This case was put on Twitter by Elisha Targonsky, who has a nice EM blog (http://thechartreview.org
). He provided it for posting here. On Twitter, he asked for an analysis of the infarct artery.
Analysis of the infarct artery is mostly an academic exercise. The patient clearly needs cath lab activation. However, it is of some clinical value: interventionalists like to know what artery is affected because it often determines which artery they will investigate first with angiography.
So it does have some value, but is not critical.
But moreover, it is an exercise which helps one understand all the ST vectors at play in an ECG.
Notice this is a 15 lead ECG, with posterior leads V8 and V9 and also Right sided lead V4R.Here was my Twitter response without any other information:Tweet 1:
|What is your analysis? See mine below.|
Prox large RCA, also to lateral and posterior walls. Ant MI is RV, not LV. V2 less STE b/o posterior MI. Tweet 2:
In other words: pseudo anterior MI (RV: V1-V4) from large RCA, to post & lat also. V2 STE attenuated by postOne must explain several findings:
1. Inferior ST elevation
2. Anterior ST elevation (V1 and V3), but very little in V2
3. ST elevation in V4-V6 (but also ST depression in aVL)
4. Posterior ST elevation
5. ST elevation in V4R
--One is tempted to call this LAD occlusion
with anterior MI and wraparound LAD to the inferior wall. But then how do you get a posterior STEMI also?
--One might say: OK, it is left main
, and that is why there is BOTH anterior (LAD) and Posterior (Circ) STEMI.
Why the inferior STE? Maybe it is a left dominant system, so the circ also goes to the inferior wall.
But then one must still explain 2 findings: the patient is still alive AND there is ST elevation in V4R.
ST elevation in V4R can conceivably be caused by LAD occlusion, as some individuals have the RV supplied by rightward branches of the LAD. This is a possibility, but you would expect such a patient to be in shock.What was the clinical scenario?
A middle-aged male with h/o CAD, HTN, DM, hyperlipidemia.
Previous LAD stent, then 2 years later had bare metal stent to RCA.
Presented without shock
, with 10/10 substernal CP. Diaphoretic and nauseated.
--So left main is very unlikely.
--What then? The ST elevation in V4R is the big clue. This is almost always due to Right Ventricular MI. RV MI also may cause anterior ST elevation mimicking anterior MI ("Pseudoanteroseptal MI")
. In these cases, the maximum ST elevation is in V1 or V2, and becomes less as one goes out to V3, V4, etc.So the IRA is the RCA.
--What does this RCA supply besides the RV? It supplies the inferior wall, the posterior wall, the inferolateral wall (STE in V4-V6 without high lateral STE in aVL)
--Why is there less STE in V2 than in V1 or V3?
1. The posterior ST elevation is exactly reciprocal to V2 and is attenuating the STE in V2.
2. That downward pull is not as opposite V3 as it is opposite to V2.
3. The RV ST elevation is greater in V1 than in V2
4. The lateral ST elevation has more "upward" pull on V3 than there is downward pull from posterior.
--Why is there ST depression in aVL but ST elevation in precordial lateral leads V5 and V6?
V5 and V6 are situated more inferior than aVL. Many inferior MI have ST elevation in V5 and V6. And all inferior STEMI have ST depression in aVL. In our series of 150 inferior STEMI, 27 had ST elevation in V5 and V6. All had ST depression in aVL.What direction is the ST vector?
There is diffuse ST elevation, except
towards leads I, aVL and V2:
To the right
Right anteriorAngiography Results:
No disease in LAD or circ
RCA dominant with acute thrombosis
Thrombectomy and stent.