A 20-something male presented from an outside facility with Chest pain. Vital signs were normal.
History: Onset of CP 2.5 hours prior to ED arrival. "Tight and pressure, radiates to right arm, + nausea, + SOB. No thromboembolism risks, not pleuritic, no radiation to the back. No cardiac risk factors, no cocaine use.
He came with this ECG from the outside facility, recorded 1 hour after pain onset:
Is this inferior ST elevation due to "early repolarization"?
No. Why not? We have found in our study comparing inferior STEMI (manuscript in preparation) to inferior early repol several distinguishing characteristics.
1. There is reciprocal ST depression in aVL. This occurred in 0 of 66 cases of early repolarization, and 99% of patients with inferior Occlusion MI (OMI).
2. There is too much ST elevation. In only 1 of 66 cases of early repol was there one lead with at least 2 mm STE.
3. Absence of ST elevation in V5 and V6. In our group with inferior early repolarization, 53 of 66 had at least 1 mm of STE in V5, and 61 of 66 had at least 0.5 mm in V5. 64 of 66 had at least 1 mm of STE in V6 and 58 of 66 had at least 0.5 mm in V6. In other words, when there is normal variant ST elevation in inferior leads, there is usually also normal variant ST elevation in V5 and V6.
4. T-waves are too tall. T-waves in inferior leads are hyperacute, out of proportion to those in early repol
5. T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia.
95 minutes later, the patient arrived in the ED and here is the triage ECG:
There should be no doubt that this is OMI. All of the above 5 points apply, but now all the features have evolved and are more apparent. In addition, there is ST depression, diagnostic of ischemia, in V3-V6.
Nevertheless, the cardiologist consulted diagnosed early repolarization. The patient did not undergo immediate cath.
22 minutes later, another ECG was recorded:
Side by side comparison of leads II and III on the first two ECGs:
First troponin I returns + at 0.252 ng/ml.
191 minutes after first ECG:
Heparin drip started. CCU consulted. Admitted to CCU. Integrilin given. Not take directly to cath lab.
A second troponin returned at 1.71 ng/ml 3 hours later.
The patient was not taken to cath for another 6 hours after this last ECG. It showed a 99% stenosis in the RCA, and proximal to a posterolateral branch. A coronary aneurysm was found. TIMI flow not reported.
Troponin I peaked at 75 ng/ml (A VERY large OMI)
Next ECG available - 2 week followup:
This ECG, and the very elevated troponin, strongly suggest that the artery re-occluded during the extra 6 hour delay.
Lessons:
1. Young people do have OMI
a. Some of these MIs in young people are due to anomolies: aneurysm from a disorder known to be associated with coronary aneurysms (left out to maintain anonymity) in this case. Young women, when they have OMI, often have coronary dissection.
b. Nevertheless, even young people have atherosclerosis and plaque rupture. We have seen many, such as this young woman. And young women have worse outcomes than other groups with STEMI because of the tendency to say, "Nah, couldn't be!"
2. When the ECG is unequivocally diagnostic, don't let young age or other atypical features deter you.
3. Know the features of OMI look-alikes. In this case, early repolarization was diagnosed by the cardiologist, who clearly was unaware of important differentiating features of inferior early repol from inferior OMI (see above)
4. Once OMI is diagnosed, the patient should go immediately to the cath lab even if the ST elevation resolves, because the risk is so high. In this case, however, the diagnosis was also simply missed.
See this case to demonstrate the danger of reperfused OMI!
5. Finally, YOU have to be the expert and YOU have to advocate for the patient. Cardiologists don't know everything, and in particular they don't know YOUR job, which is to differentiate the patients with benign symptoms (the vast majority) from those with Serious pathology. If the cardiologist disagrees and is incorrect, the only way the patient will get good care is if YOU are the expert, YOU know what findings are true positives and true negatives, and YOU can explain why you are right and Advocate.
Cardiologists need to know a whole lot, but they don't do our everyday job of screening hundreds of symptomatic patients to find the one with the real thing. They cannot be experts at that; you must be the expert. They are much more likely to demand proof of disease than emergency physicians. We demand proof of absence of disease. And the cardiologists' opinions are of course often, or even usually, correct, but insist on a respectful conversation in which reasoning and evidence, rather than authority, direct the outcome. That can only happen if YOU are well informed.
Here are two examples of early repolarization in the inferior leads:
First:
Second:
History: Onset of CP 2.5 hours prior to ED arrival. "Tight and pressure, radiates to right arm, + nausea, + SOB. No thromboembolism risks, not pleuritic, no radiation to the back. No cardiac risk factors, no cocaine use.
He came with this ECG from the outside facility, recorded 1 hour after pain onset:
 |
| There is at least 2 mm of inferior ST elevation, with reciprocal ST depression in aVL, ST flattening in V4-V6, and T-wave inversion in V2. |
No. Why not? We have found in our study comparing inferior STEMI (manuscript in preparation) to inferior early repol several distinguishing characteristics.
1. There is reciprocal ST depression in aVL. This occurred in 0 of 66 cases of early repolarization, and 99% of patients with inferior Occlusion MI (OMI).
2. There is too much ST elevation. In only 1 of 66 cases of early repol was there one lead with at least 2 mm STE.
3. Absence of ST elevation in V5 and V6. In our group with inferior early repolarization, 53 of 66 had at least 1 mm of STE in V5, and 61 of 66 had at least 0.5 mm in V5. 64 of 66 had at least 1 mm of STE in V6 and 58 of 66 had at least 0.5 mm in V6. In other words, when there is normal variant ST elevation in inferior leads, there is usually also normal variant ST elevation in V5 and V6.
4. T-waves are too tall. T-waves in inferior leads are hyperacute, out of proportion to those in early repol
5. T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia.
95 minutes later, the patient arrived in the ED and here is the triage ECG:
 |
| There is 2-2.5 mm of ST elevation in inferior leads. There is reciprocal ST depression in I and aVL, with T-wave inversion in aVL. There is relative ST depression in V2 (isoelectric: in a young man it there should be at least 1 mm of ST elevation), thre is also flattening of the ST segment in V2. There is ST depression from V3-V6. There is a negative T-wave in V3, and biphasic T-waves in V4-V6. |
There should be no doubt that this is OMI. All of the above 5 points apply, but now all the features have evolved and are more apparent. In addition, there is ST depression, diagnostic of ischemia, in V3-V6.
Nevertheless, the cardiologist consulted diagnosed early repolarization. The patient did not undergo immediate cath.
22 minutes later, another ECG was recorded:
 |
| It is slightly changed. See next image for side by side comparison |
 |
| ST elevation is higher on the repeat ECG than on the first, especially in proportion the the R-wave. There appears to be a diminution of the T-wave amplitude; however, not when the R-wave amplitude is taken into account. |
191 minutes after first ECG:
 |
| There is resolution of ischemic findings, spontaneously. There are no Q-waves. There appears to have been spontaneous reperfusion. The minimal remaining inferior ST elevation is now consistent with early repolarization |
Heparin drip started. CCU consulted. Admitted to CCU. Integrilin given. Not take directly to cath lab.
A second troponin returned at 1.71 ng/ml 3 hours later.
The patient was not taken to cath for another 6 hours after this last ECG. It showed a 99% stenosis in the RCA, and proximal to a posterolateral branch. A coronary aneurysm was found. TIMI flow not reported.
Troponin I peaked at 75 ng/ml (A VERY large OMI)
Next ECG available - 2 week followup:
 |
| There are inferior Q-waves of infarction, with T-wave inversions typical of completed inferior transmural OMI. |
Lessons:
1. Young people do have OMI
a. Some of these MIs in young people are due to anomolies: aneurysm from a disorder known to be associated with coronary aneurysms (left out to maintain anonymity) in this case. Young women, when they have OMI, often have coronary dissection.
b. Nevertheless, even young people have atherosclerosis and plaque rupture. We have seen many, such as this young woman. And young women have worse outcomes than other groups with STEMI because of the tendency to say, "Nah, couldn't be!"
2. When the ECG is unequivocally diagnostic, don't let young age or other atypical features deter you.
3. Know the features of OMI look-alikes. In this case, early repolarization was diagnosed by the cardiologist, who clearly was unaware of important differentiating features of inferior early repol from inferior OMI (see above)
4. Once OMI is diagnosed, the patient should go immediately to the cath lab even if the ST elevation resolves, because the risk is so high. In this case, however, the diagnosis was also simply missed.
See this case to demonstrate the danger of reperfused OMI!
5. Finally, YOU have to be the expert and YOU have to advocate for the patient. Cardiologists don't know everything, and in particular they don't know YOUR job, which is to differentiate the patients with benign symptoms (the vast majority) from those with Serious pathology. If the cardiologist disagrees and is incorrect, the only way the patient will get good care is if YOU are the expert, YOU know what findings are true positives and true negatives, and YOU can explain why you are right and Advocate.
Cardiologists need to know a whole lot, but they don't do our everyday job of screening hundreds of symptomatic patients to find the one with the real thing. They cannot be experts at that; you must be the expert. They are much more likely to demand proof of disease than emergency physicians. We demand proof of absence of disease. And the cardiologists' opinions are of course often, or even usually, correct, but insist on a respectful conversation in which reasoning and evidence, rather than authority, direct the outcome. That can only happen if YOU are well informed.
Here are two examples of early repolarization in the inferior leads:
First:
 |
| 1. There is inferior ST elevation without reciprocal ST depression in aVL. This is because the ST axis is leftward, not down or to the right. And thus the ST elevation in lead III is always less than or equal to that in lead II. 2. There is anterior and lateral ST elevation also; isolated ST elevation in inferior leads is relatively rare in limb lead early repol. 3. There are, in this ECG, well formed J-waves in leads V4-V6. 4. The QTc is less than 390, though we did not find this to be an accurate distinguishing feature of inferior ST elevation. 5. The ST elevation is at most 1 mm in inferior leads. |
Second:
 |
| Slightly different, but the generalizations above apply here, too. |
Thank you very much for the great case and superb discussion point.
ReplyDeleteI look at your blog often and it helps me as a paramedic
ReplyDeleteGreat one
ReplyDeleteIf you are in a facility where cath-lab not available, would you give lytics in the setting of first ECG ?
Yes. It is diagnostic of STEMI.
Delete