This is a complex case that I have reprinted from my article in the EMRA publication, EM Resident, with their permission. I'm starting with some didactics. If you want skip to the case, page down, but it is difficult to understand without knowing the background information.
Prior Myocardial Infarction/Left Ventricular Aneurysm
Approximately 60% of patients with a previous anterior transmural MI, and fewer inferior MI patients, may have persistent ST Elevation (STE),1 mimicking acute STEMI. Of those with anterior persistent STE, approximately 80% have an anatomic left ventricular (LV) aneurysm (LVA), which can be seen on echocardiogram as “diastolic distortion” or myocardial wall thinning.2, 3 In the reperfusion era, transmural MI is uncommon, and so the incidence of persistent STE is less than it once was. In a 1987 series of patients with a prior MI presenting with chest pain and STE, only 50% proved to have an acute MI.4 Persistent STE may also be associated with systolic dyskinesis, akinesis, or a large area of myocardial necrosis, even in the absence of anatomic ventricular aneurysm.5
LVA of the anterior wall results in Qr-waves (deep Q followed by a small r-wave) or QS-waves (single deep negative wave) in V1-V4, followed by a moderate degree of STE. The QS-waves indicate complete loss of anterior electrical forces during depolarization. The T-wave may be upright (but not large or hyperacute as in acute STEMI) or inverted (but not deeply inverted, as in acute Non-STEMI). Inferior LVA has STE and QR-waves, not QS-waves, and is thus much more difficult to differentiate from acute inferior STEMI.
We found the best discriminator of LVA vs. acute MI is the T wave amplitude/QRS amplitude ratio, and derived and validated this ratio: if (sum of the T wave amplitude) ÷ (sum of QRS amplitude) in V1-V4 is greater than 0.22, it favors AMI with good sensitivity and specificity.6 If any one lead has a ratio greater than 0.36, it is acute STEMI with equal accuracy. False negatives had a long time between symptom onset and ECG, so that the T-wave was no longer tall. We also validated this rule, published as an abstract (7). Just as useful is evaluation of an index ECG (prior ECG), but these are not always available. Echocardiography may also be useful if it shows dyskinesis (diastolic dysfunction); unfortunately, persistent STE after old MI also occurs without anatomic aneurysm. STE with echocardiographic regional wall akinesis or hypokinesis is present in both acute STEMI and old transmural MI. In some cases, coronary angiography will be required to make the diagnosis. New STEMI in the same location as previous Q-wave MI may also have deep QS-waves, but also has tall T-waves and an increase degree of STE.
An example of classic LV aneurysm morphology (figure 1).
Normal Right Bundle Branch Block (figure 2)
|There is QS pattern in V1-V3 with anterior STE. The T-wave amplitude is not sufficient for acute MI. If you apply either ratio rule, it turns out to be LV aneurysm. This is a classic LV aneurysm morphology.|
|This is normal RBBB, with rSR’, slight ST depression in V2 and V3, and no ST elevation anywhere.|
A non-pathologic RBBB has an rSR’ in V1-V3 and no ST elevation anywhere on the ECG. In RBBB, an absence of an r-wave in lead V1 only may be normal, but if it extends to V2 and beyond it is always abnormal, and the differential includes not only RBBB with MI but also RBBB with left ventricular hypertrophy, and RBBB with cardiomyopathy. There is usually up to 1 mm of ST depression in V2 and V3, discordant (opposite direction of) the positive R’ wave (see figure 2). If there is a very large voltage R’ wave, as in right ventricular hypertrophy, this ST depression may be greater than 1mm in the absence of acute ischemia. To determine the presence or absence of STE in RBBB, one must first determine the end of the QRS, which is the beginning of the ST segment (the J-point).
Case presentation: Right bundle branch block (RBBB) transforms a QS- into a QR-pattern, obscuring diagnosis of left ventricular aneurysm, and suggesting acute STEMI and RBBB.
A 79 year old man presented with dyspnea. He stated that he had sustained a recent myocardial infarction and that it had been painless. His presenting ECG is shown here (figure 3):
Here is a magnification of V1-V3 (figure 4):
|Arrows show the end of the QRS and thus the beginning of the ST segment; this is the J-point. It is apparent, then, that the ST segment is elevated.|
Thus there are anterior Q-waves and anterior STE. So it is an acute STEMI, right? I saw this patient in the late 1990’s (and have seen others since) and administered tPA for acute MI. Before the tPA had time to work, the rate slowed and the RBBB disappeared and showed the ECG in figure 1 above.
Old records were retrieved, and indeed the patient’s previous ECG was the same. In fact, he had presented one week earlier with the exact symptoms and exact same RBBB ECG and received tPA from one of my partners!
How is this possible? Normally, anterior LVA has no or little R-wave amplitude. However, this patient has rate-related RBBB. His right bundle has a long refractory period so that when his rate increases, his right bundle is refractory and does not conduct. In RBBB, there is automatically a large R’-wave even if there the anterior wall is dead, simply because of the sequence of depolarization. So the LVA morphology gets replaced and distorted.
How can you suspect this? On the ECG, it is nearly impossible, as far as I can tell. So you must use other clinical data. First, you have to know that this is possible. Second, you can use echocardiography to assess for aneurysm (diastolic dysfunction or bulging), but if you see only systolic dyskinesis, it could be either LVA or acute STEMI.
In contrast to LVA, patients with acute STEMI who have Q-waves have a larger T-wave. See figure 5 for an example of a patient with QS-waves but with hyperacute T-waves, such that the T/QRS ratio is high. It was an acute LAD occlusion.
|Figure 5. There are QS-waves as one would see in LV aneurysm, but there are large T-waves, as is seen in acute STEMI. The T/QRS ratio is high. It was an acute LAD occlusion.|
1. Mills RM, Young E, Gorlin R, Lesch M. Natural history of S-T segment elevation after acute myocardial infarction. Am J Cardiol 1975;35(5):609-14.
2. Visser CA, Kan G, David GK, Lie KI, Durrer D. Echocardiographic-cineangiographic correlation in detecting left ventricular aneurysm: A prospective study of 422 patients. Am J Cardiol 1982;50(2):337-41.
3. Visser CA, Kan G, Meltzer RS, Koolen JJ, Dunning AJ. Incidence, timing and prognostic value of left ventricular aneurysm formation after myocardial infarction: A prospective, serial echocardiographic study of 158 patients. Am J Cardiol 1986;57(10):729-32.
4. Miller DH, Kligfield P, Schreiber TL, Borer JS. Relationship of prior mycardial infarction to false-positive electrocardiographic diagnosis of acute injury in patients with chest pain. Arch Intern Med 1987;147:257-61.
5. Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnormalities: a two-dimensional echocardiographic study. Am J Cardiol 1984;53(11):1542-6.
6. Smith SW. T/QRS amplitude ratio best distinguishes the ST elevation of anterior left ventricular aneurysm from anterior acute myocardial infarction. American Journal of Emergency Medicine 2005;23(3):279-87.
7. Beeman W. Shroff G. Smith SW. T/QRS Amplitude Ratio Is Significantly Higher In Acute Anterior ST Elevation Myocardial Infarction Than In Previous Myocardial Infarction With Persistent ST Elevation (left Ventricular Aneurysm Morphology): A Validation (abstract 371). Annals of EM Oct 2011 Suppl 58(4): S302.