Takotsubo Cardiomyopathy

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Takotsubo cardiomyopathy (TCM) is a transient cardiac syndrome that involves left ventricular apical akinesis and mimics acute coronary syndrome (ACS). It was first described in Japan in 1990 by Sato et al. Patients often present with chest pain, have ST-segment elevation on electrocardiography (ECG), and have elevated cardiac enzyme levels consistent with myocardial infarction (MI). (See the images below.) ^{[1, 2]} However, when the patient undergoes cardiac angiography, left ventricular (LV) apical ballooning is present, and there is no significant coronary artery stenosis. (See Presentation and Workup.) ^[3]

The Japanese word takotsubo translates to “octopus pot,” resembling the shape of the left ventricle during systole on imaging studies. Although the exact etiology of TCM is still unknown, the syndrome appears to be triggered by a significant emotional or physical stressor. ^[4] (See Etiology.)

The modified Mayo Clinic criteria for diagnosis of TCM ^[5] can be applied to a patient at the time of presentation. The diagnosis requires the presence of all four of the following (see Workup):

Normal myocardium utilizes approximately 90% of its energy from fatty acid metabolism at rest and with aerobic activity. During ischemia, this pathway is suppressed, and glucose is largely utilized instead, which results in impaired cardiac function. Patients with TCM are found to shift toward the glucose pathway despite relatively normal myocardial perfusion and lack of ischemia in LV segments. ^[6]

The most commonly discussed possible mechanism for TCM is stress-induced catecholamine release, with toxicity to and subsequent stunning of the myocardium. ^[4]  Endomyocardial biopsy of patients with TCM demonstrates reversible focal myocytolysis, mononuclear infiltrates, and contraction band necrosis. The sympathetic/catecholamine theory is gaining momentum, because TCM was induced in rats exposed to physical stress and, in some instances, was prevented by pretreatment with an alpha blocker or beta blocker. Other evidence for this theory has been demonstrated through myocardial imaging studies using catecholamine analogues that evaluated cardiac sympathetic activity.

Some authors have proposed a unifying hypothesis stating that in susceptible individuals, notably women, neurohormonal stimulation results in acute myocardial dysfunction, as reflected by the characteristic LV wall-motion abnormality of TCM. Whether this is triggered by multivessel spasm, thrombosis, epicardial vessel occlusion, or direct myocardial toxicity remains to be seen. These authors point out that the wall-motion abnormality of TCM can be seen in other conditions, including those with certain left anterior descending (LAD) lesions, ^[7]  making wall motion alone insufficient for the diagnosis of TCM. ^[8]

Cases of TCM have been reported in the literature following cocaine, methamphetamine, and excessive phenylephrine use. ^{[9, 6]}  Exercise stress testing, which is known to cause increased levels of catecholamines, has resulted in false positives attributable to TCM. ^[10]  Studies have found that patients with TCM have, by a statistically significant margin, higher levels of serum catecholamines (norepinephrine, epinephrine, and dopamine) than do patients with MI. ^[11]  The apical portions of the LV have the highest concentration of sympathetic innervation found in the heart and may explain why excess catecholamines seem to selectively affect its function. ^[6]

The exact etiology of TCM is still unknown, but several theories have been proposed and are being investigated. ^[12] These include the following ^{[9, 13]} :

A significant emotional or physical stressor or neurologic injury typically precedes the development of the TCM. ^[4] Stressors include the following:

TCM has also been reported after near-drowning episodes. ^[14]

Seizures may also trigger TCM, but it is rare for TCM to result in sudden unexpected death in epilepsy (SUDEP). ^[15]

In a systematic review of 104 cases of TCM (1965-2013), investigators noted that young patients with TCM were more likely to be female and physical stress was more likely to exacerbate TCM than mental stress was. ^{[16, 17]}  The clinical presentation of TCM in this patient population was similar to that of other cardiac diseases (eg, coronary heart disease) but could be differentiated from them by means of echocardiography in conjunction with ventriculography. ^[16]

Similarly, the International Takotsubo Registry reported that patients with TCM, as compared with ACS patients, were more likely to be female (89.8%) and that physical triggers were more common than emotional triggers (36% vs 27.7%), though more than one quarter (28.5%) had no clear triggers. ^[17] Patients with TCM also had higher rates of neurologic or psychiatric disorders and a significantly lower LV ejection fraction (LVEF). The two groups (TCM and ACS) had similar rates of severe inpatient complications (eg, shock, death), and independent predictors of such complications included physical triggers, acute neurologic/psychiatric diseases, elevated troponin levels, and low LVEF. ^[17]

Studies reported that 1.7-2.2% of patients who had suspected ACS were subsequently diagnosed with TCM. ^{[18, 19]} Patients are typically Asian or Caucasian. In a literature review of cases in which race was reported, 57.2% of patients were Asian, 40% were Caucasian, and 2.8% were other races. ^[20]

Literature reviews report a mean patient age of 67 years, though cases of TCM have occurred in children and young adults ^{[9, 11]} Nearly 90% of reported cases involve postmenopausal women. ^[21]

The prognosis in TCM is typically excellent, with nearly 95% of patients experiencing complete recovery within 4-8 weeks. ^{[22, 23]} A study by Singh et al indicated that the annual recurrence rate is approximately 1.5% but that the frequency of ongoing symptoms is greater. ^[24] Estimates of mortality have ranged from 1% to 3.2%. ^{[20, 21]}

Complications occur in 20% of TCM cases, particularly in the early stage, ^[2] and include the following:

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Khallafi H, Chacko V, Varveralis N, Elmi F. “Broken heart syndrome”: catecholamine surge or aborted myocardial infarction?. J Invasive Cardiol. 2008 Jan. 20(1):E9-13. [Medline].

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Finsterer J, Bersano A. Seizure-triggered Takotsubo syndrome rarely causes SUDEP. Seizure. 2015 Sep. 31:84-7. [Medline].

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Templin C, Ghadri JR, Diekmann J, et al. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy. N Engl J Med. 2015 Sep 3. 373 (10):929-38. [Medline].

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Sharkey SW, Lesser JR, Garberich RF, Pink VR, Maron MS, Maron BJ. Comparison of Circadian Rhythm Patterns in Tako-tsubo Cardiomyopathy Versus ST-Segment Elevation Myocardial Infarction. Am J Cardiol. 2012 May 29. [Medline].

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Eric B Tomich, DO Staff Physician, Department of Emergency Medicine, Brooke Army Medical Center

Eric B Tomich, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Emily Luerssen, MD Assistant Program Director, Department of Emergency Medicine, Madigan Army Medical Center

Emily Luerssen, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents’ Association

Disclosure: Nothing to disclose.

Christopher S Kang, MD, FACEP, FAWM Attending Physician, Department of Emergency Medicine, Madigan Army Medical Center; Clinical Assistant Professor, Division of Emergency Medicine, University of Washington School of Medicine; Adjunct Assistant Professor, Uniformed Services University of the Health Sciences; Staff, Providence St Peter’s Hospital

Christopher S Kang, MD, FACEP, FAWM is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, Washington State Medical Association, Wilderness Medical Society, Society of US Army Flight Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Department of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, National Association of EMS Physicians

Disclosure: Medical Director for: SironaHealth.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Takotsubo Cardiomyopathy

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