pain.

Peak troponin 33.6 ng/mL

The impression was that this was an embolus from the aortic valve or from left atrial appendage (due to atrial fibrillation).

Echocardiogram: Previous echo EF = 56%; Now = 50%

TEE (Transesophageal echo): showed a thrombus on the mechanical aortic valve.



Myocardial infarction with previously normal coronary arteries.

I could not find any studies that looked at patients who had a previous normal angiogram and present with what appears to be acute coronary syndrome.

But there are at least several studies of patients with STEMI who normal coronary arteries at the time of the event.

This one has a nice figure showing the etiologies:

Myocardial infarction with normal coronary arteries: a conundrum with multiple aetiologies and variable prognosis: an update

Note that "concealed atherosclerosis" is one of them.
Even if there is no previous atherosclerotic stenosis on a standard angiogram, there can be significant occult atherosclerosis.  Most atherosclerotic lesions are "extraluminal" and can only be see with intravascular ultrasound or with CT coronary angiogram.  These lesions are very prone to ulcerate and thrombose.



The following study was also based on the angiogram at the time of the myocardial infarction.

Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: Experience from the PRAGUE studies

The observed prevalence of normal coronary angiography in patients presenting with acute chest pain and ST elevations was 2.6%. Most of these cases were misdiagnoses, not infarctions. A normal angiogram during a biochemically confirmed infarction is extremely rare (0.7%) and was not seen during the ongoing symptoms of ischemia.

This is the best study I could find:

In this large study of 5767 NSTEMI patients, 88% of patients with acute coronary syndrome had significant CAD (any stenosis greater than or equal to 50%), 6% had mild CAD (any stenosis of 0% to ≤50%), and 6% had no CAD (no stenosis identified).  This shows that even patients with no angiographic coronary stenosis can have unseen extraluminal plaque that ruptures and causes thrombosis and ACS.

Here is a great review in the New England Journal of Medicine:


Mechanisms of Acute Coronary Syndromes and Their Implications for Therapy. 
New Engl J Med 368(21): 2004-2013; may 23, 2013; 

Quote from article:

"Surprisingly, serial angiographic studies have revealed that the plaque at the site of the culprit lesion of a future acute myocardial infarction often does not cause stenosis that, as seen on the antecedent angiogram, is sufficiently severe to limit flow. Angiographic monitoring of responses to thrombolytic therapy has shown that after lysis of the offending thrombus, the underlying stenosis is often not the cause of the critical stenosis of the artery. In a prospective angiographic study involving patients undergoing percutaneous intervention for coronary artery disease, only half the subsequent events arose from lesions with sufficient stenosis to have warranted intervention at the time of revascularization. (CT) angiography, which permits evaluation of the arterial wall (not just the lumen), has shown that the characteristics of plaque associated with acute coronary syndromes include low attenuation (i.e., little or no calcification) and outward expansion of the artery wall, a process that tends to accommodate the growth of plaque while minimizing luminal encroachment.6-8  Intravascular ultrasonography has shown that in acute coronary syndromes, the culprits often lie proximal to the sites of maximal stenosis — the traditional targets of revascularization therapies."







Learning Points

1. A previous normal angiogram decreases the probability that any event is due to ACS, but by no means eliminates it.

2. Acute coronary occlusion may be due to other etiologies than ACS, such as embolism.  Coronay embolism is an indication for PCI.  The embolus can often be aspirated or broken up with the wire.


3. Learn the ECG features of coronary occlusion in the setting of RBBB

3 comments:

  1. Great post!Isn't there also inferior st elevation?

    ReplyDelete
    Replies
    1. George,
      With a complex that wide, one expects some ST elevation would be present without ischemia. I would apply the modified Sgarbossa (which normally is reserved for LBBB or paced rhythm) to these inferior leads. This would require that the STE at the J point be at least 25% the preceding S-wave. And, in fact, the angiogram confirms that the inferior wall was not involved.
      Steve

      Delete
  2. very informative, Dr Smith. thank you

    ReplyDelete

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