An elderly male presented with cough and dyspnea, progressive for several days. He had no chest pain. Among his many tests, the ECG was done first, and was handed to me before I ever saw the patient:
This is consistent with inferior and posterior MI (posterior STEMI), but also with subendocardial ischemia. The clinical context is critical. Although a patient with acute chest pain and this ECG is likely to have a posterior MI, a complex medical patient may have reasons for supply/demand cardiac ischemia that are not related to ACS.
Such "demand ischemia" is usually diffuse and subendocardial, but it may be focal, especially if there is a coronary stenosis in a particular territory. In such a case, it may present with ST elevation.
Subendocardial demand ischemia may have ST depression that mimics posterior STEMI. But the minimal ST elevation in lead III suggests that this really is transmural ischemia generating ST elevation of inferior and posterior walls.
On exam, the patient was slightly hypoxic and very pale; he appeared to be anemic. His hemoglobin was 4.8 g/dL and so he was transfused. He had heme + stools but no melena or gross blood. He also had pneumonia, and a core temperature was 38.5.
I knew this was not a typical ACS and so I activated our "Pathway B", which is a compromise between activating the cath lab ("Pathway A") and not activating. It is for emergent cardiologic evaluation for patients who might need emergent angiogram and PCI, but are complicated by an equivocal ECG or complicated medical problems.
The cardiologist came immediately. An emergency formal echo showed an inferolateral wall motion abnormality. In the record, an old angiogram reported a chronically occluded obtuse marginal (OM). The previous echo was normal, but a stress echo had shown induced inferolateral hypokinesis. Thus, there was prior proof that this area was vulnerable to stress; the territory of this artery was reliant on collateral circulation for oxygen delivery.
The first troponin I returned at 3.9 ng/mL.
The etiology of these ECG findings was not ACS, but rather transmural ischemia (with resulting ST elevation) in the territory of the chronically occluded OM due to poor oxygen delivery in this vulnerable area.
After resuscitation, especially with blood products, the hemoglobin was 8.8 and the ST depression was resolved. The troponin I peaked at 12 ng/mL and then fell. Here is the next day ECG:
The patient did not undergo an angiogram. He did well.
Learning Points:
Type 1 MI (due to ACS) vs. Type 2 MI (due to poor oxygen delivery and/or high oxygen demand)
1. Don't automatically activate the cath lab for ischemic ST elevation on the ECG (in this case is was posterior ST elevation). Think first about why there is ischemia.
2. Don't forget Type 2 MI as the etiology of ischemia (ECG or troponin elevation). In our studies at HCMC, 65-75% of all MI are type 2 MI.
3. Most ischemia from type 2 supply demand mismatch is subendocardial. It will usually have more diffuse ST depression.
4. The echo is likely to have no new wall motion abnormality when there is subendocardial ischemia.
5. Even MI with ST elevation may be Type 2 MI.
6. From 2-5% of Type 2 MI have ischemic ST Elevation. We believe it should not be called STEMI. See this article by Sandoval, Smith and Apple.
7. Here is the most recent review of Type II MI, by Sandoval, Smith, Thordsen, and Apple.
Here are 3 more examples of type II MI with ST elevation.
 |
| There is minimal ST elevation in inferior leads, with reciprocal ST depression in aVL and marked ST depression in V2-V5. |
This is consistent with inferior and posterior MI (posterior STEMI), but also with subendocardial ischemia. The clinical context is critical. Although a patient with acute chest pain and this ECG is likely to have a posterior MI, a complex medical patient may have reasons for supply/demand cardiac ischemia that are not related to ACS.
Such "demand ischemia" is usually diffuse and subendocardial, but it may be focal, especially if there is a coronary stenosis in a particular territory. In such a case, it may present with ST elevation.
Subendocardial demand ischemia may have ST depression that mimics posterior STEMI. But the minimal ST elevation in lead III suggests that this really is transmural ischemia generating ST elevation of inferior and posterior walls.
On exam, the patient was slightly hypoxic and very pale; he appeared to be anemic. His hemoglobin was 4.8 g/dL and so he was transfused. He had heme + stools but no melena or gross blood. He also had pneumonia, and a core temperature was 38.5.
I knew this was not a typical ACS and so I activated our "Pathway B", which is a compromise between activating the cath lab ("Pathway A") and not activating. It is for emergent cardiologic evaluation for patients who might need emergent angiogram and PCI, but are complicated by an equivocal ECG or complicated medical problems.
The cardiologist came immediately. An emergency formal echo showed an inferolateral wall motion abnormality. In the record, an old angiogram reported a chronically occluded obtuse marginal (OM). The previous echo was normal, but a stress echo had shown induced inferolateral hypokinesis. Thus, there was prior proof that this area was vulnerable to stress; the territory of this artery was reliant on collateral circulation for oxygen delivery.
The first troponin I returned at 3.9 ng/mL.
The etiology of these ECG findings was not ACS, but rather transmural ischemia (with resulting ST elevation) in the territory of the chronically occluded OM due to poor oxygen delivery in this vulnerable area.
After resuscitation, especially with blood products, the hemoglobin was 8.8 and the ST depression was resolved. The troponin I peaked at 12 ng/mL and then fell. Here is the next day ECG:
 |
| Still abnormal but no severe ischemia remains |
The patient did not undergo an angiogram. He did well.
Learning Points:
Type 1 MI (due to ACS) vs. Type 2 MI (due to poor oxygen delivery and/or high oxygen demand)
1. Don't automatically activate the cath lab for ischemic ST elevation on the ECG (in this case is was posterior ST elevation). Think first about why there is ischemia.
2. Don't forget Type 2 MI as the etiology of ischemia (ECG or troponin elevation). In our studies at HCMC, 65-75% of all MI are type 2 MI.
3. Most ischemia from type 2 supply demand mismatch is subendocardial. It will usually have more diffuse ST depression.
4. The echo is likely to have no new wall motion abnormality when there is subendocardial ischemia.
5. Even MI with ST elevation may be Type 2 MI.
6. From 2-5% of Type 2 MI have ischemic ST Elevation. We believe it should not be called STEMI. See this article by Sandoval, Smith and Apple.
7. Here is the most recent review of Type II MI, by Sandoval, Smith, Thordsen, and Apple.
Here are 3 more examples of type II MI with ST elevation.
Hi Dr.Smith
ReplyDeleteThank you for good case.
Relatively ST depression to QRS amplitude is biggest in V5,V6 than V3,
V4. Does this mean subendo ischemia than post wall MI?
Great question. When the ST depression in V3 is due to the ST elevation of the posterior wall, as recorded from anterior, it should not be measured relative to the R-wave amplitude because the R-wave amplitude is due to the anterior, not posterior, wall. It is the difference between the positive deflection of the anterior wall minus the posterior directed vector of the posterior wall. complicated, do you understand what I'm saying?
DeleteSteve Smith
Thank you very much .
DeleteWhich is more likely to be subendo ischemia or post MI only in chest leads?
DeleteI think if you read this post (the most popular ever with over 60,000 views, you will understand: http://hqmeded-ecg.blogspot.com/2012/02/five-primary-patterns-of-ischemic-st.html
Delete