Anteroseptal vs. Anteroapical – What’s the Diff?

The most common form of myocardial infarction caused by an acute occlusion of the LAD is an anteroseptal MI (nowadays we should really be saying anteroapical) MI. This statement presents two questions:

  1.  Why ARE anteroseptal (aka anteroapical) MI’s more common than anterolateral MI’s and
  2. Why are we now calling this infarction an anteroapical infarction?

The septum receives its blood supply from two sources: the LAD and whichever artery is supplying the posterior descending artery – the RCA or the LCx. It also receives blood from the RCA via an artery called the conus artery (more on this below). An occlusion in the LAD creates a dependency on the other artery to prevent infarction. Unfortunately, the second artery (RCA or LCx – rarely both) often suffers from the same disease as the LAD and is unable to prevent an infarction.

On the other hand, the lower lateral wall of the left ventricle receives its blood supply from the LAD, the LCx, the RCA and occasionally a seldom-mentioned artery called the ramus intermedius. That’s a lot of reserve if one artery is blocked. As a matter of fact, whenever I encounter an anterolateral MI, my first thought is “Why?” So, there’s the reason why there are more anteroapical MIs than anterolateral MIs.

Now, why are we now calling anteroseptal MIs anteroapical MIs? Before going on to the explanation, look at the illustration of the heart. Study the full length of the interventricular septum – beginning at the base of the heart (at the level of the AV valves and the entrance of the His bundle) and extending all the way to the apex. If there is an occlusion of the LAD proximal to the first septal perforator, where will the infarction be located? Will it involve the proximal, middle or distal septum? Here’s the issue – you cannot know anything about proximal septal involvement with any certainty from the 12-lead ECG! Remember, you can only see an infarction (or acutely ischemic area) when there is a current traveling through it; otherwise, it will not register on the ECG. And where does the depolarizing impulse first encounter ventricular myocardium? In the mid to lower septum! The proximal septum is depolarized much later during the QRS and is affected by cancellation of forces traveling to the basal-lateral area of the left ventricle. So when you see an anteroseptal/anteroapical MI on a 12-lead ECG, the only area of infarction you are seeing must be at or below the mid septum and that leads mostly to the apical area. Also, post-mortem studies have shown that almost all “anteroseptal MIs” involved the apex and para-apical myocardium and not usually the upper septum (which, in addition to the posterior descending artery, receives extra collateral circulation from a proximal branch of the RCA called the conus artery). So even if the distal RCA and/or the LCx is also diseased, that conus branch (which is often the first branch of the RCA and sometimes even has its own origin at the aorta) can provide myocardium-saving circulation.

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