Click here for more cases of posterior MI, and more explanation
Case 1.
This is a 44 yo male with h/o HTN, CABG at age 34, and 2 drug eluting stents to the first diagonal graft 3 months prior. He presented at 1810 with chest pain 5 days after stopping clopidogrel (on the instructions of another physician). The following ECG (#1) was recorded, with ECG #2 as his baseline.
#1, presenting ECG
#2, baseline from 3 months prior
#1 shows new marked ST depression in V2 and V3.
The differential diagnosis is subendocardial ischemia with probably NSTEMI vs. posterior STEMI. By ECG alone, posterior MI is more likely because of maximal ST depression in right, as opposed to left, precordial leads. However, given the history of severe 3 vessel coronary disease it is prudent to start with medical management, then observe for resolution of pain, but to also obtain an immediate echocardiogram to ascertain which wall is involved. If pain or ECG findings do not resolve, or if there is posterior wall motion abnormality, then immediate angiography with PCI is indicated.
In this case, maximal medical therapy was undertaken with Aspirin, clopidogrel, heparin, eptifibatide, metoprolol, and IV nitroglycerin and the patient was admitted to the CCU with cardiology consulted immediately. Chest pain resolved and angiogram was not done until the next day. It showed a 100% re-occluded SVG stent to D1; thrombus was suctioned out. Echo confirmed posterior wall motion abnormality. Max troponin was 47.
Case 2.
54 yo female with h/o smoking, DM, HTN, c/o chest pain for 3 hours, substernal radiating to both shoulders. She has an initial ECG which shows diffuse ST depression and she was treated for NSTEMI. She developed some pulmonary edema after metoprolol. ECG #2 was recorded:
ST depression is maximal from V2 to V4. This is due to posterior STEMI until proven otherwise. Unfortunately, it was treated as an NSTEMI for 2.5 hours until an echocardiogram showed a posterior wall motion abnormality. Cath revealed a 100% occluded circumflex. This was opened and stented, with the convalescent ECG below, which shows large upright posterior reperfusion T waves with a long QT.
How can such delay be avoided? By recording posterior leads V7-V9, at the level of the tip of the scapula and at the posterior axillary line (V7), a position midway between this and the spine (V8), and a paraspinal lead (V9). Also, obtaining a stat echo. Most of all, recognize this ECG pattern as being by far more likely to be posterior STEMI than due to subendocardial ischemia, which has maximum ST depression in leads V4-V6.
Case 3.
Here is a case of a 66 yo male with a history of CAD who presents with 1.5 hours of chest pain and is stable.
There is ST depression maximal in, again, V2-V4. The vast majority of posterior STEMI is not isolated, but rather concurrent with inferior and/or lateral involvement. In this case there is subtle ST elevtion in the inferior leads, not noticed by the treating physicians. Compare these ST segments with those of the post reperfusion ECG below:
The patient had rapid PCI of a 100% acutely thrombotically occluded mid circumflex which was opened and stented. There was 3 vessel disease.
The T-wave in posterior STEMI
Notice also that in the first (pre-reperfusion) ECG of case 3, the T wave is not upright as in previous cases. Some authors claim that the T wave must be upright for posterior STEMI. Evidence for this is lacking. In fact, an upright T wave probably indicates reperfusion of the posterior STEMI, whereas an inverted T wave is the analog of a hyperacute T wave (still occluded) but recorded from the opposite side. Either can be present in posterior STEMI, depending on the state of microvascular perfusion due to recanalization or to collateral circulation.
Are there any solid criteria to help provide a DDx between anterior or subendocardial ischemia and posterior STEMI?
This is a very good question, and not easily answered.
First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved.
Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia.
Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs. younger smoker).
Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs.
Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations).
Sixth, placement of posterior leads (take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in just one lead is very sensitive and specific for posterior MI.
Seventh, an immediate echocardiogram can make the distinction
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). Reference and link to full text below.
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.
Pride YB, Tung P, Mohanavelu S, et al. Angiographic and ClinicalOutcomes Among Patients With Acute Coronary Syndromes Presenting With IsolatedAnterior ST-Segment Depression: A TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) Substudy Journal of the American College of Cardiology: Cardiovascular Interventions 2010;3(8):806-11.
Case 1.
This is a 44 yo male with h/o HTN, CABG at age 34, and 2 drug eluting stents to the first diagonal graft 3 months prior. He presented at 1810 with chest pain 5 days after stopping clopidogrel (on the instructions of another physician). The following ECG (#1) was recorded, with ECG #2 as his baseline.
#1, presenting ECG
#2, baseline from 3 months prior
#1 shows new marked ST depression in V2 and V3.The differential diagnosis is subendocardial ischemia with probably NSTEMI vs. posterior STEMI. By ECG alone, posterior MI is more likely because of maximal ST depression in right, as opposed to left, precordial leads. However, given the history of severe 3 vessel coronary disease it is prudent to start with medical management, then observe for resolution of pain, but to also obtain an immediate echocardiogram to ascertain which wall is involved. If pain or ECG findings do not resolve, or if there is posterior wall motion abnormality, then immediate angiography with PCI is indicated.
In this case, maximal medical therapy was undertaken with Aspirin, clopidogrel, heparin, eptifibatide, metoprolol, and IV nitroglycerin and the patient was admitted to the CCU with cardiology consulted immediately. Chest pain resolved and angiogram was not done until the next day. It showed a 100% re-occluded SVG stent to D1; thrombus was suctioned out. Echo confirmed posterior wall motion abnormality. Max troponin was 47.
Case 2.
54 yo female with h/o smoking, DM, HTN, c/o chest pain for 3 hours, substernal radiating to both shoulders. She has an initial ECG which shows diffuse ST depression and she was treated for NSTEMI. She developed some pulmonary edema after metoprolol. ECG #2 was recorded:
ST depression is maximal from V2 to V4. This is due to posterior STEMI until proven otherwise. Unfortunately, it was treated as an NSTEMI for 2.5 hours until an echocardiogram showed a posterior wall motion abnormality. Cath revealed a 100% occluded circumflex. This was opened and stented, with the convalescent ECG below, which shows large upright posterior reperfusion T waves with a long QT.
How can such delay be avoided? By recording posterior leads V7-V9, at the level of the tip of the scapula and at the posterior axillary line (V7), a position midway between this and the spine (V8), and a paraspinal lead (V9). Also, obtaining a stat echo. Most of all, recognize this ECG pattern as being by far more likely to be posterior STEMI than due to subendocardial ischemia, which has maximum ST depression in leads V4-V6.
Case 3.
Here is a case of a 66 yo male with a history of CAD who presents with 1.5 hours of chest pain and is stable.
There is ST depression maximal in, again, V2-V4. The vast majority of posterior STEMI is not isolated, but rather concurrent with inferior and/or lateral involvement. In this case there is subtle ST elevtion in the inferior leads, not noticed by the treating physicians. Compare these ST segments with those of the post reperfusion ECG below:
The patient had rapid PCI of a 100% acutely thrombotically occluded mid circumflex which was opened and stented. There was 3 vessel disease.
The T-wave in posterior STEMI
Notice also that in the first (pre-reperfusion) ECG of case 3, the T wave is not upright as in previous cases. Some authors claim that the T wave must be upright for posterior STEMI. Evidence for this is lacking. In fact, an upright T wave probably indicates reperfusion of the posterior STEMI, whereas an inverted T wave is the analog of a hyperacute T wave (still occluded) but recorded from the opposite side. Either can be present in posterior STEMI, depending on the state of microvascular perfusion due to recanalization or to collateral circulation.
Are there any solid criteria to help provide a DDx between anterior or subendocardial ischemia and posterior STEMI?
This is a very good question, and not easily answered.
First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved.
Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia.
Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs. younger smoker).
Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs.
Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations).
Sixth, placement of posterior leads (take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in just one lead is very sensitive and specific for posterior MI.
Seventh, an immediate echocardiogram can make the distinction
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). Reference and link to full text below.
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.
Pride YB, Tung P, Mohanavelu S, et al. Angiographic and ClinicalOutcomes Among Patients With Acute Coronary Syndromes Presenting With IsolatedAnterior ST-Segment Depression: A TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) Substudy Journal of the American College of Cardiology: Cardiovascular Interventions 2010;3(8):806-11.
Dr Smith
ReplyDeleteThanks for highlighting this issue, as usually we do not concentrate on Posterior MI, unless there is inferior MI. In addition, junior doctors do not look well for tall R waves. Even, some disregard quickly and tell it is positional or what so ever.
While your blog does an excellent job of highlighting posterior STEMIs that were mistaken, are there any solid criteria to help provide a DDx between anterior or subendocardial ischemia and posterior STEMI? Will posterior ST alteration always be limited to v2-v4?
ReplyDeleteThis is a very good question, and not easily answered. First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved. Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia. Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs. younger smoker). Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs. Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations). Sixth, placement of posterior leads (take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in 2 consecutive leads is very accurate for posterior MI.
ReplyDeleteI make it a habit to do a V7-V9 on any patient presenting with right precordial STD or inappropriate right precordial intrinsicoid deflection of unknown origin. It doesnt cost anything besides an extra strip of paper but could save hours of precious heart muscle. A lot of our newer docs will not activate the cath lab on an ECG with right precordial STD and don't run V7-V9 or even V1R-V6R because they don't feel it's necessary. It's quite frustrating to me and poor patient care in my opinion
ReplyDeleteJust one thought: if an anterior MI has small R waves, shouldn't a posterior MI have small S waves?
ReplyDeletethe posterior and anterior walls depolarize simultaneously, so they have opposite forces. If there is old posterior MI, there is nothing to counteract the anterior forces, so you get larger anterior R-waves. If you have old anterior MI, there is nothing to counteract the posterior R-waves, so you get Q-waves.
DeleteI got that. I was just thinking that if the R wave is a Q wave for the posterior wall, then the S wave is the equivalent of the R wave for the posterior wall. And if an anterior MI amputates the R waves, then a posterior one should do the same with the S waves. Does that make sense?
Deleteexcept that S-waves are not only negative, they are also late!
Delete