A 70-something woman had acute chest pain.
The ECG was texted to me with the words: "Acute chest pain. Could this be posterior MI? What do you make of the ST depression in V4-V6?"
What do you think?
My response: "The ST depression is maximal in V1-V4. This is most consistent with a posterior MI. If it sounds clinically like acute MI then this is good for activating the cath lab."
Her response: "Yeah, I did activate. But the cardiology fellow told me he was sure it would not be a posterior MI because of diffuse ST depression. He suggested that we should have consulted cardiology rather than activating the cath lab, and treated this like a NonSTEMI."
My response: "That is not true. It is possible that it is not posterior, but about 80-90% of the time it is posterior if the STD is maximal in V1-V4. So if it turns out not to be, that does not mean he was right. He was not right."
She did give nitroglycerine, and the pain improved but did not resolve, then recorded this ECG:
The ST depression persists but is not as profound
I did not know this at the time, but because of a widened mediastinum on CXR, they did a CT aortogram that was negative (I use one CT image below to illustrate "posterior" MI).
The first troponin I returned at 4100 ng/L -- quite high for a very acute MI, usually seen in subacute MI.
Angiographic findings (done approximately 150 minutes after 1st ECG):
Brisk, TIMI III flow into all coronaries. Severe distal vessel tortuosity and moderate left coronary calcium.
1. Left main: normal.
2. LAD: Type III. Long (~35 mm) moderately calcified 70% proximal to mid LAD stenosis.
A diagonal branch distal to the stenosis has luminal irregularities.
3. LCX: Tortuous, mildly calcified with luminal irregularities in the proper vessel and a 80-90% stenosis in the proximal OM followed by a 70% stenosis downstream after two 90 degree bends. A smaller OM has luminal irregularities.
4. RCA: Long (>35 mm), 70% mid RCA stenosis stenosis. It supplies a medium sized RPDA and small RPLA
So there is severe 3 vessel disease, but all arteries are open with good flow. This seems to imply that the fellow was correct in this case, but this is not true. The arteries were clearly not all widely patent (open) at the time of ECG recording, 150 minutes earlier. Spontaneous reperfusion with TIMI-3 (normal) flow is very common, occurring in up to 19% of proven STEMI (1). When there is such full reperfusion of an occlusion (OMI), it makes it difficult to identify the culprit on angiogram unless there is clearly an ulcerated plaque on the angiogram, which apparently there was not, or the angiographer would have found it.
However, had the angiogram been done at exactly the same time as the first ECG, the culprit would have been apparent.
The fact that the proximal OM (obtuse marginal branch off the circumflex) had such a tight stenosis makes it a likely culprit for the acute plaque rupture, but not certain.
Furthermore, the arteries were "tortuous" (full of twists and turns) and so any PCI was going to be technically difficult, so it was deferred at that point in order to discuss Coronary Bypass surgery (CABG).
The troponin peaked over 21,000 ng/L. This is very high and a level more consistent with STEMI/OMI than with NonSTEMI, although there is quite a bit of overlap. Most STEMI have troponin I over 10 ng/mL (roughly equivalent to 10,000 ng/L), and most NonSTEMI have troponin I below 10 ng/mL.
The formal bubble contrast echocardiogram: "Findings are most consistent with ischemia/infarct in the diagonal and OM vascular territories." This confirms Posterior MI.
The patient refused Bypass Surgery (CABG), and so was taken back for another angiogram and intervention.
2nd angiogram, with intervention:
Culprit Lesion (s): 80% stenosis of proximal OM1 in the setting of significant tortuosity. Successful PCI of proximal OM stenosis.
All subsequent ECGs continued to have ST depression (not shown), suggesting a No Reflow phenomenon. No further troponins were measured.
Learning points:
1. Precordial ST Depression, when maximal in V1-V4 (vs. V5-V6) is reciprocal to ST Elevation in the wall opposite those leads (i.e, posterior wall, which is now often and confusingly called "Lateral" -- see below) and indicates posterior OMI in 80-90% of cases.
2. Diffuse ST depression, maximal in II, V5 and V6 is more often due to diffuse subendocardial ischemia and has reciprocal ST Elevation in aVR.
3. Even when there is 3-vessel disease, one of them is usually the acute culprit, whether it can be identified or not. Intervening can be hazardous however, which is one reason that CABG is often recommended.
4. 15-20% of OMI are reperfused by the time of the ECG. A very high troponin (TnI over 10.0 ng/mL or 10,000 ng/L; TnT over 1.0 ng/mL or 1000 ng/L) can help to ascertain whether there was occlusion at the time of the ECG. This is a crucial part of our ECG research -- when we assess the ECG, we need to figure out what the state of the artery was during its recording.
5. Echocardiogram can help to determine if precordial ST depression is due to subendocardial ischemia (absence of wall motion abnormality, or at least not in posterior location) vs. posterior (posterior or lateral WMA).
6. Posterior MI is now frequently called "Lateral" (see articles by Bayes de Luna below). I prefer the old terminology of "Posterior" (see image and explanation below) because it differentiates OMI with ST depression ONLY (V1-V4) from OMI that has ST Elevation, with or without ST depression. See this:
This is the CT scan image of this patient
The area of transmural infarct is outlined in red.
It is the lateral wall.
--However, due to rotated orientation in the chest, the lateral wall of the heart is oriented towards the posterior thorax, directly opposite V1, V2, and V3.
--Posterior leads V7-V9 would have shown STE if the voltage was high enough.
--All that lung between the heart and V7-V9 can result in insufficient QRS or ST-T voltage!
--V1-V3 are directly opposite the wall with STE (under leads V7-V9), and therefore show reciprocal ST Depression.
--Therefore, it is more appropriate to call this a posterior STEMI than a "lateral" STEMI.
--A lateral STEMI would show STE on the 12-lead in V5 and V6 (or high lateral in I, aVL)
1. Cox DA, Stone GW, Grines CL, et al. Comparative Early and Late Outcomes After Primary Percutaneous Coronary Intervention in ST-Segment Elevation and Non–ST-Segment Elevation Acute Myocardial Infarction (from the CADILLAC Trial). Am J Cardiol [Internet] 2006;98(3):331–7. Available from: http://www.sciencedirect.com/science/article/pii/S0002914906007168
Articles by Bayes de Luna which attempt to eliminate the idea of a "Posterior MI".
I find that these ideas only confuse the acute treatment of any Occlusion MI (OMI) that only manifests ST depression in leads V1-V4. By propagating the idea that there is no posterior MI, they propagate the idea that patients who do not have ST Elevation do not have OMI (or STEMI equivalent with ST Elevation vector pointing towards the posterior thorax).
… R wave in V1 is caused by a lateral not posterior myocardial infarction—new evidence based on contrast-enhanced cardiac magnetic resonance—electrocardiogram …
A Bayés de Luna, D Rovai, G Pons Llado… - European Heart …, 2015 - academic.oup.com Since 1964, a tall and broad R wave in V1–V2, in the absence of right ventricular
hypertrophy, complete right bundle-branch block, or Wolff–Parkinson–White syndrome, has
been considered the sign of a posterior myocardial infarction (MI). 1 According to this theory … Cited by 21 Related articles All 10 versions Import into BibTeX AB de Luna, JM Cino, S Pujadas… - The American journal of …, 2006 - Elsevier Q-wave myocardial infarction (MI) location is generally based on a pathologic correlation
first proposed> 50 years ago. Despite the proved reliability of contrast-enhanced
cardiovascular magnetic resonance (CE-CMR) imaging to detect and locate infarcted areas Cited by 84 Related articles All 7 versions Import into BibTeX
A Bayes de Luna, G Wagner, Y Birnbaum, K Nikus… - Circulation, 2006 - Am Heart Assoc The ECG is the most frequently used tool for evaluating myocardial infarction (MI). The ECG
provides an opportunity to describe location and extent of infarction expressed as
pathological Q waves or their equivalents. The terminology used for the left ventricular (LV) …
Dr Smith,
ReplyDeleteI'm a little confused when reading your CT image together with the MRI image from Bayes de Luna 2015 (Fig 6). Bayes de Luna referred to the infero-lateral wall as "posterior", yet from their image I don't think its vector can readily cause ST elevation in V7-9. Do you consider that region part of "posterior" wall as well or simply infero-lateral wall?
Thanks.
Jonathan
Jonathan, If I understand you correctly, that is exactly my point! They call "lateral" posterior and that does not make sense. If the wall points to the posterior thorax where V7-V9 are or would be, I consider it posterior. If it points to the lateral thorax where V5 and V6 are, then I consider it lateral. The important thing is where the ischemia is in relation to the leads.
DeleteDear Dr. Smith,
ReplyDeleteThank you very much for this illustrative case. Could we interprete the terminal positive T-waves in V1 and V2 in the second ecg as a sign of reperfusion after giving nitro?
Kind regards,
Reto
Yes, good point!
DeleteSir,the true posterior mi will have st depression with upright t waves. Our first ecg doesn't have upright t wave. So how to explain this sir.
ReplyDeleteThat is a myth that you should eliminate from your mind. Posterior STEMI in early stages may have either inverted or upright T-waves. I have explained this complex idea in other posts. Later in posterior MI, they are upright.
Delete