Friday, May 23, 2014

A Picture of Subendocardial Ischemia

This case shows a CT image of subendocardial ischemia.  The image is shown at the bottom after the case presentation.

This patient presented with a mechanical fall and had chest pain.  He had this ECG recorded:
There is slight ST elevation in lead III, with reciprocal ST depression in aVL.  However, there are also Q-waves inferiorly and the inferior T-waves are inverted, suggesting that this is an old MI with persistent ST elevation, or, alternatively, a subacute or partially reperfused, inferior STEMI.  There are somewhat large T-waves in V2 and V3 which are non-specific but could represent posterior reperfusion T-waves. There is ST depression in V4-V6. 

His previous ECG was 4 years prior and was normal.  It confirmed that the Q-waves, inferior T-wave inversion, and large T-waves in V2 and V3 were all new.

His chest pain increased and this ECG was recorded:
Now there is increasing inferior ST elevation.  There is also new ST depression in V2-V3 and increased ST depression in V4, maximal in V2 and V3.  This is all but diagnostic of inferior-posterior STEMI. However, the inferior T-waves remain inverted, and this is atypical for inferior STEMI.  

His first troponin I returned at 0.10 ng/mL (slightly elevated) and his symptoms could not be controlled with nitroglycerin, so he was taken to the cath lab and found to have:

--Severe 3 vessel Coronary artery disease involving the LM.
--Chronic Total Occlusion of the RCA filling via left to right collaterals.
--Severe Left Main disease, and chest pain with contrast injection into the LM.  This chest pain was relieved with injection of nitroglycerine, with LV end diastolic pressure (LVEDP) decreasing to 12 from 26.
--The patient was started on Heparin and NTG drips.  The pain resolved with the nitroglycerine.
--No PCI was done
--The patient went for CABG.

The post cath ECG was not recorded until the next morning:
The ischemia is almost entirely resolved.  There are inferior and posterior reperfusion T-waves.  The Q-waves appear to be smaller

Peak Troponin I was 0.106 ng/mL (not very high)

Formal Echo report, the next day:

--Regional wall motion abnormality-inferoposterior, large.
--Decreased LV systolic performance mild; ejection fraction is 47%
-- In direct comparison with the resting study from 5 years prior, the wall motion abnormality is new, as is the reduction in left ventricular systolic performance.

Summary of this case:

So the patient had transient ST elevation (transmural, not subenocardial, ischemia) of the area of the heart (inferior and posterior walls) supplied by left to right collaterals because of a chronic total occlusion of its previous supply from the RCA along with some obstruction to flow through the collateral supply from the left main.

The inferior and posterior walls are also at chronic risk of subendocardial ischemia because of this tenuous blood supply.  The remainder of the heart is also at high risk of subendocardial ischemia because of this obstructed flow in the left main and the need for the left main to supply not only its normal territory (anterior and lateral/LAD and circumflex), but also the inferior and posterior walls.

So here is the really interesting part:

The patient had had an outpatient CT scan of the abdomen done one week earlier.  It had been ordered one month prior because the patient had a complaint of abdominal pain after eating, resolved with nitroglycerine, with a "question of bowel ischemia."

There was no ECG done at the time of the scan or at the outpatient visit for abdominal pain which precipitated the CT scan.

The abdominal CT scan showed:

1. Marked atherosclerotic calcification at the origins of the celiac and superior mesenteric arteries. These arteries appear to remain patent, however a hemodynamically significant stenosis is not excluded. No
evidence for watershed ischemia.

2.  The scan also showed poor contrast enhancement of the subendocardium of the heart.  This was only seen in retrospect.
Since this is imaged with contrast, areas that are perfused should be dense (white) with contrast.  Areas that are poorly perfused will be dark (no contrast).  Notice the poor perfusion in the subendocardium of the posterior wall of the heart (dark areas pointed out by arrows below).  The inferior wall was similarly affected.

Arrows point to a poorly perfused area of subendocardial myocardium in the posterior wall (the subendocardium is the layer closest to the heart chamber).  Since this is a contrast study, well-perfused areas are bright with contrast, whereas poorly perfused areas remain dark.  The subendocardial layer is most susceptible to ischemia because it is closest to the high pressure LV chamber; that higher pressure inhibits perfusion while the subepicardial (outer) layer may still be well perfused.

Was the "abdominal pain" actually infero-posterior subendocardial ischemia?

CT myocardial perfusion imaging

Sestamibi myocardial perfusion imaging is well known, as is CT coronary angiography, but a new imaging modality is CT myocardial perfusion imaging.  This is essentially what we see in the image above.  However, CT myocardial perfusion imaging is rarely positive at rest.  Rather, it is a provocative test (a stress test) done with adenosine or dobutamine stress with before and after images, much like what is done with sestamibi, or even with stress echo.  It may have additive incremental value to the more traditional stress tests.

Mostly I think it just give interesting images that let us visualize the ischemic heart.

Here are some references:


  1. Sir in 2nd ecg in v2, V3 after t wave there is one deflection is it u wave??

  2. Can the STd in V5 V6 in ECG 1 be due to LVH strain?

  3. @ MG — Yes — it IS definitely possible that the ST-T wave depression in lateral chest leads V5 and V6 may at least partially be the result of LV “strain” because: i) There is definite voltage for LVH on this tracing (deep anterior S waves with very tall R wave in lead V5); and ii) the SHAPE of the ST-T wave depression in lead V6 especially is very typical for the gradual slow downsloping ST segment with LV “strain”. How much of this lateral chest lead ST depression is the result of LVH vs potentially new ischemia is impossible to tell from this single ECG — :)


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