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Takotsubo Cardiomyopathy

  • Author: Eric B Tomich, DO; Chief Editor: Erik D Schraga, MD  more...
 
Updated: Dec 08, 2015
 

Background

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

Electrocardiogram of a patient with takotsubo card Electrocardiogram of a patient with takotsubo cardiomyopathy demonstrating ST-segment elevation in anterior and inferior leads.
Electrocardiogram from the same patient examined i Electrocardiogram from the same patient examined in the previous ECG, obtained several days after initial presentation. This demonstrates resolution of ST-segment elevation, and now with diffuse T-wave inversion and poor R-wave progression.

The Japanese word takotsubo translates to "octopus pot," resembling the shape of the left ventricle during systole on imaging studies. Although the exact etiology 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 and must contain all 4 aspects (see Workup):

  • Transient hypokinesis, dyskinesis, or akinesis of the left ventricular midsegments, with or without apical involvement; the regional wall-motion abnormalities extend beyond a single epicardial vascular distribution, and a stressful trigger is often, but not always, present
  • Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture
  • New electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin level
  • Absence of pheochromocytoma or myocarditis [5]
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Etiology

The exact etiology of takotsubo cardiomyopathy (TCM) is still unknown, but several theories have been proposed and are being investigated.[6] These include multivessel coronary artery spasm, impaired cardiac microvascular function, impaired myocardial fatty acid metabolism, acute coronary syndrome with reperfusion injury, and endogenous catecholamine-induced myocardial stunning and microinfarction.[7, 8]

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 instead glucose is largely utilized, resulting 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 left ventricular segments.[9]

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 left ventricular wall-motion abnormality of TCM. Whether triggered by multivessel spasm, thrombosis, epicardial vessel occlusion, or direct myocardial toxicity remains to be seen. They point out that the wall-motion abnormality of TCM can be seen in other conditions, including those with certain left anterior descending (LAD) lesions,[10] making wall motion alone insufficient for the diagnosis of TCM.[11]

Cases of TCM have been reported in the literature following cocaine, methamphetamine, and excessive phenylephrine use.[7, 9] Exercise stress testing, which is known to cause increased levels of catecholamines, has resulted in false positives attributable to TCM.[12] 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 myocardial infarctions.[13] The apical portions of the left ventricle have the highest concentration of sympathetic innervation found in the heart and may explain why excess catecholamines seem to selectively affect its function.[9]

Risk factors

A significant emotional or physical stressor or neurologic injury typically precedes the development of the TCM.[4] Stressors include learning of a death of a loved one; bad financial news; legal problems; natural disasters; motor vehicle collisions; exacerbation of a chronic medical illness; a newly diagnosed, significant medical condition; surgery; an intensive care unit stay; and the use of or withdrawal from illicit drugs. 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 rather than mental stress was more likely to exacerbate TCM.[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 with the use of echocardiography in conjunction with ventriculography.[16]

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

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Epidemiology

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

Literature reviews report a mean patient age of 67 years, although cases of TCM have occurred in children and young adults[7, 13] Nearly 90% of reported cases involve postmenopausal women.[21]

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Prognosis

The prognosis in takotsubo cardiomyopathy (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 rates have ranged from 1-3.2%.[20, 21]

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

  • Left heart failure with and without pulmonary edema
  • Cardiogenic shock
  • Left ventricular outflow obstruction
  • Mitral regurgitation
  • Ventricular arrhythmias
  • Left ventricular mural thrombus formation
  • Left ventricular free-wall rupture
  • Death [25, 26]
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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Specialty Editor Board

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.

Chief Editor

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

Disclosure: Nothing to disclose.

Additional Contributors

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.

References
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Electrocardiogram of a patient with takotsubo cardiomyopathy demonstrating ST-segment elevation in anterior and inferior leads.
Electrocardiogram from the same patient examined in the previous ECG, obtained several days after initial presentation. This demonstrates resolution of ST-segment elevation, and now with diffuse T-wave inversion and poor R-wave progression.
Coronary angiogram of a patient with takotsubo cardiomyopathy demonstrating normal coronary arteries.
Coronary angiogram of a patient with takotsubo cardiomyopathy demonstrating normal coronary arteries.
Ventriculogram during systole in a patient with takotsubo cardiomyopathy demonstrating apical akinesis.
Ventriculogram during diastole in a patient with takotsubo cardiomyopathy.
Echocardiogram of a patient with takotsubo cardiomyopathy during diastole several days after presenting to the emergency department.
Echocardiogram of a patient with takotsubo cardiomyopathy during systole, which demonstrates apical akinesis. Ejection fraction is 40%.
Echocardiogram of a patient with takotsubo cardiomyopathy during systole, nearly 2 months after presenting to the emergency department. Note the improved contractility of the apex. Ejection fraction increased from 40% to 65%.
Echocardiogram of a patient with takotsubo cardiomyopathy during diastole, approximately 2 months after presenting to the emergency department.
Echocardiogram focused on left ventricle of a patient with takotsubo cardiomyopathy during diastole.
Echocardiogram focusing on left ventricle of a patient with takotsubo cardiomyopathy during systole. Note apical akinesis.
Echocardiogram focusing on left ventricle of a patient with takotsubo cardiomyopathy during systole, approximately 2 months after presenting to the emergency department. Note improved apical contraction.
Echocardiogram focusing on left ventricle of a patient with takotsubo cardiomyopathy during diastole, approximately 2 months after presenting to the emergency department.
 
 
 
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