International Journal of Academic Medicine

: 2018  |  Volume : 4  |  Issue : 1  |  Page : 78--81

Fatal reverse takotsubo cardiomyopathy in the emergency department

Kevin H Beier1, Zack M Olson1, Sara Hollis2,  
1 Department of Emergency Medicine, University of Tennessee College of Medicine/Saint Thomas Health, Knoxville, USA
2 University of Tennessee College of Medicine/Saint Thomas Health, Nashville, Tennessee, USA

Correspondence Address:
Dr. Kevin H Beier
1700 Medical Center Parkway, Murfreesboro, TN 37129


A healthy, 56-year-old female with a history of panic disorder presented to the emergency department (ED) with chest pressure. Physical examination and supporting data were within normal limits. Despite normal stress testing, she experienced recurrence of the chest pain the same day, and repeat ED assessment revealed isolated ST elevation and a troponin of 0.15. Following admission, serial troponin increased to 26.35 and subsequent coronary angiography revealed normal coronary arteries and a ventricular wall motion consistent with reverse takotsubo cardiomyopathy. The patient unexpectedly succumbed to a malignant arrhythmia on day 3. The following core competencies were addressed in this case report: Patient care, Medical knowledge, Patient education.

How to cite this article:
Beier KH, Olson ZM, Hollis S. Fatal reverse takotsubo cardiomyopathy in the emergency department.Int J Acad Med 2018;4:78-81

How to cite this URL:
Beier KH, Olson ZM, Hollis S. Fatal reverse takotsubo cardiomyopathy in the emergency department. Int J Acad Med [serial online] 2018 [cited 2022 Oct 2 ];4:78-81
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Full Text


Reverse takotsubo cardiomyopathy (RTCM) is uncommon and typically presents as chest pain and non- ST elevation myocardial infarction (NSTEMI) in patients with recent identifiable severe emotional or physiologic precipitating stressors.[1] The diagnosis of RTCM is usually made at the time of coronary angiography when patients diagnosed with NSTEMI are found to have normal or minimal coronary artery disease and characteristic ventriculography findings.[2] Echocardiography has also been utilized to establish the diagnosis, and bedside ultrasound has been described in the literature.[3] In this case, we present a case of fatal RTCM in a previously healthy woman with no clear identifiable precipitating factors, who had a normal emergency department (ED) evaluation and dynamic stress testing on the day of presentation. This case underlines the limitations of risk assessment in chest pain evaluations and shared decision-making with patients presenting with potentially life-threatening complaints.

[4],[5] It also highlights the importance of patient education and provides clear indications for ED return and precautions for risk management.[6]

 Case Report

A previously healthy, 56-year-old female presented to the ED with transient chest pressure lasting 10–15 min, bilateral arm discomfort, and symptoms that were similar but more severe and prolonged than anxiety attacks the patient had described experiencing in her past. The HEART Score (Systematic Coronary Risk Evaluation) for MACE calculation was 1, her symptoms had resolved without treatment, troponin was 0.00 ng/ml, and arrangements were made for direct transfer to an affiliated cardiologist's office for assessment and immediate dynamic cardiac stress testing. Precautions and guidance was given to return to the ED for recurrent pain. After undergoing normal stress testing without induced pain or electrocardiographic changes at the cardiology office, she was deemed safe for discharge and was released. While driving home from the cardiologist's office, her symptom complex returned, and she returned to our ED as instructed for reevaluation. Upon return, she was emotionally upset and repeat electrocardiographic testing revealed ST changes [Figure 1]. Pulmonary computed tomography angiography was performed to exclude thromboembolic disease and aortic disease and was unremarkable. She was treated with nitroglycerin, heparin, aspirin, and clopidogrel. Pain resolved and serial electrocardiograms revealed normalization of the noted ST changes. Repeat troponin assay was 0.15 ng/ml at the time of the second ED visit and peaked on day 2 at 26.35 ng/ml. Admission to the cardiology service was arranged, and the following day, the patient underwent coronary angiography demonstrating normal coronary arteries [Figure 2] and [Figure 3] and ventricular wall motion consistent with RTCM [Figure 4]. While waiting for cardiac magnetic resonance imaging on day 3 of her hospital admission, the patient suffered a cardiac arrest while sitting comfortably in her hospital room during morning rounds. Prolonged resuscitation was unsuccessful, and she died from RTCM-related malignant ventricular fibrillation.{Figure 1}{Figure 2}{Figure 3}{Figure 4}


Takotsubo cardiomyopathy (TCM), also called “stress-induced” cardiomyopathy or broken heart syndrome, is a rare cause of myocardial infarction.[1] It has a characteristic “apical ballooning” appearance on angiography that resembles Japanese fishing traps. RTCM is a variant of this disease where the base of the left ventricle balloons (as opposed to the apex of the ventricle). Both of these are felt to be variants with similar pathophysiology in that they occur in the absence of coronary artery disease and may cause severe cardiomyopathy and occasionally fatal cardiac dysrhythmias. RTCM is a less common variant, representing only 18% of cases.[1] The exact mechanism of this disease is not fully understood. It appears to be a neurohormonal phenomenon associated with catecholamine surge and subsequent toxicity to the myocardium.[7] Described precipitating causes have included everything from illicit drug use, financial loss, bereavement of spousal loss, intense physiologic or psychiatric stress, seizures, and (most recently) scuba diving.[8]

The pathophysiology underlying the catecholamine injury is not well understood. Two theories have been proposed: vascular dysfunction or vasospasm and direct catecholamine-induced toxicity. Vasospasm is strongly suspected in the TCM variant, with multifocal coronary vasospasm demonstrated in cases with apical ballooning during coronary angiography.[9]

The basal ballooning variant of TCM, or RTCM, typically presents at a younger age, mean 36 years, and may often have a clear strong emotional or physical stressful event as a precipitation factor.[10],[11] It is felt that adrenoreceptors are most concentrated in the apex of the heart in older women, which may be responsible for the predominance of TCM or the apical variant in postmenopausal women and RTCM in younger women in whom the adrenoreceptors are most concentrated at the base of the heart.[12]

There are clinical differences in presentations of TCM versus RTCM. Those patients with TCM tend to present with more dramatic clinical findings, with a higher frequency of cardiogenic shock and pulmonary edema likely related to the differences in regional wall motion abnormalities between the two variants.[10],[13]

The treatment for RTCM is supportive. Beta-blocker therapies to reduce catecholamine-induced cardiac toxicity have been suggested, although the effectiveness is uncertain. Angiotensin-converting enzyme inhibitors have retrospectively been shown to improve outcomes. Anticoagulation should be considered as 2% of cases are complicated by thrombus in the vicinity of the ventricular ballooning.[1]

The prognosis for these patients is overall good and primarily determined by the underlying stressor. However, long term, RTCM still carries a poor prognosis similar to other forms of cardiomyopathy. Approximately 7.1% of these patients will die in the acute setting. Approximately 5% of patients who survive the acute episode will die every year and 2% will have a stroke.[1] In addition, men are almost twice as likely to succumb to the illness as women while in the hospital (8.4% vs. 3.6%). This is likely due to the higher incidence of comorbidities and underlying illness in the male population.[14]


This case report describes an unusual presentation of RTCM in a patient who presented to an ED, underwent normal dynamic stress testing, and subsequently returned and succumbed to the previously undetected illness. This case underlines the limitations of risk assessment in low-risk chest pain evaluations and shared decision-making with patients presenting with potentially life-threatening complaints. It also highlights the importance of providing clear and specific indications for ED return and precautions for risk management.

Declaration of patient consent

The authors certify that they have sought appropriate patient consent documentation. However, patient consent was not feasible due to the patient's death and inability to identify any legally authorized representiative(s) despite multiple attempts.


The authors would like to acknowledge Sara Hollis for her help during the development of this article. Her guidance in the preparation of this manuscript is greatly appreciated.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, et al. Clinical features and outcomes of Takotsubo (Stress) cardiomyopathy. N Engl J Med 2015;373:929-38.
2Olechowski B, Corbett SJ, Shah BN. Reverse takotsubo cardiomyopathy: A clinical entity mimicking acute coronary syndrome. Postgrad Med J 2015;91:355-6.
3Butterfield M, Riguzzi C, Frenkel O, Nagdev A. Stimulant-related takotsubo cardiomyopathy. Am J Emerg Med 2015;33:476.e1-3.
4Paoloni R, Ibuowo R. A cohort study of chest pain patients discharged from the emergency department for early outpatient treadmill exercise stress testing. Emerg Med Australas 2013;25:416-21.
5Backus BE, Six AJ, Kelder JC, Bosschaert MA, Mast EG, Mosterd A, et al. Aprospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol 2013;168:2153-8.
6Ackermann S, Heierle A, Bingisser MB, Hertwig R, Padiyath R, Nickel CH, et al. Discharge communication in patients presenting to the emergency department with chest pain: Defining the ideal content. Health Commun 2016;31:557-65.
7Lindsay J, Paixao A, Chao T, Pichard AD. Pathogenesis of the Takotsubo syndrome: A unifying hypothesis. Am J Cardiol 2010;106:1360-3.
8Baber A, Nair SU, Duggal S, Bhatti S, Sundlof DW. Stress cardiomyopathy caused by diving: Case report and Review of the literature. J Emerg Med 2016;50:277-80.
9Ako J, Sudhir K, Farouque HM, Honda Y, Fitzgerald PJ. Transient left ventricular dysfunction under severe stress: Brain-heart relationship revisited. Am J Med 2006;119:10-7.
10Ramaraj R, Movahed MR. Reverse or inverted Takotsubo cardiomyopathy (reverse left ventricular apical ballooning syndrome) presents at a younger age compared with the mid or apical variant and is always associated with triggering stress. Congest Heart Fail 2010;16:284-6.
11Song BG, Chun WJ, Park YH, Kang GH, Oh J, Lee SC, et al. The clinical characteristics, laboratory parameters, electrocardiographic, and echocardiographic findings of reverse or inverted Takotsubo cardiomyopathy: Comparison with mid or apical variant. Clin Cardiol 2011;34:693-9.
12Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy – A novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008;5:22-9.
13Park JH, Kang SJ, Song JK, Kim HK, Lim CM, Kang DH, et al. Left ventricular apical ballooning due to severe physical stress in patients admitted to the medical ICU. Chest 2005;128:296-302.
14Brinjikji W, El-Sayed AM, Salka S. In-hospital mortality among patients with Takotsubo cardiomyopathy: A study of the National Inpatient Sample 2008 to 2009. Am Heart J 2012;164:215-21.