This 47 yo male with 2 risk factors had onset of substernal CP while watching TV and smoking a cigarette. It felt "sharp" as if "my lungs are being ripped off," and it hurt to move and take a deep breath. The following ECG was recorded:
There is minimal (less than 1.0 mm) of ST elevation in II, III, and aVF, and also ST elevation of less than 1 mm in V5 and V6. This is diagnostic of coronary occlusion, because of reciprocal ST depression in aVL, even though there is not 1 mm of ST elevation in any lead.
The patient was started on aspirin and heparin, and the cath lab was activated, but because of the widespread ST elevation, and the sharp and pleuritic nature of the pain, the interventionalist thought it was pericarditis.
However, this cannot be pericarditis because there is reciprocal ST depression in aVL. Pericarditis is almost always diffuse (around the entire heart), and creates an ST vector that is inferior, anterior, and lateral (towards inferior leads and V4-V6, especially leads II and V5). It therefore never results in ST depression in aVL. (There is, of course, a rare exception which should only be proven by a negative angiogram: that is localized pericarditis, localized to the inferior wall.)
A stat echocardiogram was done and it showed no wall motion abnormality. However, in the intervening time period, the pain had resolved and the following ECG was recorded (2 hours after the first). Also, the first troponin I returned at 0.5 ng/ml:
The elevated troponin could be due to myopericarditis, so it alone does not tell us anything definite. However, the new T-wave inversion, and resolution of ST elevation, does further prove that the findings on the first ECG are due to MI, not pericarditis. In pericarditis, T-waves do invert, and ST segments do resolve, but much more slowly than with reperfused MI.
The patient fortunately remained pain free all night. Due to rise and fall of troponin and EKG evolution, the interventionalist took the patient to the cath lab and found that the RCA was open but there was a culprit lesion with 99% stenosis of the mid 2nd posterolateral branch of the RCA.
The artery was in all likelihood occluded at the time the patient was having pain. But because the ST elevation does not meet the arbitrary "criterion" of 1 mm in two consecutive leads, this is arbitrarily called "Non-STEMI" instead of "STEMI". The terminology, as defined by mm criteria, does not achieve its purpose of identifying complete coronary occlusion. In this case, the artery opened without reperfusion therapy, as it often does, especially with aspirin and heparin.
For another example of occlusion without 1 mm ST elevation, look here:
http://hqmeded-ecg.blogspot.com/2009/01/st-depression-limited-to-inferior-leads.html
There is minimal (less than 1.0 mm) of ST elevation in II, III, and aVF, and also ST elevation of less than 1 mm in V5 and V6. This is diagnostic of coronary occlusion, because of reciprocal ST depression in aVL, even though there is not 1 mm of ST elevation in any lead.
The patient was started on aspirin and heparin, and the cath lab was activated, but because of the widespread ST elevation, and the sharp and pleuritic nature of the pain, the interventionalist thought it was pericarditis.
However, this cannot be pericarditis because there is reciprocal ST depression in aVL. Pericarditis is almost always diffuse (around the entire heart), and creates an ST vector that is inferior, anterior, and lateral (towards inferior leads and V4-V6, especially leads II and V5). It therefore never results in ST depression in aVL. (There is, of course, a rare exception which should only be proven by a negative angiogram: that is localized pericarditis, localized to the inferior wall.)
A stat echocardiogram was done and it showed no wall motion abnormality. However, in the intervening time period, the pain had resolved and the following ECG was recorded (2 hours after the first). Also, the first troponin I returned at 0.5 ng/ml:
The elevated troponin could be due to myopericarditis, so it alone does not tell us anything definite. However, the new T-wave inversion, and resolution of ST elevation, does further prove that the findings on the first ECG are due to MI, not pericarditis. In pericarditis, T-waves do invert, and ST segments do resolve, but much more slowly than with reperfused MI.
The patient fortunately remained pain free all night. Due to rise and fall of troponin and EKG evolution, the interventionalist took the patient to the cath lab and found that the RCA was open but there was a culprit lesion with 99% stenosis of the mid 2nd posterolateral branch of the RCA.
The artery was in all likelihood occluded at the time the patient was having pain. But because the ST elevation does not meet the arbitrary "criterion" of 1 mm in two consecutive leads, this is arbitrarily called "Non-STEMI" instead of "STEMI". The terminology, as defined by mm criteria, does not achieve its purpose of identifying complete coronary occlusion. In this case, the artery opened without reperfusion therapy, as it often does, especially with aspirin and heparin.
For another example of occlusion without 1 mm ST elevation, look here:
http://hqmeded-ecg.blogspot.com/2009/01/st-depression-limited-to-inferior-leads.html
Congratulations for this post. I've a similar case today.
ReplyDeleteJânio Matos Fraga
janiomatos@yahoo.com.br
São Paulo - Brazil
very nice and useful presentation,thankx.--------dr .avinash manwatkar,selu,india 431503
ReplyDeletecan you explain the ST elevation in lead v5 v6 ?
ReplyDelete@ Anonymous — There is often lateral chest lead ST elevation in association with acute inferior STEMI, when there are larger posterolateral branches off the posterior descending artery (which often originates from the RCA). In this particular case — there was 99% stenosis of the mid-2nd posterolateral branch of the RCA — and that would account for ST elevation in V5 and V6 — :)
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