Sunday, October 25, 2015

Anterorlateral STEMI? Old Anterior MI? But cath shows RCA thrombotic stenosis.

This case is from a frequent contributor, Brooks Walsh.  With additions and edits by me.

A 68 year-old man had been having chest discomforts intermittently for the past 2 weeks. About 18 hours prior to presentation, his pain began to worsen. He developed nausea, and 911 was called after he vomited once. EMS obtained an ECG:
There is subtle ST depression in II, III, and aVF. There is ST elevation in V2 – V5, with Q waves in V2 – V4.  This is all but diagnostic of anterior MI.
Is it acute? subacute? Old MI with persistent ST elevation?

EMS requested cath lab activation. The patient was given nitroglycerin 3 times, and his discomfort resolved completely before arrival to the ED. The ECG was repeated at that point:
The ST elevation in V2-V5 appears more pronounced, otherwise no significant changes.

Is this acute or chronic ST-segment elevation?
Concern was raised by cardiology that, given the duration of symptoms, as well as the anterior Q waves, that the ECG changes could reflect a chronic pattern of persistent ST-elevation (STE) following previous MI; aka “left ventricular aneurysm” (LVA). Emergent angiography for an NSTEMI might not serve an elderly patient well, they emphasized. Quite true!

However, there are elements of the ECG that suggest that, even if she does have an old anterior MI, she also likely has superimposed features of an acute anterior STEMI.


First:

Specifically, the anterior T-waves are relatively tall, compared with the QRS complexes. In both V2 and V3 we see that the T-wave height exceeds 36% of the total QRS amplitude. Recent results from Klein et al. strongly suggest that this indicates acute anterior STEMI, even in the presence of so-called LVA.
Furthermore, QR-waves commonly develop in the first hour of an anterior STEMI.

[It is important to note that QS-waves (in contrast to QR-waves - Q-waves followed by an R-wave) do NOT develop so quickly, and QS-waves are the waves one most commonly sees in LV aneurysm]
So, QR-waves cannot, by themselves, demonstrate a subacute or chronic presentation.

Second:

There is increasing ST elevation on the 2nd ECG.  This can only happen in acute STEMI.  

Therefore: the diagnosis is either:
1. acute STEMI with early Q-waves
2. subacute STEMI (prolonged occlusion with development of Q-waves, or
3. old anterior MI with superimposed acute STEMI


Clinical Course:
While awaiting the cath lab team, a second ECG was obtained:
Improvement in anterior STE and inferior ST-segment depression. New T-wave inversion in leads I and aVL now suggest that earlier ECGs showed ST segment “straightening” and hyperacute T waves in those leads. These dynamic changes support acute occlusion affecting the anterior wall, with possible spontaneous reperfusion.

The EM resident acquired a bedside echo:

There is an anterior wall motion abnormality, with severe hypokinesis/akinesis, but no overt dyskinesis or aneurysm.  There is no inferior WMA, or only a mild one.

Only one troponin I (Ortho clinical diagnostics) was obtained, pre-PCI: 1.4 ng/ml (0.034 ng/ml is 99th %)

Angiography and PCI
In angiography a 100% LAD lesion was found at the take-off from the LM.  However, this contained multiple calcifications, and was quite difficult to cross, the interventionalist felt this was chronic.

By contrast, the dominant RCA had a proximal 90% occlusion, but appeared acute. 
Pre- and post-stent deployment in the prox RCA (blue arrow = lesion).
Note that the RV branch (red arrow) is patent.

Both the LAD and the RCA lesions were stented.

Post-PCI results:
A post-cath ECG was obtained.
Inferior ST depression has resolved, as has the anterior STE. T-wave inversion is seen in leads I, aVL, and V2-V6, consistent with a reperfused anterior wall.

The post-cath echo demonstrated severe hypokinesis in the distal septal, anterior, and anterolateral segments, while the RV had normal systolic function.

This is all consistent with anterior LV STEMI.

How do you explain the ECG and echo findings by a 90% thrombotic lesion in the RCA?

Anterior STEMI – But which anterior wall?
Keep in mind that the right precordial leads are actually looking at TWO anterior walls – the anterior wall of the LV of course, but also the anterior wall of the RV.
Accordingly, there are (at least) two possible explanations for the anterior ST elevation and reversion
 RV branch of the RCA?
The first is that the RV branch of the RCA was transiently occluded. Numerous case reports have shown that occlusion of the RV branch (whether due to occlusion of a non-dominant RCA1,2,3,4 isolated occlusion of the RV branch5, or a surprisingly-common iatrogenic occlusion of the RV branch!6,7,8,9,10) can produce anterior STE without inferior STE.  In these cases of isolated RV MI, the anterior STE is produced by the ischemic anterior RV, not the antero-septal LV wall. Since the RV branch does not supply the inferior wall of the LV, STE in the inferior leads would not be expected.

However, the bedside echo, as well as the post-PCI comprehensive echo, did not reveal any RV dilation or dysfunction, making even a transient RV MI unlikely. Even though the symptoms and the ECG showed spontaneous improvement prior to PCI, it would be unusual to recover RV function so quickly and completely, even from a transient occlusion!
More importantly, an RV branch occlusion would not produce STE or T-wave inversion in aVL. Lastly, isolated RV MIs typically produce maximum STE in the right-side leads V1 and V2, whereas the maximal elevation here is more lateral, in V3-V5.

Subtotal RCA occlusion produced acute-on-old anterior MI?
Given the old compete LAD occlusion, how could the anterior wall have a “new” MI? Probably the anterior wall was being perfused by the RCA, via collaterals. After an acute RCA sub-total occlusion, the flow to the inferior wall might have been sufficient to prevent infarction of the inferior LV wall. However, the flow to the anterior wall through the collaterals might have been dramatically decreased, to the point that the anterior wall would become acutely ischemic.

In effect, this would produce an acute anterior STEMI (produced by RCA 90% occlusion) superimposed on the old anterior MI (due to LAD occlusion). This would be consistent with the ECGs (acute STE anterior and high-lateral, followed by TWI in those same leads), and with the echos (wall motion abnormalities limited to the anterior wall), virtually excluding inferior or lateral ACS.

Our explanation: All findings are explained by the presence of an old anterolateral MI which now only has collateral circulation from the RCA.   A 90% RCA occlusion remains enough to perfuse the inferior wall, but not enough to reach the anterior and lateral walls supplied by the LAD.

Without getting a detailed view of the video angiogram, this hypothesis cannot be verified.  We did not do this.


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