This was contributed by Brooks Walsh
, with a little editing and additions, plus a section of false positive cath lab activations added by me. Brooks is a fine emergency physician from the Yale residency who has a keen and talented interest in ECGs and bedside cardiac echo.Case
A middle-aged man was sent to the ED from a primary care clinic, with “ECG changes” and worry for STEMI.
|The ECG shows ST elevation (STE) across the precordium, highest in V2 and V3. There are only minimal R waves in those leads [in fact, such tiny R-waves are technically considered Q-waves, and thus the patient has "QS"-waves (deep Q-waves without any R-wave at all], with markedly deep S waves.|
The ECG from the office that day, although not available here, was essentially identical to the above ECG. He had been at the clinic for a scheduled appointment. He denied having had any chest pain, SOB, nausea, or other ischemic symptoms at any point in the day. However, records sent from the clinic indicated he had had a STEMI treated with PCI at another hospital 4 months prior.
Besides a new STEMI, what can account for the ST segment elevation?
The T waves are dramatically biphasic, with a steep descent, suggesting a Wellen’s pattern. The poor R wave progression, however, rules out Wellen’s syndrome, which requires R-wave preservation
. Additionally, the patient denies any recent symptoms. (A true Wellen’s syndrome is observed after ischemic symptoms have resolved.)
The deep S waves and ST elevation could be the result of left ventricular hypertrophy. Although R-waves may be absent in LVH, LVH has high voltage R-waves in V4-V6. So this is NOT LVH. Persistent STE after prior MI (also known as "left ventricular aneurysm morphology")
This is an ECG entity that is most accurately termed “persistent STE after prior MI,” but is more commonly (and somewhat less accurately) called left ventricular aneurysm. This is usually seen after large anterior MIs (1)
, especially in those patients who had delayed reperfusion therapy, or none. Typically, these patients show deep QS complexes in V1 – V3, or perhaps minimal r-waves with a deep S wave. STE will usually be mild, less than 3mm, and most prominent in leads V1-V3.
The correlation with anatomic aneurysm is imprecise – patients with persistent STE might not have a true anatomic aneurysm on echocardiography, and instead may only manifest systolic dyskinesis. (2)
Conversely, many patients with dyskinesis or aneurysm do not have persistent STE. (3)
|From Arvan and Varat, reference 2|
The problem with persistent STE is that patients may be inappropriately administered or denied reperfusion therapy if they present with new ischemic-type symptoms. How can we be sure that he isn’t having a new STEMI on top of his old STEMI?
Differentiating persistent STE from “acute on chronic STE”
The first method involves analyzing the height of the T waves relative to the amplitude of the QRS complexes (i.e. height of R + depth of S).
Dr. Stephen Smith has derived and validated two calculations that can help differentiate new MI versus persistent STE. (4, 5)
|The second is the best and easiest to use.|It is important to know that this rule only applies to cases in which the differential diagnosis is anterior STEMI vs. anterior LV aneurysm. This is the case when there are deep well-formed Q-waves (usually QS-waves).
Two other words of caution:
1. In patients with prolonged chest pain (> 6 hours), the T-waves become less hyperacute and these were the only cases of false negatives.
2. Acute STEMI can be superimposed on LV aneurysm. In this case, the T-wave becomes hyperacute again, so the formula works even though there is an underlying LV aneurysm.
Apply the rule to this case:
In this case, I overestimated the height of the T wave in V4, but the formula still supports persistent STE over STEMI.
|The lead with the highest ratio is V4 at 0.25, which is substantially below 0.36|
, a bedside echo demonstrated an aneurysmal, akinetic apex, with a thin wall. Acute STEMI usually has an akinetic wall, but it will not be thin-walled.
This is consistent with an old LAD-distribution MI. While akinesis can also be seen in either persistent STE or acute MI, the dyskinesis and thinned wall strongly supports persistent STE.
It is also dilated
. It takes time for the heart to dilate after MI; it is not present at the time of acute STEMI.
Here is a still image of the latter part of the video:
A note of caution:
|Red line indicates thin, dyskinetic apex and distal septum|
Focused echocardiography (unlike comprehensive echo) should not be used to guide reperfusion decisions in patients with concerning symptoms, where the likelihood of acute coronary occlusion is high. This patient was entirely symptom-free, and the echo was simply supportive of clinical judgment, and was used in the context of old ECGs and cath reports.
Old ECG when patient did have a STEMI:
Lastly, the records were obtained from the hospital where PCI was performed many months ago
, including a full sequence of ECGs. The patient had developed chest pain early in the morning, and called 911. An ECG was obtained by EMS.
|Mild ST-segment elevation in V1 and V2, but there is also characteristic ST-depression, followed by a peaked T-wave, in V3 and V4. This is a de Winter pattern, suggesting proximal LAD occlusion.|
In the ED, the ECG evolved to that of a classic anterior STEMI.
|There are marked ST elevations in the precordium. The loss of anterior S waves, and elevated J point, has been described as grade 3 ischemia, and predicts a poor response to reperfusion therapy. |
The patient was transferred for reperfusion. The ECGs obtained post-PCI, unfortunately, shows persistent STE.
|Not only does this predict a larger infarct, but also strongly predicts chronic microvascular damage.(6) This damage might explain why persistent STE is better correlated with myocardial dysfunction (e.g. dyskinesis) than with true aneurysm. Indeed, his pre-discharge echo showed an EF of 20% - 30%, and dyskinesis of the distal septum and apex.|
Such persistent STE is called the "No-Reflow" phenomenon
. There is such severe downstream clogging of arterioles with platelet-fibrin aggregates, that, in spite of large vessel reperfusion, there is no true reperfusion. This can be assessed on angiography as "blush" or TIMI myocardial perfusion grading. The outcome of cases is predicted better by the ECG than by angiography
, with persistent STE portending a bad outcome even with an open artery!Case progression
In our ED, he had negative serial troponins. After the old records were obtained he was discharged home.
Images were reproduced under the "Fair Use" in Copyright Law, which allows such reproduction for non-profit educational purposes.Does LV Aneurysm Morphology Result in False Cath Lab Activation?
Before the publication of these studies by Smith and Klein, anterior LVA was very difficult to differentiate from anterior STEMI on the ECG, and was perhaps the most commonly misinterpreted etiology of false positive STE in patients presenting to the emergency department with ischemic symptoms [7, 8, 9, 10, 11, 12, 13]. Brady et al. showed eleven ECGs to 450 emergency physicians (EPs). The ECG of LVA was misdiagnosed as acute STEMI by 72% of EPs, a higher misclassification rate than any other ECG. The misclassification would have led to inappropriate thrombolytic therapy by 28% of EPs . In a second study by the same authors, there were 202 ECGs with STE and 12 ECGs were misdiagnosed – five ECGs showed LVA, two of which were diagnosed as STEMI . All would have been identified by the rule. Miller et al. studied 100 patients admitted to a cardiac care unit for suspicion of MI. Of these patients, 31 had STE on the ECG; 21 of 21 without prior infarction and 5 of 10 withprior infarction had AMI. All 5 false positive ECGs with STE were in the location of the previous Q-wave infarct (LVA), and the STE did not represent acute injury . In a large, more recent study, Larson et al. showed that 20 out of 123 false catheterization laboratory activations were due to LVA .
In all of these studies, and also in Rokos et al.  every ECG that was shown as a false positive cath lab activation, would have been unequivocally identified as LV aneurysm by the Smith-Klein rules!References
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2. Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnormalities: A 2-dimensional echocardiographic study. Am J Cardiol. 1984;53(11):1542-1546. doi:10.1016/0002-9149(84)90576-9.
3. Madias JE. Discordance of diagnosis of ventricular aneurysm made by the electrocardiogram and myocardial imaging: “ST-segment counterpoise” as a hypothetical mechanism. J Electrocardiol. 2006;39(3):340-341. doi:10.1016/j.jelectrocard.2006.02.009.
4. Smith SW. T/QRS Amplitude Best Distinguishes Acute Anterior MI from Anterior Left Ventricular Aneurysm. American Journal of Emergency Medicine 2005; 23(3):279-287.
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11. Miller DH, Kligfield P, Schreiber TL, Borer JS. Relationship of prior myocardial infarction to false-positive electrocardiographic diagnosis of acute injury in patients with chest pain. Arch Intern Med 1987;147: 257- 61.
12. Larson DM, Menseen KM, Sharkey SW, Duval S et al. “False-positive” cardiac catheterization laboratory activation among patients with suspected ST-segment elevation myocardial infarction. JAMA. 2007 Dec 19; 298 (23):2754-60.
13. Rokos IC, French WJ, Mattu A, Nichol G, et al. Appropriate cardiac cath lab activation: optimizing electrocardiograph interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003.