This is the eleventh and penultimate article in our latest series, The 12 Leads of Christmas, where each day we examine an individual electrocardiographic lead.
Today we’re going to discuss V3, and there’s no way I can do that without talking about isolated posterior myocardial infarction. Of all twelve, fifteen, eighteen, or even twenty leads you may examine on the ECG, V3 usually shows the most prominent ST/T-wave abnormalities during isolated posterior STEMI. Sometimes V2 is more dramatic, or less often V4, but in the grand scheme of things the ST-depression we see during acute posterior injury tends to be centered on V3.
The good news is that the word is out about posterior STEMI. Thanks to the work of folks like Bob Page, Amal Mattu, and many others, most prehospital and in-hospital emergency medicine providers are aware of the diagnosisâ€”including the use of posterior leads V7â€“V9.
This article presumes that you know how to identify both acute (ST-depression in V2â€“V4) and old (tall R-waves in V1â€“V3) posterior MI. If you’re not comfortable with the diagnosis just yet, I suggest checking out these other resources instead. This is a pretty advanced discussion aimed at folks who are already strong at reading ECG’s.
Okay, so isolated posterior STEMI usually presents with ST-depression that is maximal in V3. To be honest, this is all a setup for the next post on V6, so with that V3 learning pearl out of the way, our real goal is to examine just what causes an isolated posterior STEMI on the ECG.
As a word of warning: this is a longer post than I usually like, but I promise it’ll take less time to read than the years I’ve spent working it out myself.
The Posterior Wall
Before even examining the ECG, however, let’s identify the posterior wall of the heart.
It seems like a simple taskâ€”the posterior wall should be the part of the heart directly opposite the anterior chestâ€”but if we learned anything from our analysis of V2, it’s that the terminology used to describe the regions of the heart isn’t straightforward. In fact, the very existence of a “true posterior wall” has been hotly debated (point/counter-point).
Our human obsession with representing nature as simplified models never seems to go quite as smoothly as we would like.
Recall that when we discuss the localization of MI’s using the standard 12-lead, the only walls of the heart we really care about are those constituting the left ventricle (LV). The right ventricle (RV) and atria are left out of this discussion because they usually exert little effect with regards to ST and T-wave changes in the structurally normal heart. Removing those bits, what we’re left with is a prolate spheroid (an American football or rugby ball) with one end lopped off.
As shown in the gif above, there are five main regions of the heart: the anterior (ANT), septal (SEPT), inferior (INF), and lateral (LAT) walls… and the apex (APEX).
It would be nice if the heart was oriented at right angles to the patient’s torso, but sadly for us that is not the case. Instead it is rather oblique, with the base typically pointed towards the patient’s right scapula and the apex aimed downward towards V4 or V5â€”though this can vary depending on individual anatomy.
The problem with setting the heart at an oblique angle is that now the nice, simple naming system used on the football gif is no longer intuitive (wtf, evolution!?).
Rather than pointing straight ahead, the apex points to the left and somewhat downward. That’s simple enough.
The inferior wall is the only true wall that retains roughly the same orientation. In both cases it is the most caudal, resting on the diaphragm.
The anterior wall of the heart is actually the most superior, and while it is tilted a fair bit ventral towards the chest, I really think that life would be a whole lot easier if we just called it the superior wall. Plus, it’s pretty much directly opposite the inferior wall, so… yeah.
The septal wall is still what separates the cavity of the LV from that of the RV, but you may notice that it is also quite anterior, angled towards the patient’s right pectoral. An argument could be made that it is just as “anterior” as the true anterior wall, but I want to change the name of that region anyway so I guess we can keep this one the way it is.
And finally, the lateral wall. You’ll notice that it’s not pointed toward directly lateralâ€”or perpendicular to the anterior chest wallâ€”as its name would suggest, but rather a bit posterior. That turns out to be important…
Having listed all the major territories of the heart, where is the posterior wall? Well, as mentioned earlier, that question is debated. It’s not included as one of the seventeen segments of the heart currently described by the AHA, but since it’s a term we commonly throw aroundâ€”especially in electrocardiographyâ€”and it doesn’t look like that’s changing any time soon, we should probably figure out where it has gone.
Just as with Jurassic Park and so many mid-century B-movies, the thoughtless (but cool!) march of science is to blame for this mess.
This is an imperfect review, but as best I can piece it together, the story goes thatÂ electrocardiography was the only game in town for localizing ischemia for most of the 20th century. As a result, the regions of the heart were described based on how infarction Q-waves were distributed on the ECG. Leads II, III, and aVF “look” downward, therefore an infarction in those leads was called an inferior MI. Likewise, the electrodes for V2â€“V4 are located on the anterior part of the torso, so Q-waves in those leads were said to correlate to anterior MI. Lastly, since I, aVL, V5, and V6 tend to “look” towards the lateral aspect of the torso, Q-waves in that distribution were thought of as corresponding to lateral MI.
In that world it would make sense for an infarctionÂ on the “back of the heart,” opposite the anterior wall,Â to be called a posterior infarction. And so tall R-waves in the right-precordial leadsâ€”reciprocal to Q-waves in the opposite territoryâ€”were said to correspond with posterior MI.
Now, I realize that hardly anyone discusses Q-wave MI’s anymore. We’re starting there because most of the literature that developed our current terminology predates the 1980’s and 90’s, and thus was only concerned with Q-wave MI’s. ST-elevation was recognized as an ischemic phenomenon before those decades but since thrombolytics, coronary angiography, and PCI (our STEMI management options) are all relatively modern developments, chronic Q-wave MI’s were the main concern for most of the 20th century.
Then echocardiography (and nuclear imaging… and CT… and MRI… and other advanced imaging modalities) came on the scene and messed up our simple naming system. Offering a multitude of views of the heart, it became clear that more than three or four basic regions were needed to fully describe the walls of the left ventricle. And, with these new images, the frame-of-reference shifted from indirect landmarks on the chest to ones based on direct visualization of the heart.
When you’re looking at an echocardiogram you don’t think in terms of the sagittal, coronal, and transverse planes that we typically use, but instead consider the axis formed by the “tube” of the left ventricle and how the walls relate to that.
As we showed before, the heart sits at an oblique angle in the chestâ€”not really lining up with the walls of the torso. Now that the heart can be examined in isolationâ€”no longer constrained by torso anatomy or landmarksâ€”using it’s own anatomy as the reference,Â the anterior wall is no longer truly anterior nor the lateral wall truly lateral. But we’re here to talk about the posterior wall, so what happened there?
It was assimilated.
In the minds of most cardiologists the classic posterior wall, sometimes called the “true posterior wall,” was (and still is) thought of as being the infero-basal section of the LV (section #4 on the AHA’s “bull’s-eye” diagram above). We will call that the “classic posterior wall” in this article.There are, however, a few issues with calling that the “true posterior wall.”
You know how everyone says that a tall R-wave in V1 and V2 is a sign of old posterior infarct; being reciprocal to a “posterior” Q-wave? When they say that, the usual implication is that there is an infarction of the infero-basal wall we just described. Dr. Antoni BayÃ©s de Luna, a true master of electrocardiography (and I don’t toss that term around lightly), has headed a couple of papers deconstructing why that may not be the case [edit: I found a brand new one the night after posting this]. He instead argues that V1 is reciprocal to the lateral wall, not the “classic posterior wall,” and in his papers MRI correlations have shown the EKG sign of a tall R-wave in V1 to be very specific for lateral wall infarction (excluding non-infarction causes of a tall R, of course).
He believes we should be calling the basal-lateral wall the “posterior wall,” not the infero-basal wall.
It makes some intuitive sense . If you have a Q-wave originating from the classic posterior wall (aka the infero-basal wall), drawing a vector away from that region through the “electrical center” of the heart would put you near V3 or V4. According to BayÃ©s de Luna’s logic and research, infarction of this posterior wall still gives you a tall reciprocal R-wave, except that it shows up best in V3.
If, on the other hand, you draw a line (R-wave vector) from the basal section of the lateral wall through the “electrical center” of the heart, you end up near V1. Likewise, in BayÃ©s de Luna’s research, patients with an infarction of this basal-lateral wall on MRI were more likely to show a tall R-wave in V1.
But his arguments all have to do with completed Q-wave MI’s; how does that correlate to the acute STEMI’s we care about?
It’s more the principle of the matter that is important for now.
You see, regardless of whether a “true posterior wall” exists, there is still an electrocardiographic entity of acute posterior STEMI. I almost think of it as a “syndrome,” with a certain constellation of signs (right-precordial ST-depression chief among them) that, when seen together, produce the posterior STEMI syndrome. Even if there is no consensus regarding the exact anatomy on echocardiography or MRI, there are still patients who present with ST-depression confined to the right precordial leads and ST-elevation on posterior leads V7â€“V9. They have an acute coronary lesion.
That much is a certainty.
It really doesn’t matter if the ischemic territory is the “classic” infero-basal wall or BayÃ©s de Luna’s basal-lateral wallâ€”in a purely electrocardiographic sense the patient is experiencing an isolated posterior STEMI. The ECG doesn’t even care if they have a posterior wall or not; there is an “injury vector” (ST-elevation) directed towards the patient’s back and we choose to call that a posterior MI.
But we’ll describe why BayÃ©s de Luna is probably right…
I quote Bill Cosby yet again: “I told you that story to tell you this one,” (and, a month since I last used this quote, it’s still a questionable reference).
There seem to be three major causes of the “posterior infarction syndrome.” Don’t call it that thoughâ€”no one will know what you’re talking about:
- Obstruction of a dominant right coronary artery (RCA) or a dominant left-circumflex artery (LCx). The two look pretty similar from the left ventricle’s point-of-view and are often indistinguishable on the standard 12-lead, so we’ll list them as one cause.
- Obstruction of a non-dominant LCx.
- Obstruction of a branch off the LCxâ€“regardless of dominance.
In my experience, posterior STEMI from a dominant RCA or dominant LCx culprit (situation #1) is almost always accompanied by signs of inferior STEMI.
Sometimes it’s subtleâ€”just a bit of straightening of the ST-segments with a slightly early take-off of the J-points in III and aVF, as seen belowâ€”but it’s unusual to see an RCA occlusion produce a truly “isolated” posterior STEMI.
The reason why you almost always see inferior STEMI when the dominant artery is obstructed has to do with what defines the anatomy: the “dominant” artery is the one that gives rise to the posterior descending artery (PDA); also called the posterior interventricular artery.
Though individual anatomy varies, the PDA’s job is to supply blood to the inferior portion of the septumâ€”especially the basal-septal territory.
And here is the key: despite its name, the posterior descending artery does not supply either vision of the posterior wall that we discussed before. Its main concern is the septum, and while it does its job well, it doesn’t over-extend itself to reach the infero-basal or basal-lateral walls. An isolated occlusion of the PDA will produce a picture that looks either like a pure inferior STEMI (or rarely an infero-anterior STEMI)â€”not a infero-posterior or isolated posterior STEMI.
So, the posterior wall is not supplied by the posterior descending artery.
In a right-dominant circulation, at least part of the nebulous “posterior” territory can be supplied by a extension off the end of the RCA called the right postero-lateral artery (PLA); also known as the retro-ventricular artery. Sometimes it’s just a nub extending past the PDA or even absent, but sometimes it can be quite large. It typically supplies a portion of the inferior wall and on occasion can even extend through the LCx’s usual territory on the lateral wall.To produce a posterior STEMI via the RCA with a right-dominant circulation (shown above), you can either block the postero-lateral artery by itself (a rare event) or any portion the RCA that feeds it (the usual case). As we just described, however, if you block the RCA that feeds the postero-lateral artery, you’re also going to cut off blood-flow to the posterior descending arteryâ€”forcing an inferior infarction!
Also, since a well-developed postero-lateral tends to supply a good portion the inferior wallâ€”not just the infero-basal segmentâ€”even an isolated PLA occlusion could still result in a mixed infero-posterior STEMI.
As you see, it’s rather hard to create an isolated posterior infarction via the RCA, so that kind of rules-out the right side of the circulation as the culprit for most isolated posterior STEMI’s. What about when there’s a left-dominant circulation?If you block the LCx with a left-dominant circulation you can cause ischemia to the posterior territory, but just as with the RCA during right-dominance, you’re also going to affect the posterior descending artery downstream and the branches before it that supply the inferior wall; again causing an infero-posterior STEMI.
So, yet again, that really limits our ability to create an isolated posterior STEMI.
CONCLUSION: The real culprit
Getting to the heart of the matter, there are two main acute lesions we see that cause an isolated posterior STEMI pattern on the ECG:
- Acute obstruction of a non-dominant LCx.
- Acute obstruction of an obtuse marginal (OM) off the LCx, or similar artery.
And this is why we’ve come so far.
All of the prior nonsense was just to pave the way for the following statement: Isolated acute posterior STEMI is almost always caused by a culprit lesion in either the non-dominant circumflex itself or an obtuse marginal artery off either a dominant or non-dominant circumflex.
In our next post we’re going to get into some more practical aspects of diagnosis isolated posterior STEMI, but to show why the above statement is (mostly) true, we had to examine:
- How the regions of the heart got their names, and why they are inaccurate.
- Why the proper “posterior” wall may actually be the basal-lateral wall.
- Why the right coronary artery and its branches cannot usually create a region of ischemia isolated to the “posterior” territory, whether infero-basal (classic posterior) or basal-lateral.
- Why, even if the infero-basal territory is ischemic (regardless of culprit), the inferior wall is also usually affected, producing an infero-posterior STEMI.
I hope that walk-through was enlightening, and hopefully it will pay dividends when we start to examine some real-world ECG patterns of isolated posterior STEMI later this week.
Though I pieced together the above post from seeing a lot of cases and studying a lot of coronary anatomy, it’s not all made up. In addition to numerous case studies, there are a few papers that have examined the infarct-related artery in isolated posterior STEMI and all have shown that, in the preponderance of cases, the culprit is either the LCx or one of its obtuse-marginal branches.
- Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7â€“9: â€œhiddenâ€ ST-segment elevations revealing acute posterior infarction.
- 80% due to LCx, 20% due to OM-1, 0% due to RCA.
- Angiographic and Clinical Outcomes Among Patients With Acute Coronary Syndromes Presenting With Isolated Anterior ST-Segment Depression.
- 48.4% due to LCx, 17.8% due to RCA (secondary analysis of a large study, probably flawed in its ability to assess for truly isolated posterior STEMI).
- Clinical use of posterior electrocardiographic leads: a prospective electrocardiographic analysis during coronary occlusion.
- Balloon occlusion of the RCA always resulted in concomitant inferior elevation (n=34).
- Importance of posterior chest leads in patients with suspected myocardial infarction, but nondiagnostic, routine 12-lead electrocardiogram.
- Of 16 patients with suspect posterior MI who went to cath and showed a culprit, in 100% of cases it was the LCx.
I hope youâ€™re enjoying our 12 Leads of Christmas series. You can check out the rest of the posts below (updated as new posts come out):
12 Leads of Christmas: Lead I
12 Leads of Christmas: Lead II
12 Leads of Christmas: Lead III
12 Leads of Christmas: aVL
12 Leads of Christmas: aVF
12 Leads of Christmas: aVR
12 Leads of Christmas: V1
12 Leads of Christmas: V2
12 Leads of Christmas: V4
12 Leads of Christmas: V5
12 Leads of Christmas: V6