Prolonged Chest Pain. Is this LV aneurysm or acute anterior STEMI? Acuteness of STEMI and viable myocardium.
Posted May 21 2012 12:04pm
This patient had no significant past medical history. He presented with chest pain of 48 hours duration which became worse in the previous several hours. The pain was stabbing and 10/10 and associated with SOB. The pain was partly relieved with sublingual nitroglycerin. Here is the initial ECG
There are QS-waves in leads V1-V3, and a QR in lead V4. It looks like anterior LV aneurysm. Is it? Answer below.
Rule 1: TV1 + TV2 + TV3 + TV4 divided by QRS V1 + QRS V2+ QRS V3 + QRS V4 If the value is less than 0.22, then it is usually LV aneurysm. If greater than or equal to 0.22, then acute anterior STEMI. Applied to this ECG: 4.5 +4 + 3.5 + 4 divided by 20 + 22 + 8.5 + 4 = 16/54.5 = 0.29 (> 0.22 correlates with anterior STEMI)
Rule 2. If there is any one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is likely to be anterior STEMI. Applied to this ECG: Lead V4 is 4/4 = 1 (>0.36 correlates with anterior STEMI).
The problem with this method: Almost all of our false negatives (in both the derivation and validation groups) were in patients who had at least 6 hours of pain. In other words, in a subacute anterior MI there may be well formed QS-waves and the T-wave amplitude diminishes as the infarct progresses. Therefore, in this patient with 48 hours of symptoms you would be particularly suspicious of a negative result.
He had a previous normal ECG and had no history of MI, so new Q-waves are that much more suspicious for subacute STEMI.
Is there benefit to PCI in patients with prolonged symptoms and persistent ST elevation?
Schomig et al. (JAMA 2005;293:2865-72) showed in a randomized trial that such patients who underwent PCI had a smaller left ventricular infarct size than those show did not.
How accurate is time from symptom onset in determining the amount of viable myocardium remaining? Not very. In this study of "aborted" STEMI, 11% of patients with a 5 hours symptom onset to PCI time had no significant biomarker elevation. These patients had a lower mortality than those with more elevated biomarkers, and much lower if they had > 70% ST resolution after artery opening (This ECG marker is the best sign of restored microvascular reperfusion, even better than TIMI flow in the artery).
The ECG may be much better than time since symptom onset at determining viable myocardium and benefit from reperfusion. There are several papers on the Anderson Wilkins Acuteness score , which uses a complex equation involving measurements of T-waves and Q-waves. In one such study , the ECG was better than time since symptom onset at measuring the "acuteness" of the infarct. High T-wave amplitude is associated with higher acuteness (more viable myocardium at risk and more benefit to reperfusion); in contrast, well-formed Q-waves are associated with lower acuteness and with less benefit. A recent study by Engblom et al. that used pre- and post-reperfusion myocardial imaging to compare ischemic myocardium at risk to final infarct size did not substantiate this, but there are problems with the study, including prolonged time from ECG to tracer injection and with the equation itself, which does not use proportions: T-wave amplitude is absolute and not relative to the QRS.
The cath lab was activated. His initial troponin I returned at 13 ng/ml, confirming prolonged duration of STEMI. Angiogram revealed a 100% mid LAD occlusion which was stented.