I just posted this case:
Today I post another case that nicely demonstrates the significance of inferior ST depression.
A middle-aged female presented to the ED with chest pain. It had been intermittent all day.
Here was her first ED ECG with active pain:
(Up-down T-waves are sometimes due to hypokalemia - the upright "T" wave is actually a U-wave in these cases. This is usually in leads V2 and V3. See these cases for examples)
Isolated ST depression in II, III, and aVF should be considered to be reciprocal to subtle ST elevation in aVL and to indicate that there is occlusion of the Diagonal, Obtuse Marginal, or even the LAD.
Time 40 minutes:
She remained pain free all night.
It is wise to put these patients on continuous 12-lead ST segment monitoring, as re-occlusion can occur without any chest pain.
Next morning:
Echo showed anteroapical wall motion abnormality. Troponin I peaked at 2.5 ng/mL.
Angiogram showed 99% thrombotic stenosis with TIMI-II flow in proximal LAD. It was stented.
Comment:
At time zero, during maximal chest pain, she had a full proximal LAD occlusion. After NTG, it opened enough for adequate perfusion, chest pain relief, and T-wave inversion.
Note how subtle this occlusion was: it is only seen by some subtle ST depression in II, III, and aVF and subtle STE in aVL.
Note also that the ischemia was in the LAD territory, but the ST depression was "inferior."
Isolated "Inferior" ST Segment Depression: Not a Sign of Inferior Ischemia
Today I post another case that nicely demonstrates the significance of inferior ST depression.
A middle-aged female presented to the ED with chest pain. It had been intermittent all day.
Here was her first ED ECG with active pain:
 |
| There are abnormal ST segments in "inferior" leads, and very subtle STE in aVL, with T-wave inversion. There are "down-up" T-waves in the inferior leads, which are almost always due to ischemia. |
Isolated ST depression in II, III, and aVF should be considered to be reciprocal to subtle ST elevation in aVL and to indicate that there is occlusion of the Diagonal, Obtuse Marginal, or even the LAD.
Initial troponin I was 0.65 ng/mL.
After she was initiated on ASA/Plavix/Heparin and Nitro, her chest pain resolved.
After she was initiated on ASA/Plavix/Heparin and Nitro, her chest pain resolved.
Time 40 minutes:
 |
| The ST depression is resolved. "Inferior" T-waves are now fully upright, consistent with reperfusion in the territory of aVL. Now there are Wellens' waves in anterolateral leads, consistent with reperfusion in the proximal LAD. This strongly suggests that while the patient was having chest pain, the proximal LAD was occluded. |
She remained pain free all night.
It is wise to put these patients on continuous 12-lead ST segment monitoring, as re-occlusion can occur without any chest pain.
Next morning:
 |
| Evolution of T-wave inversion confirms Wellens' waves. There is no doubt that this will be a proximal LAD lesion |
Echo showed anteroapical wall motion abnormality. Troponin I peaked at 2.5 ng/mL.
Angiogram showed 99% thrombotic stenosis with TIMI-II flow in proximal LAD. It was stented.
Comment:
At time zero, during maximal chest pain, she had a full proximal LAD occlusion. After NTG, it opened enough for adequate perfusion, chest pain relief, and T-wave inversion.
Note how subtle this occlusion was: it is only seen by some subtle ST depression in II, III, and aVF and subtle STE in aVL.
Note also that the ischemia was in the LAD territory, but the ST depression was "inferior."
*Proximal* LAD lesions produce currents of injury at the *base* of the LV and those produce an ST segment vector that points upward in the frontal plane and has no correlate in the precordial plane (unless the ischemia extends towards the mid and apical LV, when there will be ST segment elevation in V1,V2,V3). Accordingly, one could see subtle ST segment elevation in aVL and aVR and ST depression in the inferior leads, as in this case.
ReplyDeleteDr Smith,
ReplyDeleteIf the ECG shows feature of reperfusion (t-wave inversion) + pain reducing (eg; pain score from 8 down to 3). Will thrombolytic benefits the patient if PCI is not available?
Tq,
Andey
Good question and no one knows the answer. However, the ACC/AHA now recommend tPA for patients with diffuse ST depression and STE in aVR (which is indicative of subendocardial ischemia and due to incomplete occlusion). However, they also believe (inaccurately, they misrepresent the paper they reference) that these ECG findings represent Left Main occlusion.
DeleteI believe that nonocclusive thrombus is lysed by tPA probably even better than occlusive, because there is better flow in the artery.
Neurologists believe in giving tPA in reperfusing cerebral arteries (symptoms improving), which I think is interesting.
Very interesting cases, as usual.
ReplyDelete1.I feel like there is a bit of ST depresion in V6 in the first ECG; also in the previous post, in V5,V6 there's ST straightening. Shouldn't these findings put subendocardial ischemia a bit higher on the differential?
2.In a previous post (unfortunately I can't find it) you said that circumflex occlusion can also present itself without a diagnostic STEMI ECG and ST depresion in the inferior leads.
Thank you !
Adrian,
Deleteyes, there is a bit of ST depression. This could be subendocardial ischemia (the artery probably has some flow in it at this point. that is why the T-waves are up-down). Alternatively, if it is still occluded, proximal LAD occlusion can lead to septal ischemia with reciprocal ST depression in V5 and V6.
Steve Smith
In the second point I made I wanted to ask if circumflex occlusion can also manifest as ST depression in the inferior leads( because it isn't in your list of possible causes and I remembered a post discusing that).
DeleteYes, especially occlusion of one of the obtuse marginal branches off the circ!
Delete