This 51 yo male presented with Chest pain.
There is ST depression, greater than 3 mm in some leads, in I-III, aVF, and V3-V6. aVR also has ST elevation.
Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main origin.
This patient was treated with nitroglycerine, ASA, and heparin. His pain diminished substantially but did not go away altogether. An ED ultrasound showed an anterior, apical, and septal wall motion abnormality. Repeat ECG showed most of the ST depression resolved (but not all).
There is no ST elevation, no evidence of occlusion that will cause imminent necrosis of a myocardial wall. But there is evidence of a very unstable atherosclerotic plaque that could completely thrombose at any moment. Also, his ongoing pain signified ongoing ischemia, which is an indication for immediate angiography and PCI. Therefore he was taken emergently (in the evening) to the cath lab. There was a severe ostial LAD thrombosis that was very close to the left main.
He went for emergent bypass that evening and had a good outcome.
ST elevation in aVR is often thought to represent left main occlusion. However, it really just signifies widespread and diffuse subendocardial ischemia which could be due to left main or 3-vessel disease, or severe proximal LAD disease. Left Main occlusion generally causes rapid death; most who survive left main ACS have some flow and thus often have widespread ST depression.
Think of aVR as (-)aVR. (-)aVR is 180 degrees opposite aVR and thus is between leads I and II. Thus, if I and II have ST depression, the (-) aVR must have ST depression, and (+) aVR must have ST elevation.
There is ST depression, greater than 3 mm in some leads, in I-III, aVF, and V3-V6. aVR also has ST elevation.
Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main origin.
This patient was treated with nitroglycerine, ASA, and heparin. His pain diminished substantially but did not go away altogether. An ED ultrasound showed an anterior, apical, and septal wall motion abnormality. Repeat ECG showed most of the ST depression resolved (but not all).
There is no ST elevation, no evidence of occlusion that will cause imminent necrosis of a myocardial wall. But there is evidence of a very unstable atherosclerotic plaque that could completely thrombose at any moment. Also, his ongoing pain signified ongoing ischemia, which is an indication for immediate angiography and PCI. Therefore he was taken emergently (in the evening) to the cath lab. There was a severe ostial LAD thrombosis that was very close to the left main.
He went for emergent bypass that evening and had a good outcome.
ST elevation in aVR is often thought to represent left main occlusion. However, it really just signifies widespread and diffuse subendocardial ischemia which could be due to left main or 3-vessel disease, or severe proximal LAD disease. Left Main occlusion generally causes rapid death; most who survive left main ACS have some flow and thus often have widespread ST depression.
Think of aVR as (-)aVR. (-)aVR is 180 degrees opposite aVR and thus is between leads I and II. Thus, if I and II have ST depression, the (-) aVR must have ST depression, and (+) aVR must have ST elevation.
Quick question regarding your explanation of -aVR. You said -aVR is between I & II, if you are referring to the hexial diagram, I think I understand this part. When you said that "I & II have ST depression, the (-) aVR must have ST depression and (+) aVR must have elevation," are you referring to the + or - deflection of the QRS complex? So if I & II have ST Depression the negative complex should have depression? Would this be normal or abnormal?
ReplyDeleteThanks, for the great site and book.
Geoff
I am referring to the entire PQRSTU. Just reverse polarity on all parts of aVR and it is -aVR. -aVR would lie between I and II, so that if both of those have ST depression, then -aVR must have ST depression. If -aVR has ST depression, then aVR must have ST elevation.
ReplyDeleteThis is a roundabout way of saying that: if there is ST depression in I and II, then there is ST elevation in aVR.
There are quite a few studies on STE in aVR being related to Left Main stenosis, or three vessel disease. Dr. Amal Mattu has some great research out there on this. I believe the rule is if STE in aVR is > than STE in v1 than there is a high probability of a LMCA partial occlusion. If I understand you correctly, you are saying this STE is more due to ischemia than infarct as with typical STE.
ReplyDeleteWhether ST elevation in aVR is due to left main occlusion, left main ischemia, severe 3 vessel ischemia, or a combination is very difficult to extract from the literature because the studies have small numbers, non-standardized criteria, and don't always correct for ST depression. More importantly, most left main survivors either have subtotal occlusion (there is still flow) or collateral flow to the LAD. It is generally not specified in the studies whether the patients have some flow to the affected myocardium, or no flow.
ReplyDeleteThe ECG when there is no flow (LM occlusion without collaterals) vs. some flow (subtotal or collaterals) will be completely different and the studies do not differentiate. With some flow, there will be diffuse ST depression (and the mandatory ST elevation in aVR if there is ST depression in I and II). There will be little ST elevation (that is, no or little STE in V1 or aVL)
Theoretically: With NO flow there will be widespread ST elevation, including posterior ST elevation from no flow in the circumflex. This manifests as ST depression in anterior leads, but because there is simultaneous ST elevation in anterior leads due to lack of flow in the LAD, the anterior and posterior walls cancel out and you get attentuated ST elevation in V2-V3. In other words, some of the findings cancel each other out. But aVL and V1 remain elevated due to absence of flow in the LAD, and thus the first diagonal (which manifests in aVL). Inferior leads will have ST depression (reciprocal to aVL), and aVR thus has ST elevation.
Electrically, ST elevation in aVR cannot be independent of ST depression elsewhere; that would be impossible. Since aVR is opposite (-)aVR, which is between leads I and II, if there is STE in aVR, there must be ST depression in one or both of I and II.
In any case, ST elevation in aVR is a bad sign and a result of severe ischemia, whether due to no flow or low flow, whether in left main or 3 vessel. The important thing is to recognize it and gather your resources when you find it.
I will write a more extensive piece on this later.
Another word: Szymanski et al published a paper in AJEM in 2009 (Szymanski FM, Grabowski M, Filipiak KJ, Karpinski G, Opolski G. Admission ST-segment elevation in lead aVR as the factor improving complex risk stratification in acute coronary syndromes. Am J Emerg Med 2008; 26:408-12.)
ReplyDeleteIn it, they find that ST elevation in aVR is independent of ST depression in other leads. This is an interesting finding, but must be taken with the fact that the definition of ST elevation was greater than or equal to 0.5 mm (as was the definition of ST depression). Furthermore, the vast majority of patients with STE in aVR had between 0.5 and 1.0 mm. Thus, it seems that perhaps there may be 0.5-1.0 mm STE in aVR without any ST depression of at least 0.5 mm.
However, any large amount (greater than or equal to 1.0 mm) will have some ST depression.
Thanks for the post, Steve. Had a case just the other day with a good short history that fit and very subtle widespread ST depressions and a tiny elevation in aVR and the PCI team agreed on immediate cath, before the first troponin came in. It came in at 250 (Roche hsTnT, cutoff 15). Had 90-95% left main and 80% LAD to boot. Good outcome.
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