2 Cases of Acute Ischemic Stroke -- What is the Etiology?

Case 1.

An elderly patient had sudden onset of severe hemiplegia.  He had no chest symptoms.  Head CT was negative.  tPA (alteplase) was started and an ECG was subsequently recorded:

There are well formed QS-waves in V2 and V3, suggestive of old MI with LV aneurysm.
Is the ST elevation due to LV aneurysm?
Unlikely: there is too much ST elevation.
V3 especially has a high T/QRS ratio, with 4 mm of T-wave divided by 7.5 mm of QRS, for a ratio of 0.55.  A value in any of leads V1-V4  greater than 0.36 makes acute STEMI far more likely than LV aneurysm.
However, there is also T-wave inversion, suggesting an open artery or prolonged (subacute) MI.

So this is either:
1.  Subacute STEMI (~24 hours old), or
2.  Old anterior STEMI (with probable aneurysm) with superimposed acute and reperfused STEMI (with inverted reperfusion T-waves).
3.  Recent (within a week or two) anterior STEMI with "no-reflow" resulting in marked persistent ST elevation.

An initial troponin I returned at 0.788 ng/mL.

If this were a subacute STEMI, already having formed well developed QS-waves, the initial troponin would be substantially higher.

Therefore, this is either #2 or #3.

When someone has a stroke and has old QS-wave MI, or especially a recent QS-wave STEMI on the ECG, one should be looking for LV thrombus.  LV aneurysm results in an akinetic (immobile) LV wall, which results in blood stasis which is thrombogenic.  Subacute STEMI adds inflammation to the endocardium, which enhances thrombogenicity.

Formal echo was therefore done:

1. Regional wall motion abnormality-distal septum anterior and apex akinetic
2. LV thrombus

The patient was treated medically for the MI.  (I now can't remember if the patient went for stent retrieval and, if so, the outcome.)

Subsequent troponins trended down and hit a plateau at a slightly lower level of 0.660 ng/mL.

This suggests the MI was recent (within many days to a week or so), not subacute.

This model fits best with the presentation, as a recent transmural STEMI in the LAD territory would result in a thrombogenic endocardium and LV thrombus, which is then at risk to embolize and result in stroke.

In the era before reperfusion therapy (early 1980's), all anterior STEMI were routinely put on heparin drips to prevent the occurrence of LV thrombus with its attendant stroke risk.

Diagnosis: Recent completed anterior wall STEMI with subsequent akinetic anterior wall, thrombus formation, and subsequent embolism with large middle cerebral artery ischemic stroke.  And that entire diagnosis could be gleaned from the clinical presentation and the ECG.

Case 2

This elderly patient had sudden onset of left-sided hemiplegia.  He had this ECG recorded before going for a head CT:

ECG:

There are wide, well-formed Q-waves in inferior leads, diagnostic of subacute or old inferior MI.
Not all LV aneurysms have persistent ST elevation, especially in the inferior location.
Additionally, inferior aneurysms usually do NOT have QS-waves (as they do with anterior MI); rather, they have QR-waves, as here.
So absence of QS-wave does not rule out inferior LV aneurysm.   

He also had this ED bedside echo done prior to head CT.  Here is the parasternal short axis:


What do you see in addition to a dense inferior wall motion abnormality?  (Answer is below)

Clinical course:

The head CT showed no bleed and tPA was given.

Here is one image from the head CT.  What do you see?

What do you see?

There is a hyperdense MCA sign in the left Middle Cerebral Artery [radiodenseity (white) in upper right part of brain].  Hyperdense MCA sign is seen more commonly in cerebral embolism (though most embolism is from atrial fibrillation) than in carotic artery thrombosis, as the thrombus is mature and more radiodense at the time of stroke onset.  So this is further evidence that there is a cardio-embolic source.  Since the patient is not in atrial fibrillation, that embolic source is likely to be a mural thrombus.  Since the patient has a dense inferior wall motion abnormality to go along with the large Q-waves, this is the likely source.


Bedside Ultrasound Legend:

Here is a still shot at the 1 second mark of the above ultrasound, where the ultrasound is pointed closer to the apex than the base:

Here I have circled the finding of the ultrasound:

There is a myocardial rupture with pseudoaneurysm of the inferior wall, with thrombus filling the pseudoaneurysm.

Clinical course:

CT angiogram stroke protocol revealed thrombus in the right internal carotid artery and middle cerebral artery.  The patient received tPA (alteplase) very quickly, then went for a stent retrieval. Unfortunately, the clot could not passed with the stent retrieval system, consistent with a mature thrombus.  It could not be retrieved.  The patient was started on long term anticoagulation.

Here the interpretation of the subsequent formal ultrasound (this formal US is not shown):

Regional wall motion abnormality, inferoposterior, akinetic with rupture and thrombus filled left ventricular pseudoaneurysm.

Clinical course:

The tPA did not cause catastrophic bleeding in this patient with a myocardial rupture, as the thrombus in the pseudoaneurysm was quite mature.  The stroke completed, as this mature thrombus is resistant to thrombolysis and could not be retrieved.

Learning Points

LV aneurysm can be diagnosed by ECG.  In the context of stroke, it strongly suggests cardioembolic source.