Editorial preface: I will be occasionally using the term occlusion myocardial infarction (OMI) to signify acute coronary occlusions which should be emergently reperfused (thrombolysis or percutaneous coronary intervention). Unfortunately, as OMI inherently does not have ‘false negatives’, I will still begrudgingly include the phrases ACS and STEMI as many are familiar with and still use these terms. For further explanation, read the OMI manifesto (1) or listen to its synopsis on EMCrit.
Answer: Trick question! The coronary angiogram finds no lesion. So what could it be?
First let’s breakdown the ECG:
Rate: 72/min
Rhythm: regular, wide complex, occasional P (seen in V1; not conducted by AV node).
This likely represents accelerated idioventricular rhythm (AIVR). Clues to suggest this is the presence of “taller left rabbit ear sign” which is highly specific for ventricular origin (2). AIVR is typically benign, self-limiting rhythm resulting from an ectopic ventricular pacemaker that exceeds sinus rate (2). The rhythm typically spontaneously resolves when the sinus rate exceeds the ventricular rate (2). In settings of low output cardiac states, atropine can be trialed to restore AV synchrony and atrial contribution to preload (2). AIVR has many different causes, including reperfusion after acute myocardial infarction, drug toxicity (such as digoxin), electrolyte abnormality, cardiomyopathy and others (2).
Axis: Left axis deviation
Intervals: Wide QRS, right bundle branch block with left anterior fascicular block (right bundle branch block + left axis deviation)
ST-T-Q: ST elevations in I, aVL, V1, V2, aVR with ST depressions in II, III, aVF
ST elevation in I, aVL, ST depression in inferior leads may represent a high lateral MI (3). A visual aid to remember these characteristic ECG findings has been termed the “South African Flag Sign” (4).
An example of the South African Flag Sign on the same ECG is shown below. This visual aid helps to point out that in a high lateral MI, the ST segments with derangements are most noticeable in the green segment of the flag: leads I, III, aVL, V2 (4).
Now getting back to our patient:
Although with ST elevation in aVR and V1, the ECG pattern of ST abnormalities did not completely fit a single acute coronary occlusion, the patient was taken to the cath lab as a “STEMI”. The angiogram demonstrated “clean coronaries”.
Take a look at the ventriculogram:
And the echocardiogram:
Both clips demonstrate diffuse hypokinesis most evident in the apical, anterior and septal regions. Thus, without angiographic evidence of obstruction, the patient was diagnosed with takotsubo cardiomyopathy.
The patient required intubation and was started on low dose dobutamine for inotropic support. After diuresis, the patient was successfully extubated and dobutamine was tapered. The remainder of the patient’s hospital course went well and the patient was discharged and remains alive and well.
What is Takotsubo cardiomyopathy?
Takotsubo cardiomyopathy, derived from the japanese words “tako tsubo” for the traditional ceramic octopus trap, is estimated to account for 2% of suspected ST elevation myocardial infarctions (STEMI) in the United States (6). The condition is most commonly found in postmenopausal women (6, 7), however in Japan it is more prevalent in men (8). Patients tend to present with symptoms similar to acute coronary syndrome (ACS), mainly with chest pain (68-75%), dyspnea (18-46%), and syncope (8%) (6, 7). Although classically, the diagnosis is associated with an emotional trigger (hence its other name, ‘broken heart syndrome’), such a trigger is only identified in 25% of cases. More commonly, it is associated with a physical stressor (e.g asthma exacerbation, endoscopy), and in a third of cases there is no identifiable trigger at all (6, 7). Nonetheless, the history is an important aspect in the diagnosis, as over half of patients with Takotsubo have psychological or neurological disorders, compared to only 25% of those with ACS (7).
Electrocardiographically, the condition may be mistaken as STEMI, as 82% of cases are associated with ST elevation. ST elevations most commonly are found in the precordial leads, however it may also be seen in inferior and lateral leads (6, 9). Other ECG findings may include new right bundle branch block, non-specific T wave changes, q waves, QTc prolongation, sinus tachycardia, or no abnormal findings (6, 7, 9). Interestingly, takotsubo has a lower incidence of ST depression (8%) than ACS (31%) (7).
Laboratory evaluation is not typically helpful in distinguishing between the two conditions, as troponin is commonly elevated (87%) in Takotsubo, although not to the degree typically seen in ACS (6, 7, 9). One clue in establishing the diagnosis is an elevated brain natriuretic peptide (82%), which typically exceeds the mean value in those with ACS (7).
Ultimately, the diagnosis is made by coronary angiography. As takotsubo by definition is not a result of acute plaque rupture and thrombosis, patients typically do not have significant coronary lesions that would explain the associated ECG changes or regional wall motion abnormalities. As such, 80% of patients with the condition are found to have normal coronary arteries, with the remainder having incidental atherosclerosis that is not consistent with the pattern of acute myocardial dysfunction (6).
Angiography or echocardiography can further clarify the diagnosis by detecting moderate to severe ventricular dysfunction, classically with apical hypokinesis or ballooning, however other variants including basal and mid-ventricular forms have been described (10, 11, 12). Importantly, the distribution of regional wall motion abnormalities typically does not correlate with a single coronary artery distribution, a key feature distinguishing this condition from OMI (8).
The patient presenting with history, exam, ECG abnormalities, and troponin elevation consistent with OMI provides a therapeutic dilemma for the emergency provider – especially one who does not have access to coronary angiography, as the decision to utilize fibrinolytic therapy will carry possible harm without any benefit. Thus, patients with features concerning for either condition should be expeditiously transferred to a center with angiography capabilities to further clinch the diagnosis and provide the appropriate therapy.
Stay tuned for an upcoming post about additional “ST mimickers”.
References:
- Meyer P, Weingart S, Smith S. The OMI Manifesto. April 2018. http://hqmeded-ecg.blogspot.com/2018/04/the-omi-manifesto.html
- Burns E. Accelerated Idioventricular Rhythm AIVR). Life In The Fast Lane. March 2019. https://litfl.com/accelerated-idioventricular-rhythm-aivr/
- Durant E, Singh A. Acute first diagonal artery occlusion: a characteristic pattern of ST elevation in noncontiguous leads. Am J Emerg Med. 2015 Sep;33(9):1326
- Littmann L. South African flag sign: a teaching tool for easier ECG recognition of high lateral infarct. Am J Emerg Med. 2016 Jan;34(1):107-9.
- Sharkey, et al. (2011). Takotsubo (stress) cardiomyopathy. American Heart Association.
- Gianni M, et al. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review.Eur Heart J. 2006;27(13):1523. Epub 2006 May 23.
- Templin C, Ghadri JR, Diekmann J, et al. Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med. 2015;373(10):929.
- Aizawa K, Suzuki T. Takotsubo cardiomyopathy: Japanese perspective. Heart Fail Clin 2013;9:243-247
- Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J 2008;155:408-417
- R.T. Hurst, J.W. Askew, C.S. Reuss, et al. Transient midventricular ballooning syndrome: a new variant. J Am Coll Cardiol, 48 (2006), pp. 579-583
- S.O. Van de Walle, S.A. Gevaert, P.J. Gheeraert, et al. Transient stress-induced cardiomyopathy with an “inverted Takotsubo” contractile pattern. Mayo Clin Proceed, 81 (2006), pp. 1499-1502
- D. Haghi, T. Papavassiliu, S. Fluchter, et al. Variant form of the acute apical ballooning syndrome (Takotsubo cardiomyopathy): observations on a novel entity. Heart, 92 (2006), pp. 392-394
Robby
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