Diffuse ST Elevation. What do you think?
What do you think of this ECG, without any clinical information?
There is inferior and lateral ST elevation and ST depression in V1 and V2, just what would be present in an infero-postero-lateral STEMI. What other finding is there?
An extremely long QTc is present, and this was even noted by the computer algorithm, which accurately measured it at 575 ms. This strongly suggests stress cardiomyopathy (SCM). This immediately caught my eye when shown to me and SCM immediately came to mind.
The patient presentation is of course critical to the diagnosis of SCM: this patient presented with altered mental status and a Na of 107 mEq/L. She had presumably had a seizure.
An echocardiogram revealed multiple wall motion abnormalities, though not the typical "Takotsubo" Apical Ballooning.
Here are 5 other cases of Stress Cardiomyopathy
Here is a case of Reverse Takotsubo
When I saw this ECG, I also thought "hypokalemia," Why? There is a "wavy" pattern in V2 which is caused by an inverted T-wave followed by a large U-wave. See this annotated version:
The lines show the "wavy" pattern and the arrow points to the large U-wave (arrow). The wavy pattern could be mistaken for a down-up T-wave, which is common in Posterior MI, but in this case it would be a far too long QT interval for this to be T-wave..
Here are some more examples of the wavy pattern of hypokalemia.
Peak troponin I was 2.5 ng/mL. ECG findings quickly resolved. There was no angiogram.
How to suspect takotsubo stress cardiomyopathy from the presenting symptoms, signs and ECG
First, it is believed to by caused by diffuse small vessel ischemia due to catecholamines, and thus has the same electrophysiologic substrate as STEMI. It affects the entire heart except the base, resulting in diffuse circumferential wall motion abnormalities that only spare the base (top) of the heart. These diffuse wall motion abnormalities (lateral, posterior, inferior, septal, anterior, apical) result in systolic "apical ballooning" which looks like a Japanese octopus trap (a takotsubo).
Of course, the clinical presentation can help to suspect this: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214344/
It is most common in postmenopausal women and is associated with severe emotional upset (stress) or severe physiologic stressors such as respiratory failure.
Stress Cardiomyopathy (Apical Ballooning syndrome, or Takotsubo cardiomyopathy) only presents with ST elevation in about 1/3 of cases, but when it does, it is one of the most difficult mimics of anterior STEMI, and often the only way to tell the difference is to do an angiogram.
ECG Differentiation of SCM from STEMI
First, a very long QT is quite specific for SCM, but not sensitive. In this study, the mean QTc for SCM was 567 (+/- 81) ms vs. 489 (+/- 61) ms for anterior STEMI.
A review and analysis of the literature in ECG differentiation of the two entities (1-6) reveals that an analysis of ST elevation vector is a good predictor of anterior STEMI vs. stress cardiomyopathy. In anterior STEMI, whether proximal, mid, or distal LAD occlusion, there is ST elevation in V1 (1 mm measured at 80 ms after the J-point) in about 80% of cases, whereas this is present in 20% of cases of SCM. SCM also has a negative ST segment in aVR and is more likely to have ST elevation in inferior leads, or at least absence of ST depression in inferior leads (however, 40% of anterior STEMI lack inferior ST depression). Finally, precordial ST elevation in SCM is more pronounced in V3-V5 vs. V2-V4.
Putting these all together, it is apparent that the ST vector in anterior STEMI is more commonly anterior and superior (V1-V4), without STE in inferior leads, whereas in SCM the ST Vector it is more inferior and lateral (V2-V5, with STE in inferior leads and ST depression in aVR). This correlates with the location of wall motion abnormalities in SCM (diffuse and toward the apex, similar to pericarditis, including inferior and lateral walls) vs. anterior STEMI (anterior as well as septal-apical).
In this very interesting study by Kosuge et al., the combination of the presence of ST-segment depression in lead aVR and the absence of ST-segment elevation in lead V1 identified SCM (vs. anterior STEMI) with 91% sensitivity, 96% specificity, and 95% predictive accuracy, which was superior to any other electrocardiographic findings.
1. Tamura A et al. A New Electrocardiographic Criterion to Differentiate Between Takotsubo Cardiomyopathy and Anterior Wall ST-Segment Elevation Acute Myocardial Infarction. Am J Cardiol Sept 2011; 108(5):630-633.
2. Ogura R, et al. Specific findings of the standard 12-lead ECG in patients with "takotsubo" cardiomyopathy: comparison with the findings of acute anterior myocardial infarction. Circ J 2003;67:687– 690.
3. Inoue M, et al. Differentiation between patients with takotsubo cardiomyopathy and those with
anterior acute myocardial infarction. Circ J 2005;69:89 –94.
4. Bybee KA, et al. Electrocardiography cannot reliably differentiate transient left ventricular
apical ballooning syndrome from anterior ST-segment elevation myocardial infarction. J Electrocardiol 2007;40:38.e1–38.e6.
5. Jim MH, et al. A new ECG criterion to identify takotsubo cardiomyopathy from anterior
myocardial infarction: role of inferior leads. Heart Vessels 2009;24:124–130.
6. Kosuge M, et al. Simple and accurate electrocardiographic criteria to differentiate takotsubo
cardiomyopathy from anterior acute myocardial infarction. J Am Coll Cardiol 2010;55:2514 –2516.
http://content.onlinejacc.org/article.aspx?articleid=1142882
7. Kosuge M, et al. Similar abstract from 2012: http://content.onlinejacc.org/article.aspx?articleid=1204510
Posted by Steve Smith at 9:13 AM
Labels: PseudoSTEMI, stress cardiomyopathy
Would have you done a coronary angiogram to this patient if you were in charge at presentation ?
Steve Smith February 2, 2018 at 2:48 PM
If confronted with chest pain, yes. But this patient had altered mental status, seizure, and Na of 107. So I would not.
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