This case was contributed by one of my talented colleagues, Johanna Moore, MD. She is our research director and is doing some great research on cardiac arrest. Check out her research on Head-up CPR!
There is more interesting stuff on Head up CPR here. And here.
Case
A patient with a history of CABG in 1998, with subsequent ischemic cardiomyopathy, called his clinic to report he had a few minutes of burning chest and epigastric pain, associated with walking, that was now gone. They told him to call 911. Medics arrived and recorded this ECG (pain free) about 15 minutes after the resolution of chest discomfort:
The paramedics were worried by his ECG and had a physician check the patient and ECG at the door.
The patient arrived and was free of discomfort.
After briefly reviewing the patient's previous ECG, the physicians decided to expedite the patient's care by placing him in a critical care area despite the patient's well appearance. This first ED ECG was recorded at 15 minutes after the previous prehospital ECG and 30 minutes after resolution of discomfort.
1 year prior
The physicians were concerned regarding the change from the patient's previous ECG and degree of absolute ST segment elevation on the new ECG.
On further history, the patient reported no associated symptoms. He was a reticent historian, and only after repeated pointed questioning was better history obtained. He stated that the discomfort was brought on by walking, lasted for "just a few minutes" and relieved with rest. When asked more about the duration of the pain, the patient stated the pain lasted for 15-20 minutes. When specifically asked if he had any recent episodes like this, he stated he had a few similar pains in recent weeks, but was unable to state how this episode was different today.
He looked very comfortable, and stated he felt back to normal. He had a blood pressure of 137/85, pulse of 77, and O2 sat of 95%.
The patient reported he had not had an angiogram since the CABG was performed in 1998. The last echocardiogram on file from 2012 showed an EF of 43%, with inferior, septal, and posterior wall motion abnormalities. The ED physicians performed a bedside echo:
This shows globally severe systolic dysfunction.
Based on the history, ECG, and bedside echo, the ED physicians called the on call cardiologist for an emergent consult. The cardiologist was present within 10 min and also performed a history and physical.
This repeat ECG was performed 16 min later, and 31 min after the prehospital ECG:
The cardiologist and ED physician debated what to do. Both thought the patient would eventually need an angiogram either later that day or the next. It was reassuring to them the patient appeared well, but he had a concerning medical history and HPI for unstable angina, especially taking his cardiac ultrasound and ECG into account as well. As they were talking with the patient, the troponin I returned at 0.516 ng/mL.
At this point, the physicians did not have a good alternative explanation to ACS for why this troponin would be positive and both agreed he should go to the cath lab.
The angiogram showed a "99%" LAD lesion that was hazy, but had TIMI-3 flow.
Here is the post PCI ECG:
Troponin I peaked at 1.390 ng/mL the next AM, and this ECG was recorded:
Smith comment
What happened here?
This is the most likely scenario:
The patient had a completely occluded LAD, or nearly so, at the time of the chest discomfort. The flow was less than TIMI 3 at that moment. If an ECG had been recorded, the ST Elevation would have been even higher (or the S-wave amplitude lower), and it would probably have been high enough to meet the Modified Sgarbossa criteria.
However, the artery opened, the ischemia was resolving, and the pain resolved. By the time of the first ECG, it was no longer diagnostic (no longer met Modified Sgarbossa criteria). Nevertheless, the physicians used very good judgment to take the patient to the cath lab, where although there was TIMI-3 flow, there was an acute lesion due to ACS.
As the ischemia resolved, the ST/S ratio fell from 0.174 to 0.158 in just 16 minutes, then to 0.132, then 0.114
There is more interesting stuff on Head up CPR here. And here.
Case
A patient with a history of CABG in 1998, with subsequent ischemic cardiomyopathy, called his clinic to report he had a few minutes of burning chest and epigastric pain, associated with walking, that was now gone. They told him to call 911. Medics arrived and recorded this ECG (pain free) about 15 minutes after the resolution of chest discomfort:
 |
| Left Bundle Branch Block, but with both S-waves and T-waves cut off due to high voltage. You can see quite a bit of discordant ST depression in V5 and V6, but not out of proportion |
The paramedics were worried by his ECG and had a physician check the patient and ECG at the door.
The patient arrived and was free of discomfort.
After briefly reviewing the patient's previous ECG, the physicians decided to expedite the patient's care by placing him in a critical care area despite the patient's well appearance. This first ED ECG was recorded at 15 minutes after the previous prehospital ECG and 30 minutes after resolution of discomfort.
 |
| There is LBBB with 7.5 mm of STE in lead V2 (the lead with the highest ST/S ratio) The S-wave is 43 mm. The ratio is 7.5/43 = 0.174. This is below the Modified Sgarbossa cutoff of 0.25 In Smith's studies, 0.20 was more sensitive but less specific than 0.25; 0.17 is less than either. Nevertheless, there is a big and scary change from the previous ECG (below). |
 |
| LBBB with a relatively narrow QRS and much less ST deviation |
The physicians were concerned regarding the change from the patient's previous ECG and degree of absolute ST segment elevation on the new ECG.
He looked very comfortable, and stated he felt back to normal. He had a blood pressure of 137/85, pulse of 77, and O2 sat of 95%.
The patient reported he had not had an angiogram since the CABG was performed in 1998. The last echocardiogram on file from 2012 showed an EF of 43%, with inferior, septal, and posterior wall motion abnormalities. The ED physicians performed a bedside echo:
This shows globally severe systolic dysfunction.
Based on the history, ECG, and bedside echo, the ED physicians called the on call cardiologist for an emergent consult. The cardiologist was present within 10 min and also performed a history and physical.
This repeat ECG was performed 16 min later, and 31 min after the prehospital ECG:
 |
| There is slightly less ST elevation in V2, at 6 mm, for a ratio of 6/38 = 0.158. The ST segment, and the ratio, are falling. Now there is also much less ST depression in V5 and V6 |
The cardiologist and ED physician debated what to do. Both thought the patient would eventually need an angiogram either later that day or the next. It was reassuring to them the patient appeared well, but he had a concerning medical history and HPI for unstable angina, especially taking his cardiac ultrasound and ECG into account as well. As they were talking with the patient, the troponin I returned at 0.516 ng/mL.
At this point, the physicians did not have a good alternative explanation to ACS for why this troponin would be positive and both agreed he should go to the cath lab.
The angiogram showed a "99%" LAD lesion that was hazy, but had TIMI-3 flow.
Here is the post PCI ECG:
 |
| 5 mm STE in lead V2. Ratio = 5/38 = 0.132 The ratio is still falling |
Troponin I peaked at 1.390 ng/mL the next AM, and this ECG was recorded:
 |
| 4 mm of STE in lead V2. Ratio = 4/35 = 0.114 (normal) |
Smith comment
What happened here?
This is the most likely scenario:
The patient had a completely occluded LAD, or nearly so, at the time of the chest discomfort. The flow was less than TIMI 3 at that moment. If an ECG had been recorded, the ST Elevation would have been even higher (or the S-wave amplitude lower), and it would probably have been high enough to meet the Modified Sgarbossa criteria.
However, the artery opened, the ischemia was resolving, and the pain resolved. By the time of the first ECG, it was no longer diagnostic (no longer met Modified Sgarbossa criteria). Nevertheless, the physicians used very good judgment to take the patient to the cath lab, where although there was TIMI-3 flow, there was an acute lesion due to ACS.
As the ischemia resolved, the ST/S ratio fell from 0.174 to 0.158 in just 16 minutes, then to 0.132, then 0.114
In spite of Occlusion, the troponin I peaked at only 1.390 ng/mL. By our research methods, this would not qualify as an Occlusion MI (OMI), even though it is!! Even though this OMI put a lot of myocardium at risk, reperfusion was so fast that only a small amount of myocardium actuallly died
Learning Point:
There can be severe ACS, even with "99%" stenosis, and TIMI-3 flow at the same time. The ECG will not be diagnostic of occlusion when there is TIMI-3 flow, even if the artery is severely narrowed by thrombus.
Learning Point:
There can be severe ACS, even with "99%" stenosis, and TIMI-3 flow at the same time. The ECG will not be diagnostic of occlusion when there is TIMI-3 flow, even if the artery is severely narrowed by thrombus.
GREAT case with some important clinical lessons to be learned — especially that even when Sgarbossa (or modified Sgarbossa) Scores don't suggest acute STEMI — that a critical lesion (and need for timely cath) may still be there. Also, that clinical judgment is irreplaceable, with serial tracings helpful to sort out unusual findings (ie, Why despite no appreciable change in heart rate the amount of ST elevation in this LBBB became so much less ... ). THANKS for presenting!
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