A 50 something presented with 10/10 bilateral arm and pain between the shoulder blades that started at work. It felt like a "tearing," and was associated with diaphoresis.
BP was 250/140. He appeared distressed.
Here is the initial ECG:
Of course the initial fear was aortic dissection, with the classic pain and severely elevated BP. And it is not uncommon for a dissection to dissect down the coronary arteries, especially the RCA, so one might find an ECG like this in aortic dissection. (Though only a tiny minority of RCA STEMI are caused by aortic dissection!)
The patient was given labetolol without much effect, then esmolol and nitroprusside until the BP was under control.
He was sent to the CT scanner where no dissection was found.
At this point the ECG findings must be attributed to acute coronary syndrome. A repeat ECG is indicated to look for evolution or resolution.
Before another ECG was obtained, the pain resolved. This was recorded at 90 minutes:
The first troponin was slightly elevated. The ischemia was thought to be due to severe hypertension (a type 2 MI). The cath lab was not activated.
Only less than 5% of type 2 MI present with subepicardial ischemia (ST elevation). Demand ischemia from hypertension would be unlikely to manifest such focal STEMI on the ECG.
Progress
While waiting for a bed, he developed chest pain again, and this ECG was recorded at 120 minutes:
The cath lab was activated.
While waiting, the pain subsided again 10 minutes later (recorded at 130 minutes):
10 minutes later, the pain recurred again (time 140 minutes):
Cath showed a 100% thrombotic occlusion of the RPAV off the RCA, stented.
Reperfusion was so fast that there was no wall motion abnormality the next day.
BP was 250/140. He appeared distressed.
Here is the initial ECG:
 |
| This is diagnostic of inferoposterior MI, with acute coronary occlusion. There are hyperacute T-waves in inferior leads, ST depression and T-wave inversion in aVL, and ST depression with T-wave inversion in V2 and V3. There is also ST depression in V4-V6. |
Of course the initial fear was aortic dissection, with the classic pain and severely elevated BP. And it is not uncommon for a dissection to dissect down the coronary arteries, especially the RCA, so one might find an ECG like this in aortic dissection. (Though only a tiny minority of RCA STEMI are caused by aortic dissection!)
The patient was given labetolol without much effect, then esmolol and nitroprusside until the BP was under control.
He was sent to the CT scanner where no dissection was found.
At this point the ECG findings must be attributed to acute coronary syndrome. A repeat ECG is indicated to look for evolution or resolution.
Before another ECG was obtained, the pain resolved. This was recorded at 90 minutes:
 |
| Normalization was attributed to normalization of the severely elevated BP. |
The first troponin was slightly elevated. The ischemia was thought to be due to severe hypertension (a type 2 MI). The cath lab was not activated.
Only less than 5% of type 2 MI present with subepicardial ischemia (ST elevation). Demand ischemia from hypertension would be unlikely to manifest such focal STEMI on the ECG.
Progress
While waiting for a bed, he developed chest pain again, and this ECG was recorded at 120 minutes:
 |
| Now there is obvious inferoposterior STEMI |
The cath lab was activated.
While waiting, the pain subsided again 10 minutes later (recorded at 130 minutes):
 |
| ST segments and hyperacute T-waves have normalized. |
10 minutes later, the pain recurred again (time 140 minutes):
 |
| Obvious STEMI again. |
Cath showed a 100% thrombotic occlusion of the RPAV off the RCA, stented.
Reperfusion was so fast that there was no wall motion abnormality the next day.
Sorry, I wonder If there was only a thrombotic occlusion or a thrombotic occlusion on atherom plaque.
ReplyDeleteCould Prinzmetal angina induce a thrombotic occlusion , especially If a patient has a prothrombotic and procoagulant status?
No, Prinzmetal's does not cause thrombotic occlusion. This was from eroded/fissured atheromatous plaque.
DeleteAccording to UptoDate, it can:
DeleteMyocardial infarction (MI) in patients with variant angina is usually due to concurrent obstructive coronary artery disease [83,84]. With variant angina alone, coronary vasospasm may trigger thrombus formation. Lipoprotein(a) may play a role in this setting. It interferes with fibrinolysis by competing with plasminogen binding to molecules and cells, and elevated serum Lp(a) is associated with a history of prior myocardial infarction in patients with coronary vasospasm [85].
Thanks for correcting that. But this was from atheroma. The vast majority of repeated opening and closing of coroanry arteries is due to thrombus, not spasm. And the vast majority of thrombus is due to ruptured plaque. Prinzmetal's angina was a popular diagnosis years ago before the pathophysiology of intracoronary repeated formation and lysis of thrombus was recognized.
DeleteWouldn't it be safer and faster for the patient to perform a bedside echocardiogram and not wait until the ECG becomes diagnostic?
ReplyDeletePanagiotis,
DeleteI would have just made the diagnosis and activated the cath lab. Or if one is uncertain one can either do a bedside ultrasound or just do serial ECGs. They certainly could have been done more quickly. But you can see that any static ECG, or ultrasound, could be normal if obtained between episodes of occlusion.
Steve Smith
This is obviously making a bit of a leap, but another reason I believe there was diagnostic confusion is that, by my eye, the first EKG shows subendocardial ischemia (likely secondary to the severe HTN) superimposed on the subtle inferior STEMI.
ReplyDeleteOn that first EKG there is ST-depression in V5 and V6 that is not present on the later two EKG's showing clear inferior STEMI (#3 and #5). Also, there frontal ST-vector is right about 180 degrees on the nose, quite a bit superior of the 110–120 degrees we usually see with run-of-the-mill inferior STEMI (and in fact see on EKG's #3 and 5). I'd suggest that this is due to the combination of the diffuse subendocardial ischemia vector, which points in the 240 degree range, averaging with the inferior subepical ischemia vector, pointed at 120 degrees, to yield 180 degrees on-the-nose.
Obviously the math's note that simple since the magnitude of the two ST-vectors isn't necessarily equal, nor is their angle guaranteed, but that's the gist of it.
Also, the magnitude of the ST-depression in V3 is actually equal between the first EKG (showing subtle STEMI) and the third ECG (showing obvious STEMI), suggesting there is another factor at play increasing the ST-depression on that first ECG. The same could be said for V4, which actually shows MORE ST-depression on the first ECG compared to the third.
It's a minor point, but I think it could help explain why that first ECG looks a bit atypical.