There is ST depression with upright T-wave in leads V2-V6, maximal in V3. There is no ST elevation anywhere on the ECG. There are those who deny the existence of posterior STEMI; they argue that coronary anatomy makes it "extremely unlikely." But fact has a way of overturning theory.
After therapy with IV nitroglycerine and an aspirin, the ST depression and chest pain resolved. Because of issues with some contraindications to antiplatelet and anticoagulation therapy, and because the ECG and symptoms had resolved, he was not taken immediately for cath. He did have an echo confirming a new posterolateral wall motion abnormality.
Next day cath showed a 100% Ramus intermedius occlusion; it was opened and stented. Max TnI was 14 ng/ml. Echo showed corresponding new WMA and EF was 54%.
There are many studies that indirectly reveal that the percent of STEMIs that are isolated posterior is between 3 and 11% (about 8%). More recently, a substudy of the recent TRITON-TIMI 38 trial comparing Prasugrel to Clopidogrel for ACS enrolled 13,608 patients; 1198 had isolated ST depression in V1-V6. Of these, 314 (26%) had occlusion (TIMI 0 or 1 flow) of the infarct-related artery (i.e., STEMI).
There were 3534 other STEMIs in this study, not including the 314 with ST depression only (posterior STEMI). Add these 314 to the 3534 and you have 314/3848 (8.1%) of STEMI have pure isolated posterior STEMI. This conforms with the previous smaller studies. Moreover, the cath was done a median of 29.4 hours after presentation, so this does not account for those arteries that spontaneously reperfused (about 25% of STEMI will reperfuse with antiplatelet and antithrombotic therapy alone within one day -- old data). Thus, there were probably even more occluded arteries.
Only 14/314 (4.5%) were interpreted by the investigator as STEMI. None of the patients with an occluded artery had an ECG to PCI time <6 hours.
This is not a "rare" event.
"Only 14/314 (4.5%) were interpreted by the investigator as STEMI. None of the patients with an occluded artery had an ECG to PCI time <6 hours."
ReplyDeleteThis is a scary statistic given the fact that the investigator is using a 12 lead EKG. They are the first line of recognition in a potential explosive situation. Do you think it is because of lack of education or experience with the issue? While it is not a rare event to have posterior wall MI, it is more uncommon that other varieties, thus limiting providers with credible experience. Or is it just an overall taken-for-granted approach when the EKG looks normal, but the patient says otherwise?
The EKG does NOT look normal. But it has no ST elevation. Because most cases with some new ST deprression do not have occlusion, physicians are uncomfortable diagnosing STEMI in those that do. Use of posterior leads and echocardiography would help.
ReplyDeleteThe patient's ECG was not normal with the ST depression in V2-V5 (ok, maybe a little bit in V6). I've had this discussion with an ED Doc who did not totally understand the reciprocal changes that happen with a posterior MI presenting with anteriolateral ischemia (or anteroseptal). This is a problem. If a patient comes into the ED with a STEMI, the cath-lab is activated. But, if they present in the ED with anterolateral wall ischemia, they wait for labs and are treated medically if negative (go to the ICU). A patient with a posterior STEMI needs a cath-lab just as fast as other STEMI's (time is muscle). I will do posterior lead placement on everyone who: (1) presents with chest pains and has an unremarkable EKG with standard placement.....(looking for posterior wall ischemia) (2) Any ST segment depression in the anteroseptal region. (3) Inferior wall MI's, to try and distinguish between an isolated marginal block, mid RCA, or (with the help of V4R) a proximal RCA occlusion. If V4R is also elevated but not in V8 or V9, the patient is left dominant or codominant.
ReplyDeleteI had a "discussion" with an ED doctor one time about this exact senerio. Another crew brought in a pt with CP. The 12-lead EKG shows ST depression in the anteroseptal region (ischemia). The ambulance crew did not think to do posterior lead placement to check for a STEMI. Although the patient was being treated with meds, he was being admitted into the ICU for treatment, tests (serial Troponins), and observation. I talked with the physician who was caring for him and mentioned the fact that this ST depression could be reciprocal to a posterior wall STEMI. I then suggested a repeat EKG with posterior lead placement. He dismissed my idea saying that the ST depression was not in V1 also, so it couldn't be a posterior STEMI.
ReplyDeleteIf the posterior leads were placed and a STEMI was found, the cath-lab team would be activated and the patient would go directly to the cath-lab. Since the MD did not beleive this to be a posterior STEMI, and did not bother to check for one, the patient went to the ICU. This puts the patient in danger of more muscle damage, since "Time is muscle".
All ischemic changes in the anterolateral region should be considered to be a posterior wall STEMI until ruled out.
I would NOT recommend posterior leads on everyone with chest pain and nondiagnostic ECG, only the ones with very high risk (character of pain, risk factors, more suspicious ECG). Studies of routine posterior leads show that it is not useful.
ReplyDeleteHow can a ramus intermedius occlusion cause an isolated posterior MI? The infarct related artery should be either a PDA or less likely postero-lateral branches coming off the right or circumflex, or even rarer a wraparound LAD going past the apex to supply a portion of the posterior wall. Unless I'm mistaken, the one coronary artery that should not be able to cause an isolated posterior MI is the ramus.
ReplyDeleteThe ramus intermedius often wraps around to the posterior wall. It may supply territories which are usually supplied by the circumflex through the obtuse marginals. That was the case here.
ReplyDeleteHi Steve,
ReplyDeleteAny comments on the upright-nature of the T-Waves in V2 & V3 here in this Isolated Posterior STEMI?
Sam
This is really complicated.
DeleteThere are some who say that an upright T-wave is a necessary part of acute posterior STEMI. They are wrong. The orientation of the T-wave in posterior STEMI at the time of occlusion has not ever, to my knowledge, been demonstrated in the literature.
However, I think it can be demonstrated by studying it during simultaneous inferior STEMI. When the RCA supplies the inferior and posterior walls and is occluded, and the inferior ST elevation with upright T-wave proves that the artery is occluded, one must look to V2 and V3 (which have ST depression) and study the orientation of the T-wave. In such situations, I have usually seen the T-wave inverted. A large upright T-wave indicates reperfusion of the posterior wall if it is large (what I call "posterior reperfusion T-waves").
But one that is not large could be present with either persistent occlusion or with reperfusion.
The reason that posterior T-wave analysis gets complicated is that they are being monitored from the anterior wall and the anterior wall's T-waves predominate because they are so much closer to the leads.
Without ischemia: The anterior T-waves are normally upright. The posterior T-waves, as seen from the anterior wall, would be inverted (in anterior leads) if there was no interference from the anterior T-waves. They are a mirror image of what would be seen with posterior leads. But the anterior T-waves obscure this.
In STEMI: The posterior T-waves would be more inverted (hyperacute) if there were no interference from anterior T-waves.
In reperfusion: the posterior T-wave from the posterior perspective turns down (inverts). But as recorded from the anterior wall, it turns up! Then it is added to the upright anterior T-waves and they are very large.
Complicated.
Steve