A middle-aged woman with a history of CAD and stents, but also a history of several subsequent visits for non-cardiac chest pain, called 911 for chest pain of 5+ hours duration.
The medics recorded this ECG at time zero:
Down-up T-waves in right precordial leads during chest pain is likely posterior MI.
When I showed this to a resident, she asked if these are Wellens' waves. I pointed out that Wellens waves are 1) up-down and 2) after resolution of pain. And they indicated, of course, LAD thrombus with a reperfused artery (good flow), whereas this is indicative of no or low flow to the posterior wall. I did add that subendocardial ischemia is also possible.
The medics gave NTG, and the chest pain resolved. This was recorded at time 12 minutes:
The patient was brought to the ED, at which time she had pain again, and this ECG was recorded at time 30 minutes (nearly 6 hours after onset of pain):
The patient's chest was quite tender, and the initial contemporary troponin was below the level of detection (0.010 ng/mL).
I activated our "Pathway B." Pathway B is intermediate between "admit for serial troponins" and "activate the cath lab (Pathway A)". That means I call the cardiologist on call, and he/she gets further evaluation going immediately.
The interventionalist came down immediately and talked to the patient, looked at the ECG, and decided to take her to the cath lab.
Angiogram:
100% In-stent Occlusion of a large circumflex, easy to cross with wire. There was no collateral filling. A stent was placed.
However, it is very puzzling:
All serial troponins remained below the LoD!
But to the angiographer the lesion was not a chronic total occlusion.
The echocardiogram showed a new inferolateral wall motion abnormality, but it was only hypokinesis, not akinesis, and the EF was 60%. One cardiologist did not initially see the WMA. This suggests either ischemia with stunning (unstable angina) or small infarct.
Here is the post procedure ECG, 5 hours after PCI:
The patient had no more of what she describes as her "heart attack" type chest pain.
This was recorded the next day:
Coronary thrombosis is a Dynamic process!
The artery opens and closes spontaneously. Thrombus propagates and lyses (remember there is endogenous tPA). If the occlusion is brief, then there is no infarct and troponins are negative. There might still be stunning from ischemia with a WMA. Then if it occludes again just prior to the angiogram, the angiogram shows 100% occlusion, even if it has only been brief.
This appears to be a case of unstable angina due to coronary occlusion that was complete at the time of the angiogram, though opening and closing prior to the angiogram.
Alternatively (and I think less likely), it could be that she had her MI more than 2 weeks prior and all troponins are now negative. The lesion might still be easy to cross with the wire. She would have a wall motion abnormality. However, with no collateral circulation and a total occlusion, there should be a dense wall motion abnormality (but it was not dense). If this hypothesis is correct, then she was having post-infarct angina (but that begs the question of why? Where was the new angina/ischemia originating from?)
Unstable angina still exists. And it may have an occluded artery at angiogram.
My next post will show another example of unstable angina due to occlusion, with all negative troponins.
In our UTropIA study (see here at clinicaltrials.gov) of about 2000 consecutive ED patients who had troponin ordered, we measured both contemporary and high sensitivity troponins (Abbott Architect Troponin I) and found that one of 9 STEMI patients (there were quite a few more patients who had ECGs diagnostic of occlusion but that did not meet STEMI criteria) had an initially undetectable high sensitivity troponin. About half had an initial hs trop below the 99% reference value.
The medics recorded this ECG at time zero:
 |
| Note the downsloping ST depression in V1-V3, with down-up T-waves in V2 and V3. |
Down-up T-waves in right precordial leads during chest pain is likely posterior MI.
When I showed this to a resident, she asked if these are Wellens' waves. I pointed out that Wellens waves are 1) up-down and 2) after resolution of pain. And they indicated, of course, LAD thrombus with a reperfused artery (good flow), whereas this is indicative of no or low flow to the posterior wall. I did add that subendocardial ischemia is also possible.
The medics gave NTG, and the chest pain resolved. This was recorded at time 12 minutes:
 |
| Now V2 and V3 have a long flat ST segment with a tiny upright T-wave. This is also highly suspicious for posterior MI, probably resolving. V5 and V6 appear to have smaller T-waves now as well. |
The patient was brought to the ED, at which time she had pain again, and this ECG was recorded at time 30 minutes (nearly 6 hours after onset of pain):
 |
| New but subtle downsloping ST depression with down-up T-waves in V2 and V3. Interestingly, limb leads are not very helpful here. |
The patient's chest was quite tender, and the initial contemporary troponin was below the level of detection (0.010 ng/mL).
I activated our "Pathway B." Pathway B is intermediate between "admit for serial troponins" and "activate the cath lab (Pathway A)". That means I call the cardiologist on call, and he/she gets further evaluation going immediately.
The interventionalist came down immediately and talked to the patient, looked at the ECG, and decided to take her to the cath lab.
Angiogram:
100% In-stent Occlusion of a large circumflex, easy to cross with wire. There was no collateral filling. A stent was placed.
However, it is very puzzling:
All serial troponins remained below the LoD!
But to the angiographer the lesion was not a chronic total occlusion.
The echocardiogram showed a new inferolateral wall motion abnormality, but it was only hypokinesis, not akinesis, and the EF was 60%. One cardiologist did not initially see the WMA. This suggests either ischemia with stunning (unstable angina) or small infarct.
Here is the post procedure ECG, 5 hours after PCI:
 |
| ST segments and T-waves are mostly normalized, supporting acute ischemia on the previous ECGs |
The patient had no more of what she describes as her "heart attack" type chest pain.
This was recorded the next day:
 |
| Fairly normal |
Coronary thrombosis is a Dynamic process!
The artery opens and closes spontaneously. Thrombus propagates and lyses (remember there is endogenous tPA). If the occlusion is brief, then there is no infarct and troponins are negative. There might still be stunning from ischemia with a WMA. Then if it occludes again just prior to the angiogram, the angiogram shows 100% occlusion, even if it has only been brief.
This appears to be a case of unstable angina due to coronary occlusion that was complete at the time of the angiogram, though opening and closing prior to the angiogram.
Alternatively (and I think less likely), it could be that she had her MI more than 2 weeks prior and all troponins are now negative. The lesion might still be easy to cross with the wire. She would have a wall motion abnormality. However, with no collateral circulation and a total occlusion, there should be a dense wall motion abnormality (but it was not dense). If this hypothesis is correct, then she was having post-infarct angina (but that begs the question of why? Where was the new angina/ischemia originating from?)
Unstable angina still exists. And it may have an occluded artery at angiogram.
My next post will show another example of unstable angina due to occlusion, with all negative troponins.
In our UTropIA study (see here at clinicaltrials.gov) of about 2000 consecutive ED patients who had troponin ordered, we measured both contemporary and high sensitivity troponins (Abbott Architect Troponin I) and found that one of 9 STEMI patients (there were quite a few more patients who had ECGs diagnostic of occlusion but that did not meet STEMI criteria) had an initially undetectable high sensitivity troponin. About half had an initial hs trop below the 99% reference value.
