I was reading through ECGs on the system when I saw this one:
|Sinus tachycardia, rate 120
Computerized QTc = 380 ms
What do you think?
I was immediately worried about a proximal LAD occlusion. Although sinus tachycardia generally argues against ACS, a large anterior MI may result in such poor stroke volume that there is compensatory tachycardia and possibly impending cardiogenic shock.
I looked to see if there was an ED cardiac ultrasound, and there was:
Parasternal Long Axis:
Poor image, but one can see that there is poor apical function
Parasternal short axis:
This shows poor contractility of the anterior wall.
Contrast the shortening and thickening of the posterior wall (opposite the transducer) to the anterior wall (closest to the transducer)
Apical 4 chamber:
Apical wall motion abnormality
The base is contracting well.
At this point I still knew nothing about the patient, but was worried about an acute anterolateral STEMI (Proximal LAD occlusion).
I went to talk with the treating clinicians. They too were worried about LAD occlusion and had consulted cardiology.
Here is the history:
An elderly woman with history of diabetes and hypertension presented ambulatory with acute onset of crushing 10/10 chest pain that radiates to the back. It started one hour prior to arrival. She has never had anything like this before.
With that history, I had no doubt about the diagnosis.
Cardiology performed a formal echo. Here is the result. (She had previous normal echo with 65% ejection fraction):
–Normal left ventricular size, thickness and severely depressed systolic function.
–The estimated left ventricular ejection fraction is 27%.
–Very large area of regional wall motion abnormality, akinetic, involving apex, mid and apical segments of the anterior, lateral, inferior and septal walls along with hyperdynamic base.
Let’s take one more look at the ECG:
|There is STE in V2 and V3 of about 1 mm at the J-point (up to 1.5 mm “normal” for women)
However, there is 2 mm in V4-V6, so this is diagnostic of STEMI, by criteria.
There is also some STE in aVL and I, with reciprocal ST depression in III and aVL.
Just for interest’s sake, how do the formulas perform? (Really, since V4-V6 are diagnostic, as is the echo, we should not let a low number dissuade us from the diagnosis)
QTc = 380, STE60V3 = 2, RAV4 = 8; QRSV2 = 7
3-variable: 22.20 (low); 4-variable: 18.68 (high)
(4-variable is more accurate, but not validated)
Interestingly, there is also a bit of ST elevation in lead II. This suggests that there may be inferior ST elevation that does not fully manifest in III and aVF because the STE in aVL results in an opposing force to depress the ST segments in III and aVF.
So perhaps there is competing ST elevation in I and aVL on the one hand, and II, III, aVF on the other. This would mean there is not only anterolateral MI, but also inferior MI, and implicates a “wraparound” (type III) LAD to the inferior wall. This is also supported by the echo which shows diffuse wall motion abnormalities.
The patient was taken for emergent angiography:
The coronaries were clean. The LAD was type II (NOT a wraparound). Thus, even an autolysed thrombus in the LAD would not explain the ECG (a type II LAD occlusion would not produce this inferior findings on the ECG and on the echo).
Takotsubo stress cardiomyopathy became the most likely, or certain, diagnosis.
Troponin returned at 0.222. No other troponins were drawn.
Shortly afterwards, the patient spiked a fever and was diagnosed with pyelonephritis.
Here is the post cath ECG:
|T-waves are not nearly as tall, and ST elevation is less
Here is the next day ECG:
|Wellens’ waves?? Looks like it, but can happen with takotsubo also.
And then the day after:
|Very wide, rather bizarre inverted T-waves.
These are very typical of takotsubo.
Takotsubo stress cardiomyopathy, with an unusual onset of crushing chest pain, presumably due to sepsis from pyelonephritis.
Could this have been diagnosed by the ECG?
In retrospect, from the ECG alone, takotsubo may have been strongly suspected based on ST depression in aVR, absence of ST elevation in V1, and STE in lead II. However, all these findings may be present with a wraparound LAD to the inferior wall.
Pathophysiology of Takotsubo
Diffuse small vessel ischemia, with resulting ischemic pain, wall motion abnormalities, and ECG findings. It is only the distribution of these findings that is, or may be, different between STEMI and Takotsubo.
Can one reliably differentiate the ST Elevation of Takotsubo from the ST Elevation of LAD occlusion?
The quote below is from our paper just published online:
David F. Miranda, M.D, Angie Lobo, M.D, Brooks Walsh, M.D, Yader Sandoval, M.D,
Stephen W. Smith, M.D.
New Insights into the Use of the 12-lead Electrocardiogram for Diagnosing Acute Myocardial Infarction in the Emergency Department.
Canadian Journal of Cardiology 34(2):132; February 2018. Issue: Advances and Controversies in Cardiac Emergency Care.
(in Press, Accepted Manuscript)
Takotsubo may manifest T-wave inversion, but also STE that mimics STEMI. Although earlier work had suggested that ECG criteria might distinguish this STE from anterior STEMI,57 recent literature does not support this result.58 59 Although the specificity of various combinations of ECG elements for Takotsubo may be > 95%, the positive predictive value may be as low as 67% due to the low prevalence of Takotsubo. Many anterior STEMI, especially due to wraparound LAD to the inferior wall, have similar ECG findings and also apical ballooning.60 Therefore, coronary angiography is often essential to rule out acute coronary occlusion, even when the STE pattern and cardiac ultrasound both suggest Takotsubo.
57. Kosuge M, Ebina T, Hibi K, et al. Simple and accurate electrocardiographic criteria to differentiate takotsubo cardiomyopathy from anterior acute myocardial infarction. Journal of the American College of Cardiology 2010;55:2514-6.
58. Frangieh AH, Obeid S, Ghadri JR, et al. ECG Criteria to Differentiate Between Takotsubo (Stress) Cardiomyopathy and Myocardial Infarction. Journal of the American Heart Association 2016;5.
59. Vervaat FE, Christensen TE, Smeijers L, et al. Is it possible to differentiate between Takotsubo cardiomyopathy and acute anterior ST-elevation myocardial infarction? J Electrocardiol 2015;48:512-9.
60. Mugnai G, Pasqualin G, Benfari G, et al. Acute electrocardiographic differences between Takotsubo cardiomyopathy and anterior ST elevation myocardial infarction. J Electrocardiol 2015;48:79-85.
Annotated Bibliography (relevant quotes from abstracts)
57. Kosuge et al.:
“The absence of abnormal Q waves, absence of reciprocal changes, presence of ST-segment elevation in lead −aVR (i.e., ST-segment depression in lead aVR), and absence of ST-segment elevation in lead V1identified TC with sensitivities of 42%, 94%, 97%, and 94%, specificities of 74%, 49%, 75%, and 71%, and predictive accuracies of 71%, 53%, 77%, and 73%, respectively.”
58. Frangieh et al.:
“When comparing STEMI and STE-TTC, ST-elevation in –aVR (ST depression in aVR) was characteristic of STE-TTC with a sensitivity/ specificity of 43% and 95%, positive predictive value (PPV) 91%, and a negative predictive value (NPV) 62% (Pwhen ST depression in aVR is accompanied by ST-elevation in inferior leads, sensitivity/specificity were 14% and 98% (PPV was 89% and NPV 52%) (P=0.001), and 12% and 100% when associated with ST-elevation in anteroseptal leads (PPV 100%, NPV 52%) (P On the other hand, STEMI was characterized by ST-elevation in aVR (sensitivity/specificity of 31% and 95% P
59. Vervaat et al. assessed these previous criteria:
“The existing ECG criterion was less accurate (76%) than in the original study (95%), with a large difference in sensitivity (26% vs. 91%). Only a frontal plane ST-vector of 60° could significantly distinguish TC from all acute anterior STEMI subgroups (p < 0.01) with an overall diagnostic accuracy of 81%. The mean amplitude in inferior leads II and aVF was significantly higher for patients with TC compared to all patients with acute anterior STEMI (p < 0.01 and p < 0.05 respectively) and the mean amplitude in the precordial leads V1 and V2 was significantly lower compared to proximal and mid LAD occlusion (p < 0.01)."
60. Mugnai et al.
“The absence of abnormal Q waves, the ST depression in aVR and the lack of ST elevation in V1 were significantly associated with TC (respectively: 52% vs 18%, p = 0.01; 47% vs 11%, p = 0.01; 80% vs 41%, p = 0.01). The combination of these ECG findings identified TC with a specificity of 95% and a positive predictive value of 85.7%.”
More cases of Takotsubo Stress Cardiomyopathy
COPD exacerbation, what do the ECG and bedside echo show?
Is the Right Ventricle involved in Takotsubo Stress Cardiomyopathy?
RV SCM has been described, appears to accompany LV takotsubo cardiomyopathy up to 25% of the time and be associated with worse LV function. See this article: and also this article:
There is no more vexing ECG mimic of acute STEMI than SCM because the underlying cellular pathophysiology is the same. It is unusual to make the diagnosis without an angiogram.