A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG
Here is the patient's previous ECG
Normal
Here is the patient's presenting ED ECG:
What do you think?
There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation. Precordial ST depression may be subendocardial ischemia or posterior STEMI. How can we tell the difference?
See the list below.
If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)]. This was indeed done:
Notice the limb leads have been reversed (axes of every lead are inverted!). But we are now concerned with the precordial leads. V7-V9 (labelled V4-V6) have no ST elevation.
Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. In this case, the patient had failed to take his atenolol in the AM and was having reflex tachycardia in addition to ACS. BP was 160/100. He was given metoprolol IV which succuessfully brought his heart rate and BP down.
His chest pain resolved completely, but his ECG continued to show profound ST depression. We performed a
bedside echo and found a posterior wall motion abnormality.
The cath lab was activated and the patient went for immediate angiography, which showed a 95% hazy thrombotic lesion with TIMI III flow in a large first obtuse marginal (OM-1) off the circumflex. Therefore, the angiographer had time to visualized the other arteries. The RCA was chronically occluded but supplied a small area. The LAD had a 75% proximal lesion that by fractional flow reserve was hemodynamically significant. So there was 3-vessel disease, but with an acute posterior STEMI. The OM-1 was opened and stented, then the LAD was stented 3 days later.
The acute infarct-related artery was off the circumflex and the affected wall was posterior (STEMI).
The posterior leads were falsely negative. See far below for data on posterior leads.Does this matter that the posterior ECG was a false negative? If there is ST depression (as there is here), it is ACS. Whether it is subendocardial ischemia or posterior STEMI,
if you cannot get it to resolve, you must activate the cath lab. And even if it is STEMI, if you get it to resolved with medical therapy, then you have opened the artery without intervention and a delay is acceptable.
This is very popular post from almost 4 years ago on posterior MI . At the bottom are 7 ways to help differentiate the ST depression of posterior STEMI from subendocardial ischemia. I have copied them here
Some ways to differentiate subendocardial ischemia from posterior STEMIFirst, 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. These are very difficult and it is very hard to detect a posterior wall motion abnormality unless you are very experienced. I recommend a formal study with Definity before concluding there is no posterior wall motion abnormality.
Eighth, see above. Whether or not it is STEMI, the cath lab should be activated if the ischemia cannot be controlled medically: aspirin, nitro, beta blockers, clopidogrel, heparin/enoxaparin, GP IIb/IIIa inhibitor.
Here is a short summary of data on posterior leads, from: Critical Decisions in Emergency and Acute Care Electrocardiography. William Brady and JD Truwit, editors. Blackwell Publishing 2009. (Smith SW as editor of section on Acute Coronary Syndromes). This is a quoted excerpt from a chapter that was written by Daniel T. O’laughlin, MD, and edited by me.
Here is the patient's previous ECG
There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation. Precordial ST depression may be subendocardial ischemia or posterior STEMI. How can we tell the difference? See the list below.
If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)]. This was indeed done:
Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. In this case, the patient had failed to take his atenolol in the AM and was having reflex tachycardia in addition to ACS. BP was 160/100. He was given metoprolol IV which succuessfully brought his heart rate and BP down. His chest pain resolved completely, but his ECG continued to show profound ST depression. We performed a bedside echo and found a posterior wall motion abnormality.
The cath lab was activated and the patient went for immediate angiography, which showed a 95% hazy thrombotic lesion with TIMI III flow in a large first obtuse marginal (OM-1) off the circumflex. Therefore, the angiographer had time to visualized the other arteries. The RCA was chronically occluded but supplied a small area. The LAD had a 75% proximal lesion that by fractional flow reserve was hemodynamically significant. So there was 3-vessel disease, but with an acute posterior STEMI. The OM-1 was opened and stented, then the LAD was stented 3 days later.
The acute infarct-related artery was off the circumflex and the affected wall was posterior (STEMI). The posterior leads were falsely negative. See far below for data on posterior leads.
Does this matter that the posterior ECG was a false negative? If there is ST depression (as there is here), it is ACS. Whether it is subendocardial ischemia or posterior STEMI, if you cannot get it to resolve, you must activate the cath lab. And even if it is STEMI, if you get it to resolved with medical therapy, then you have opened the artery without intervention and a delay is acceptable.
This is very popular post from almost 4 years ago on posterior MI . At the bottom are 7 ways to help differentiate the ST depression of posterior STEMI from subendocardial ischemia. I have copied them here
Some ways to differentiate subendocardial ischemia from posterior STEMI
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. These are very difficult and it is very hard to detect a posterior wall motion abnormality unless you are very experienced. I recommend a formal study with Definity before concluding there is no posterior wall motion abnormality.
Eighth, see above. Whether or not it is STEMI, the cath lab should be activated if the ischemia cannot be controlled medically: aspirin, nitro, beta blockers, clopidogrel, heparin/enoxaparin, GP IIb/IIIa inhibitor.
Here is a short summary of data on posterior leads, from:
Critical Decisions in Emergency and Acute Care Electrocardiography. William Brady and JD Truwit, editors. Blackwell Publishing 2009. (Smith SW as editor of section on Acute Coronary Syndromes). This is a quoted excerpt from a chapter that was written by Daniel T. O’laughlin, MD, and edited by me.