Takotsubo cardiomyopathy

Other names: Transient apical ballooning syndrome, apical ballooning cardiomyopathy, Gebrochenes-Herz syndrome,[1] acute stress-induced cardiomyopathy, broken-heart syndrome, takotsubo syndrome[2]
(A) Drawing of takotsubo cardiomyopathy (B) Compared to a normal heart
Specialty| Cardiology
Symptoms| Chest pain, shortness of breath, brief loss of consciousness[3][1]
Complications| Heart failure, arrhythmia, stroke, sudden cardiac death[1]
Usual onset| Sudden[3]
Types| Primary (emotional), secondary (physical factors)[1]
Causes| Significant stress (physical or emotional)[3]
Diagnostic method| Cardiac catheterization[3]
Differential diagnosis| Heart attack, coronary artery spasm, myocarditis, esophageal spasm[3][1]
Treatment| Supportive care[3]
Frequency| 2 to 7% of heart attacks[4][3]
Deaths| 4% risk of death[3]

Takotsubo cardiomyopathy, also known as stress cardiomyopathy, is a type of heart disease in which there is a sudden temporary weakening of part of the heart muscule without blockage of the arteries to the heart.[1][3] Symptoms may include chest pain, shortness of breath, and brief loss of consciousness.[3][1] Complications may include heart failure, arrhythmia, stroke, and sudden cardiac death.[1]

It usually occurs as a result of significant stress, either physical or emotional.[3] This may include death of a loved one, divorce, public speaking, assault, chemotherapy, pheochromocytoma, and vomiting.[3][4] The mechanism is believed to involve a surge of catecholamines, including adrenaline and norepinephrine, which increases the work of and decreases blood flow to the heart.[5] Diagnosis is based on cardiac catheterization finding unblocked coronary arteries together with ballooning of the left ventricle.[3] ECG findings may be similar to a myocardial infarction (MI).[3] Troponin elevation may occur, though is generally low.[1]

Initial management involves supportive care.[3] There is no evidence that treatment can prevent recurrence.[6] Although the heart generally returns to normal over days to week, about 4% of people die during the initial episode, and there is a 12% risk of recurrence.[3] Cases due to physical illness rather than emotional stress are associated with worse outcomes.[1]

Takotsubo cardiomyopathy occurs worldwide.[6] It occurs more commonly in women after menopause.[6] It is thought to be responsible for about 2 to 7% of what are initially though to be heart attacks.[4][3] It was first described in 1990 by Sato.[3] The name comes from the Japanese word takotsubo meaning "octopus trap", as the heart takes the shape of an octopus trap.[7] It has colloquially been called "broken heart syndrome".[3][2]

## Contents

* 1 Signs and symptoms
* 2 Risk factors
* 2.1 Stress
* 2.2 Sex
* 2.3 Genetics
* 2.4 Hormones
* 3 Pathophysiology
* 4 Diagnosis
* 5 Treatment
* 5.1 Heart failure
* 5.2 Blood pressure
* 6 Prognosis
* 7 Epidemiology
* 8 History
* 9 Popular culture
* 10 References
* 11 External links

## Signs and symptoms[edit | edit source]

The typical presentation of takotsubo cardiomyopathy is chest pain with or without shortness of breath and associated electrocardiogram (ECG) changes mimicking a myocardial infarction of the anterior wall. During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted. It is the hallmark bulging-out of the apex of the heart with preserved function of the base that earned the syndrome its name takotsubo "octopus trap", in Japan, where it was first described.[8]

Stress is the main factor in takotsubo cardiomyopathy, with more than 85% of cases set in motion by either a physically or emotionally stressful event that prefaces the start of symptoms.[9] Examples of emotional stressors include grief from the death of a loved one, fear of public speaking, arguing with a spouse, relationship disagreements, betrayal, and financial problems.[9] Acute asthma, surgery, chemotherapy, and stroke are examples of physical stressors.[9] In a few cases, the stress may be a happy event, such as a wedding, winning a jackpot, a sporting triumph, or a birthday.[10][11]

## Risk factors[edit | edit source]

### Stress[edit | edit source]

Although there have been documented cases of TTS without a triggering stressor, it is widely recognized that TTS is preceded by a stressful event.[12] Case series looking at large groups of patients report that some patients develop takotsubo cardiomyopathy after an emotional stress. Some patients have a preceding clinical stressor (such as a brain injury, asthma attack or exacerbation of a chronic illness) and research has indicated that this type of stress may even occur more often than emotionally stressful triggers.[13] Roughly one-third of patients have no preceding stressful event.[14] A 2009 large case series from Europe found that takotsubo cardiomyopathy was slightly more frequent during the winter season. This may be related to two possible/suspected pathophysiological causes: coronary spasms of microvessels, which are more prevalent in cold weather, and viral infections – such as Parvovirus B19 – which occur more frequently during the winter.[15]

### Sex[edit | edit source]

Women, specifically postmenopausal women, are at greatest risk of developing TTS.[12] This has led some researchers to theorize about the possible protective effects of estrogen in preventing TTS.[16][4]

### Genetics[edit | edit source]

It is currently being investigated if certain genetic traits associated with catecholamine receptors found on cardiac muscle cells play a role in the development of TTS.[16] There is limited evidence tying TTS directly to a specific genetic expression or mutation, however there is currently a widely held hypothesis supporting the idea of the interaction between environmental factors and the interplay of genetic predisposition leading to the susceptibility to microvascular alterations that contribute to the TTS disease process.[4]

### Hormones[edit | edit source]

Certain endocrine diseases including pheochromocytoma and thyrotoxicosis have been identified as potential risk factors for TTS.[17][18] The relationship between thyroid function and stress cardiomyopathy is marked by a dual phenotype, where both impending primary hyperthyroidism and a high set point of thyroid homeostasis (encoding type 2 allostatic load) are common phenomena.[19] A multi-centre observation study found normal thyroid function to be the exception rather than the rule in TTS.[19] Especially hyperthyroidism is highly prevalent in takotsubo cardiomyopathy, and it seems to predict a poor prognosis in terms of complications and mortality.[20]

## Pathophysiology[edit | edit source]

The cause of takotsubo cardiomyopathy is not fully understood, but several mechanisms have been proposed.[21] It is well documented that elevated catecholamine levels have been implicated in the vast majority of TTS cases. Theories suggest a link between brain activation of stress-related biochemicals and the effects these chemicals have on areas of the heart. More specifically, adrenal stimulation by the sympathetic nervous system has been noted in cases ranging from physical events such as ischemic stroke, to emotional events such as depression or loss of a loved-one.[22] How these increased levels of catecholamines act in the body to produce the changes seen with TTS is not clearly understood.[4][6][12][16] Research supports the widely-held understanding that microvascular dysfunction and coronary vasospasm caused by a rapid influx of catecholamines to cardiac myocytes results in apical stunning and transient cardiomyopathy.[4][6][12]

1. Microvascular dysfunction/Transient vasospasm: Some of the original researchers of takotsubo suggested that multiple simultaneous spasms of coronary arteries could cause enough loss of blood flow to cause transient stunning of the myocardium.[23] Other researchers have shown that vasospasm is much less common than initially thought.[24][25][26] It has been noted that when there are vasospasms, even in multiple arteries, that they do not correlate with the areas of myocardium that are not contracting.[27] However, the idea of coronary artery vasospasm is still believed to contribute to the TTS disease process. The theory of vasospasm is not easily separated from that of microvascular dysfunction and in fact, microvascular dysfunction could explain vasospasticity.[12] Impaired microvascular function is seen in a vast majority, if not all, of patients with TTS and is currently one of the most supported theories.[4][16] Most of the dysfunction occurs as a result of abnormalities within the endothelial linings of blood vessels supplying the heart.[16] In TTS, these highly sensitive interior linings of the vessels have reduced functionality which create dysregulation of vascular tone and predispose the individual to vasoconstriction. When the increased vasoconstrictor effects of catecholamines are introduced, the result is acute cardiac ischemia.[4][12][16]
2. Catecholamine-induced myocyte injury: It has been suggested that the response to catecholamines (such as epinephrine and norepinephrine, released in response to stress) leads to heart muscle dysfunction that contributes to takotsubo cardiomyopathy.[12] The effects of this toxicity can be greater in those with a predisposition to anxiety or panic disorders.[6] Delivery of catecholamines (epinephrine, norepinephrine) via circulating blood and through direct delivery from cardiac nerves is increased by the stimulation of stress control centers of the brain.[6] During an emotionally or physically stressful event, brain centers initiate the sympathetic nervous pathways and increase myocardial activity. Excessive catecholamine stimulation has a toxic effect on cardiac muscle cells which creates necrosis of the contractile units of cells similarly seen during acute myocardial infarction.[4][12] The increased workload of cardiac muscle created by the stimulation of catecholamines, increases the need for more blood and oxygen to these muscles to sustain function. When these demands are unable to be met, the heart is starved of blood and oxygen and begins to die.[6] Included in the cytotoxic sequela of catecholamine toxicity is the molecular transformation of the cardiac myocyte to produce apical stunning.
3. Mid-ventricular obstruction, apical stunning: It has been suggested that a mid-ventricular wall thickening with outflow obstruction is important in the pathophysiology.[28] This stunning is largely seen as a protective effect produced by the flood of excess catecholamines into the cardiac muscle cell.[12] Overstimulation of catecholamine receptors create physiological changes in the receptor which has an inverse effect on cardiac cellular function. Termed 'cellular-trafficking', this property of the cardiac muscle cell is actually a molecular transformation of the cell to produce a down-regulation of catecolaminergic sensitivity.[6] This means that in the presence of excess epinephrine, a normal cardiac contraction is inhibited in an effort to reduce energy demands, prevent hyperactivity and spare the integrity of the cell.[6][12] Further bolstering this idea is the concentration of these kinds of receptors in the heart. Higher concentrations of the receptor effected to produce cardiac stunning are found closer to the apex of the ventricle. This is what creates the classic ballooning effect of the ventricle.[6][12]

It is likely that there are multiple factors at play that could include some amount of vasospasm and failure of the microvasculature. These factors can overlap and create the complex sequela leading to ischemia and left ventricle contraction abnormality.[12] For instance, estrogen, which confers protection to women by improving blood flow to heart muscle, is one biochemical pathway implicated in the TTS disease process. Once this protective mechanism is reduced through the decreased production of estrogen after menopause, there is thought to be an increase in endothelial dysfunction predisposing an individual to vasoconstriction and cardiac ischemia.[6] An inciting stressful event elicits the release of catecholamines into the blood stream to create increased heart muscle activity and metabolism. This leads to further cardiac microvascular endothelial dysfunction through oxidative stress, alteration of ion-mediated channels, and electrolyte disturbances which ultimately alter myocardial cell membrane permeability and dysfunction.[4][12] Coupled with direct heart muscle toxicity, this crescendo of factors are implicated in the ballooning and heart failure characteristically seen in TTS.[4][6][12][16]

A 2019 case involved a 60-year-old woman presenting with Takotsubo cardiomyopathy due to over-consumption of wasabi, mistaking it for avocado.[29]

## Diagnosis[edit | edit source]

Echocardiogram showing the effects of the disease[30]

Several well regarded institutions of medical research have produced clinical criteria useful in diagnosing TTS. One of the first sets of guidelines was initially published in 2004 and again in 2008 by the Mayo Clinic. Other research institutions proposing diagnostic criteria include the Japanese Takotsubo Cardiomyopathy Study Group, Gothenburg University, Johns Hopkins University, the Takotsubo Italian Network and the Heart Failure Associates TTS Taskforce of the European Society of Cardiology.[31] All of the research institutions agree on at least two main criteria needed to accurately diagnose TTS: 1) transient left ventricular wall motion abnormality and 2) the absence of a condition obviously explaining this wall motion abnormality (coronary artery lesion, hypoperfusion, myocarditis, toxicity, etc.). Other commonly acknowledged criteria necessary for diagnosis include characteristic EKG changes and mild to modest elevation in cardiac troponin.[31]

Transient apical ballooning syndrome or takotsubo cardiomyopathy is found in 1.7–2.2% of patients presenting with acute coronary syndrome.[15] While the original case studies reported on individuals in Japan, takotsubo cardiomyopathy has been noted more recently in the United States and Western Europe. It is likely that the syndrome previously went undiagnosed before it was described in detail in the Japanese literature. Evaluation of individuals with takotsubo cardiomyopathy typically includes a coronary angiogram to rule out occlusion of the left anterior descending artery, which will not reveal any significant blockages that would cause the left ventricular dysfunction. Provided that the individual survives their initial presentation, the left ventricular function improves within two months.[citation needed]

The diagnosis of takotsubo cardiomyopathy may be difficult upon presentation. The ECG findings often are confused with those found during an acute anterior wall myocardial infarction.[32][33] It classically mimics ST-segment elevation myocardial infarction, and is characterised by acute onset of transient ventricular apical wall motion abnormalities (ballooning) accompanied by chest pain, shortness of breath, ST-segment elevation, T-wave inversion or QT-interval prolongation on ECG. Cardiac enzymes are usually negative and are moderate at worst, and cardiac catheterization usually shows absence of significant coronary artery disease.[15]

The diagnosis is made by the pathognomonic wall motion abnormalities, in which the base of the left ventricle is contracting normally or is hyperkinetic while the remainder of the left ventricle is akinetic or dyskinetic. This is accompanied by the lack of significant coronary artery disease that would explain the wall motion abnormalities. Although apical ballooning has been described classically as the angiographic manifestation of takotsubo, it has been shown that left ventricular dysfunction in this syndrome includes not only the classic apical ballooning, but also different angiographic morphologies such as mid-ventricular ballooning and, rarely, local ballooning of other segments.[15][34][35][36][37]

The ballooning patterns were classified by Shimizu et al. as takotsubo type for apical akinesia and basal hyperkinesia, reverse takotsubo for basal akinesia and apical hyperkinesia, mid-ventricular type for mid-ventricular ballooning accompanied by basal and apical hyperkinesia, and localised type for any other segmental left ventricular ballooning with clinical characteristics of takotsubo-like left ventricular dysfunction.[35]

In short, the main criteria for the diagnosis of takotsubo cardiomyopathy are: the patient must have experienced a stressor before the symptoms began to arise; the patient's ECG reading must show abnormalities from a normal heart; the patient must not show signs of coronary blockage or other common causes of heart troubles; the levels of cardiac enzymes in the heart must be elevated or irregular; and the patient must recover complete contraction and be functioning normally in a short amount of time.[38]

* a)Diastolic phase b) systolic phase shows apical ballooning with sparing of apex indicative of takotsubo cardiomyopathy

* Left ventriculography during systole showing apical ballooning akinesis with basal hyperkinesis in a characteristic takotsubo ventricle

* Left ventriculogram during systole displaying the characteristic apical ballooning with apical motionlessness in a patient with takotsubo cardiomyopathy

* (A) Echocardiogram showing dilatation of the left ventricle in the acute phase (B) Resolution of left ventricular function on repeat echocardiogram six days later

* ECG showing sinus tachycardia and non-specific ST and T wave changes from a person with confirmed takotsubo cardiomyopathy

## Treatment[edit | edit source]

The treatment of takotsubo cardiomyopathy is generally supportive in nature, for it is considered a transient disorder.[39] Treatment is dependent on whether patients experience heart failure or acute hypotension and shock. In many individuals, left ventricular function normalizes within two months.[40][41] Aspirin and other heart drugs also appear to help in the treatment of this disease, even in extreme cases.[42][43] After the patient has been diagnosed, and myocardial infarction (heart attack) ruled out, the aspirin regimen may be discontinued, and treatment becomes that of supporting the patient.[44] There is currently no internationally agreed protocol for treatment of this condition.[citation needed]

While medical treatments are important to address the acute symptoms of takotsubo cardiomyopathy, further treatment includes lifestyle changes.[45] It is important that the individual stay physically healthy while learning and maintaining methods to manage stress, and to cope with future difficult situations.[citation needed]

Although the symptoms of takotsubo cardiomyopathy usually go away on their own and the condition completely resolves itself within a few weeks, some serious short and long-term complications can happen that must be treated.[46] These most commonly include congestive heart failure and very low blood pressure, and less commonly include blood clotting in the apex of the left ventricle, irregular heart beat, and tearing of the heart wall.[46]

### Heart failure[edit | edit source]

For patients in acute heart failure, ACE inhibitors, angiotensin receptor blockers, and beta blockers, are considered mainstays of heart failure treatment. But use of beta blockers specifically for takotsubo cardiomyopathy is controversial, because they may confer no benefit.[39]

### Blood pressure[edit | edit source]

For people with cardiogenic shock, medical treatment is based on whether a left ventricular outflow tract (LVOT) obstruction is present.[47] Therefore, early echocardiography is necessary to determine proper management. For those with obstructed LVOTs inotropic agents should not be used, but instead should be managed like patients with hypertrophic cardiomyopathy, (e.g. phenylephrine and fluid resuscitation).[39] For cases in which the LVOT is not obstructed, inotropic therapy (e.g. dobutamine and dopamine) may be used, but with the consideration that takotsubo is caused by excess catecholamines.[47]

Furthermore, mechanical circulatory support[48] (MCS) with an intra-aortic balloon pump (IABP) is well-established as supportive treatment.[47][49]

## Prognosis[edit | edit source]

Despite the grave initial presentation in some of the patients, most of the patients survive the initial acute event, with a very low rate of in-hospital mortality or complications. Once a patient has recovered from the acute stage of the syndrome, they can expect a favorable outcome and the long-term prognosis is excellent for most.[15][8][34] Even when ventricular systolic function is heavily compromised at presentation, it typically improves within the first few days and normalises within the first few months.[15][24][25][26] Although infrequent, recurrence of the syndrome has been reported and seems to be associated with the nature of the trigger.[15][14] Stress cardiomyopathy is now a well-recognized cause of acute congestive heart failure, lethal abnormal heart rhythms, and rupture of the heart wall.[7]

## Epidemiology[edit | edit source]

Takotsubo cardiomyopathy is common, affecting between 1.2% and 2.2% of people in Japan and 2% to 3% in Western countries who suffer a myocardial infarction. It also affects far more women than men with 90% of cases being women, most postmenopausal. Scientists believe one reason is that estrogen causes the release of catecholamine and glucocorticoid in response to mental stress. It is not likely for the same recovered patient to experience the syndrome twice, although it has happened in rare cases.[50] The average ages at onset are between 58 and 75 years. Less than 3% of cases occurred in patients under age 50.[51]

## History[edit | edit source]

Japanese octopus traps after which this disease is named[7]

Rees wrote in 1967 that the death of a close relative increases the risk of dying within one year by a factor of seven.[52]

Engel wrote about sudden and rapid death during psychological stress in 1971 and itemized 8 causation categories: (1) on the impact of the collapse or death of a close person; (2) during acute grief; (3) on threat of loss of a close person; (4) during mourning or on an anniversary; (5) on loss of status or self-esteem; (6) personal danger or threat of injury; (7) after the danger is over; (8) reunion, triumph, or happy ending. He proposed these events provoke neurovegetative responses, involving both the flight-fight and conservation-withdrawal systems, conducive to lethal cardiac events, particularly in individuals with preexisting cardiovascular disease.[53]

Although the first scientific description of takotsubo cardiomyopathy was not until the 1990s, Cebelin and Hirsch wrote about human stress cardiomyopathy in 1980. The two looked at homicidal assaults that had happened in Cuyahoga County, Ohio, the past 30 years, specifically those with autopsies who had no internal injury, but had died of physical assault. They found that 11 of 15 had myofibrillar degeneration similar to animal stress studies. In the end, they concluded their data supported "the theory of catecholamine mediation of these myocardial changes in man and of the lethal potential of stress through its effect on the heart".[54]

The first studied case of takotsubo cardiomyopathy was in Japan in 1991 by Sato et al. More cases of the syndrome appeared in Japan within the next decade, although western medicine had still not acknowledged it. The syndrome finally occurred in 1997 when Pavin, et al., wrote about two cases of "reversible LV dysfunction precipitated by acute emotional stress". The western world had not heard of such a thing at the time, as it was incredibly rare and often misdiagnosed. The Japanese at last reported about the syndrome to the west in 2001 under the name "transient LV apical ballooning" though at this point the west had already heard of numerous cases. The syndrome reached international audiences through the media in 2005 when the New England Journal of Medicine wrote about the syndrome.[55]

## Popular culture[edit | edit source]

The name and title track of the 2021 album Tako Tsubo by French band L'Impératrice refers to the intense emotional stress which may provoke this syndrome.

## References[edit | edit source]

1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 Ahmad, SA; Brito, D; Khalid, N; Ibrahim, MA (January 2022). "Takotsubo Cardiomyopathy". PMID 28613549. `{{cite journal}}`: Cite journal requires `|journal=` (help)
2. ↑ 2.0 2.1 "Takotsubo Cardiomyopathy". Archived from the original on 16 June 2022. Retrieved 21 July 2022.
3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 Dawson, DK (January 2018). "Acute stress-induced (takotsubo) cardiomyopathy". Heart (British Cardiac Society). 104 (2): 96–102. doi:10.1136/heartjnl-2017-311579. PMID 28824005.
4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 Ghadri, Jelena-Rima; Wittstein, Ilan Shor; Prasad, Abhiram; Sharkey, Scott; Dote, Keigo; Akashi, Yoshihiro John; Cammann, Victoria Lucia; Crea, Filippo; Galiuto, Leonarda; Desmet, Walter; Yoshida, Tetsuro (2018-05-29). "International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology". European Heart Journal. 39 (22): 2032–2046. doi:10.1093/eurheartj/ehy076. ISSN 0195-668X. PMC 5991216. PMID 29850871.
5. ↑ Tavazzi, G.; Zanierato, M.; Via, G.; Iotti, G. A.; Procaccio, F. (December 2017). "Are Neurogenic Stress Cardiomyopathy and Takotsubo Different Syndromes With Common Pathways?: Etiopathological Insights on Dysfunctional Hearts". JACC Heart Failure. 5 (12): 940–42. doi:10.1016/j.jchf.2017.09.006. PMID 29191302.
6. ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 Akashi, Y. J.; Nef, H. M.; Lyon, A. R. (July 2015). "Epidemiology and pathophysiology of Takotsubo syndrome" (PDF). Nature Reviews Cardiology. 12 (7): 387–397. doi:10.1038/nrcardio.2015.39. hdl:10044/1/25730. PMID 25855605. S2CID 24742760. Archived from the original (PDF) on 28 February 2021. Retrieved 19 January 2022.
7. ↑ 7.0 7.1 7.2 Akashi YJ, Nef HM, Möllmann H, Ueyama T (2010). "Stress cardiomyopathy". Annual Review of Medicine. 61: 271–86. doi:10.1146/annurev.med.041908.191750. PMID 19686084.
8. ↑ 8.0 8.1 Gianni M, Dentali F, et al. (December 2006). "Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review". European Heart Journal. 27 (13): 1523–1529. doi:10.1093/eurheartj/ehl032. PMID 16720686.
9. ↑ 9.0 9.1 9.2 Sharkey, S.; Lesser, J.; Maron, B. (2011). "Takotsubo (stress) cardiomyopathy". Circulation. American Heart Association. 124 (18): e460-2. doi:10.1161/CIRCULATIONAHA.111.052662. PMID 22042929. Archived from the original on 31 December 2014. Retrieved 19 January 2022.
10. ↑ Coghlan, Andy (12 March 2016). "Shock of good news can hurt your heart as much as grief". New Scientist. Archived from the original on 2 February 2022. Retrieved 19 January 2022.
11. ↑ Jelena Ghadri; et al. (March 2016). "Happy heart syndrome: role of positive emotional stress in takotsubo syndrome". European Heart Journal. 37 (37): 2823–2829. doi:10.1093/eurheartj/ehv757. PMC 5841222. PMID 26935270.
12. ↑ 12.00 12.01 12.02 12.03 12.04 12.05 12.06 12.07 12.08 12.09 12.10 12.11 12.12 12.13 Pelliccia, Francesco; Kaski, Juan Carlos; Crea, Filippo; Camici, Paolo G. (13 June 2017). "Pathophysiology of Takotsubo Syndrome" (PDF). Circulation. 135 (24): 2426–2441. doi:10.1161/CIRCULATIONAHA.116.027121. ISSN 1524-4539. PMID 28606950. S2CID 207581288. Archived (PDF) from the original on 24 February 2021. Retrieved 19 January 2022.
13. ↑ Templin, C.; Ghadri, J; Diekmann, J.; Napp, C.; Bataiosu, D.; Jaguszewski, M.; Cammann, V.; Sarcon, A.; Geyer, V.; Neuman, C.; Seifert, B.; Hellermann, J. (2015). "Clinical features and outcomes of takotsubo (stress) cardiomyopathy" (PDF). New England Journal of Medicine. 373 (10): 929–938. doi:10.1056/NEJMoa1406761. PMID 26332547. Archived (PDF) from the original on 9 March 2021. Retrieved 19 January 2022.
14. ↑ 14.0 14.1 Elesber, A. A.; Prasad, A.; Lennon, R. J.; Wright, R. S.; Lerman, A.; Rihal, C. S. (July 2007). "Four-Year Recurrence Rate and Prognosis of the Apical Ballooning Syndrome". Journal of the American College of Cardiology. 50 (5): 448–452. doi:10.1016/j.jacc.2007.03.050. PMID 17662398.
15. ↑ 15.0 15.1 15.2 15.3 15.4 15.5 15.6 Eshtehardi P, Koestner SC, Adorjan P, Windecker S, Meier B, Hess OM, Wahl A, Cook S (July 2009). "Transient apical ballooning syndrome—clinical characteristics, ballooning pattern, and long-term follow-up in a Swiss population". International Journal of Cardiology. 135 (3): 370–5. doi:10.1016/j.ijcard.2008.03.088. PMID 18599137. Archived from the original on 16 December 2019. Retrieved 19 January 2022.
16. ↑ 16.0 16.1 16.2 16.3 16.4 16.5 16.6 Komamura, K.; Fukui, M.; Iwasaku, T.; Hirotani, S.; Masuyama, T. (2014). "Takotsubo cardiomyopathy: Pathophysiology, diagnosis and treatment". World Journal of Cardiology. 6 (7): 602–609. doi:10.4330/wjc.v6.i7.602. PMC 4110608. PMID 25068020.
17. ↑ Y-Hassan, S.; Falhammar, H. (30 July 2020). "Cardiovascular Manifestations and Complications of Pheochromocytomas and Paragangliomas". Journal of Clinical Medicine. 9 (8): 2435. doi:10.3390/jcm9082435. PMC 7465968. PMID 32751501.
18. ↑ Kalra, S; Lakhani, OJ; Chaudhary, S. (October 2020). "Takotsubo Endocrinopathy". European Endocrinology. 16 (2): 97–99. doi:10.17925/EE.2020.16.2.97. PMC 7572168. PMID 33117439.
19. ↑ 19.0 19.1 Aweimer, A; El-Battrawy, I.; Akin, I.; Borggrefe, M.; Mügge, A.; Patsalis, P. C.; Urban, A.; Kummer, M.; Vasileva, S.; Stachon, A.; Hering, S.; Dietrich, J. W. (12 November 2020). "Abnormal thyroid function is common in takotsubo syndrome and depends on two distinct mechanisms: results of a multicentre observational study". Journal of Internal Medicine. 289 (5): 675–687. doi:10.1111/joim.13189. PMID 33179374.
20. ↑ Scudiero, F.; Arcari, L.; Silverio, A.; Citro, R.; Bossone, E.; Autore, C.; Muraca, I.; Chinati, P.; Sanna, G.; Piti, A.; Parodi, G. (25 November 2020). "Hyperthyroidism in Takotsubo syndrome: prevalence, clinical features and long-term outcomes". European Heart Journal. 41 (Supplement_2): ehaa946.1812. doi:10.1093/ehjci/ehaa946.1812.
21. ↑ Veillet-Chowdhury, M.; Hassan, S. F.; Stergiopoulos, K. (March 2014). "Takotsubo cardiomyopathy: a review". Acute Cardiac Care. 16 (1): 15–22. doi:10.3109/17482941.2013.869346. PMID 24552225. S2CID 8577417.
22. ↑ Redfors, B.; Shao, Y.; Omerovic, E. (2013). "Stress-induced cardiomyopathy (Takotsubo) – broken heart and mind?". Vascular Health and Risk Management. 9: 149–154. doi:10.2147/VHRM.S40163. PMC 3632585. PMID 23626469.
23. ↑ Kurisu S, Sato H, Kawagoe T, et al. (2002). "Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction". American Heart Journal. 143 (3): 448–455. doi:10.1067/mhj.2002.120403. PMID 11868050.
24. ↑ 24.0 24.1 Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I (July 2001). "Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan". Journal of the American College of Cardiology. 38 (1): 11–8. doi:10.1016/S0735-1097(01)01316-X. PMID 11451258.
25. ↑ 25.0 25.1 Kawai et al. JPJ 2000
26. ↑ 26.0 26.1 Desmet WJ, Adriaenssens BF, Dens JA (September 2003). "Apical ballooning of the left ventricle: first series in white patients". Heart. 89 (9): 1027–1031. doi:10.1136/heart.89.9.1027. PMC 1767823. PMID 12923018.
27. ↑ Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H (5 March 2003). "Assessment of clinical features in transient left ventricular apical ballooning". Journal of the American College of Cardiology. 41 (5): 737–742. doi:10.1016/S0735-1097(02)02925-X. PMID 12628715.
28. ↑ Merli, E.; Sutcliffe, S.; Gori, M.; Sutherland, G. G. (January 2006). "Tako-Tsubo cardiomyopathy: insights into the possible underlying pathophysiology". European Journal of Echocardiography. 7 (1): 53–61. doi:10.1016/j.euje.2005.08.003. PMID 16182610.
29. ↑ Finkel-Oron, A.; Olchowski, J.; Jotkowitz, A. (2019). "Takotsubo Cardiomyopathy Triggered by Wasabi Consumption: Can Sushi Break Your Heart?". BMJ Case Reports. 12 (9): e230065. doi:10.1136/bcr-2019-230065. PMC 6768342. PMID 31540920.
30. ↑ "UOTW No. 74 - Ultrasound of the Week". Ultrasound of the Week. 20 September 2016. Archived from the original on 29 October 2016. Retrieved 27 May 2017.
31. ↑ 31.0 31.1 Redfors, B.; Shao, Y.; Lyon, A.; Omerovic, E. (2014). "Diagnostic criteria for takotsubo syndrome: A call for consensus". International Journal of Cardiology. 176 (1): 274–6. doi:10.1016/j.ijcard.2014.06.094. PMID 25043217. Archived from the original on 10 March 2021. Retrieved 19 January 2022.
32. ↑ Azzarelli S, Galassi AR, Amico F, Giacoppo M, Argentino V, Tomasello SD, Tamburino C, Fiscella A (2006). "Clinical features of transient left ventricular apical ballooning". American Journal of Cardiology. 98 (9): 1273–1276. doi:10.1016/j.amjcard.2006.05.065. PMID 17056345.
33. ↑ Bybee KA, Motiei A, Syed IS, Kara T, Prasad A, Lennon RJ, Murphy JG, Hammill SC, Rihal CS, Wright RS (2006). "Electrocardiography cannot reliably differentiate transient left ventricular apical ballooning syndrome from anterior ST-segment elevation myocardial infarction". J Electrocardiol. 40 (1): 38.e1–6. doi:10.1016/j.jelectrocard.2006.04.007. PMID 17067626.
34. ↑ 34.0 34.1 Pilgrim TM, Wyss TR (March 2008). "Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: A systematic review". International Journal of Cardiology. 124 (3): 283–292. doi:10.1016/j.ijcard.2007.07.002. PMID 17651841.
35. ↑ 35.0 35.1 Shimizu M, Kato Y, Masai H, Shima T, Miwa Y (August 2006). "Recurrent episodes of takotsubo-like transient left ventricular ballooning occurring in different regions: a case report". Journal of Cardiology. 48 (2): 101–7. PMID 16948453.
36. ↑ Hurst RT, Askew JW, Reuss CS, Lee RW, Sweeney JP, Fortuin FD, Oh JK, Tajik AJ (August 2006). "Transient midventricular ballooning syndrome: a new variant". Journal of the American College of Cardiology. 48 (3): 579–583. doi:10.1016/j.jacc.2006.06.015. PMID 16875987.
37. ↑ Yasu T, Tone K, Kubo N, Saito M (June 2006). "Transient mid-ventricular ballooning cardiomyopathy: a new entity of Takotsubo cardiomyopathy". International Journal of Cardiology. 110 (1): 100–1. doi:10.1016/j.ijcard.2005.05.060. PMID 15996774.
38. ↑ Golabchi, A; Sarrafzadegan, N. (2011). "Takotsubo cardiomyopathy or broken heart syndrome: A review article". Journal of Research in Medical Sciences. 16 (3): 340–345. PMC 3214344. PMID 22091255.
39. ↑ 39.0 39.1 39.2 McPhee, Stephen J.; Rabow, Michael W.; Papadakis, Maxine A. (1 September 2016). Current medical diagnosis & treatment 2017. Papadakis, Maxine A.,, McPhee, Stephen J.,, Rabow, Michael W. (Fifty-sixth ed.). New York. ISBN 978-1259585111. OCLC 957316517.
40. ↑ Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Koike H, Sasaka K (2003). "The clinical features of takotsubo cardiomyopathy". QJM. 96 (8): 563–73. doi:10.1093/qjmed/hcg096. PMID 12897341.
41. ↑ Nyui N, Yamanaka O, Nakayama R, Sawano M, Kawai S (2000). "'Tako-Tsubo' transient ventricular dysfunction: a case report". Japanese Circulation Journal. 64 (9): 715–719. doi:10.1253/jcj.64.715. PMID 10981859.
42. ↑ "Medics 'can mend a broken heart'". BBC NEWS. 27 March 2009. Archived from the original on 21 October 2017. Retrieved 29 June 2017.
43. ↑ Shah, Sandy; Bhimji, Steve (2017). "Cardiomyopathy, Takotsubo Syndrome (Transient Apical Ballooning, Stress-Induced Cardiomyopathy, Gebrochenes-Herz Syndrome)". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 28613549. Archived from the original on 8 March 2021. Retrieved 19 January 2022.
44. ↑ Derrick, Dawn (2009). "The 'Broken Heart Syndrome': Understanding Takotsubo Cardiomyopathy". Critical Care Nurse. 29 (1): 49–57. doi:10.4037/ccn2009451. PMID 19182280.
45. ↑ "Broken Heart Syndrome". National Heart, Lung, and Blood Institute. Archived from the original on 5 October 2017. Retrieved 2 January 2018.
46. ↑ 46.0 46.1 Kurisu, S.; Kihara, Y. (2014). "Clinical management of takotsubo cardiomyopathy". Circulation Journal. 78 (7): 1559–1566. doi:10.1253/circj.cj-14-0382. PMID 24964980.
47. ↑ 47.0 47.1 47.2 "Management and prognosis of stress (takotsubo) cardiomyopathy". www.uptodate.com. Archived from the original on 21 October 2017. Retrieved 21 October 2017.
48. ↑ Mariani, Silvia; Richter, Jannik; Pappalardo, Federico; Bělohlávek, Jan; Lorusso, Roberto; Schmitto, Jan D.; Bauersachs, Johann; Napp, L. Christian (2020-10-01). "Mechanical circulatory support for Takotsubo syndrome: a systematic review and meta-analysis". International Journal of Cardiology. 316: 31–39. doi:10.1016/j.ijcard.2020.05.033. ISSN 1874-1754. PMID 32473281. Archived from the original on 2 February 2022. Retrieved 19 January 2022.
49. ↑ Akashi, Yoshihiro J.; Goldstein, David S.; Barbaro, Giuseppe; Ueyama, Takashi (16 December 2008). "Takotsubo Cardiomyopathy: A New Form of Acute, Reversible Heart Failure". Circulation. 118 (25): 2754–2762. doi:10.1161/CIRCULATIONAHA.108.767012. ISSN 0009-7322. PMC 4893309. PMID 19106400.
50. ↑ Schneider B.; Athanasiadis A.; Sechtem U. (2013). "Gender-Related differences in Takotsubo Cardiomyopathy". Heart Failure Clinics. 9 (2): 137–146. doi:10.1016/j.hfc.2012.12.005. PMID 23562114.
51. ↑ Prasad A, Lerman A, Rihal CS (March 2008). "Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): A mimic of acute myocardial infarction". American Heart Journal. 155 (3): 408–17. doi:10.1016/j.ahj.2007.11.008. PMID 18294473.
52. ↑ Rees WD, Lutkins SG (1967). "Mortality of Bereavement". British Medical Journal. 4 (5570): 13–16. doi:10.1136/bmj.4.5570.13. PMC 1748842. PMID 6047819.
53. ↑ Engel, George L. (1971). "Sudden and Rapid Death During Psychological Stress: Folklore or Folk Wisdom?". Annals of Internal Medicine. 74 (5): 771–783. doi:10.7326/0003-4819-74-5-771. PMID 5559442.
54. ↑ Cebelin, Hirsch (1980). "Human stress cardiomyopathy. Myocardial lesions in victims of homicidal assaults without internal injuries". Human Pathology. 11 (2): 123–132. doi:10.1016/s0046-8177(80)80129-8. PMID 7399504.
55. ↑ Wittstein I (2007). "The broken heart syndrome". Cleveland Clinic Journal of Medicine. 74 (1): S17–S22. doi:10.3949/ccjm.74.Suppl_1.S17. PMID 17455537.

## External links[edit | edit source]

* Krishnan, Lakshmi; Marchalik, Daniel (8 September 2018). "Understanding Heartbreak: From Takotsubo to Wuthering Heights". The Lancet. 392 (10150): 812. doi:10.1016/S0140-6736(18)32061-0. S2CID 54271789. Archived from the original on 2 February 2022. Retrieved 25 September 2019.
* Wagner, Judith N. (Fall 2014). "Death by voodoo: truth or tale?". Hektoen International Journal. 6 (4). ISSN 2155-3017. Archived from the original on 18 April 2021. Retrieved 19 January 2022.

Classification|

* ICD-10: I42.8
* ICD-9-CM: 429.83
* MeSH: D054549
* DiseasesDB: 33976

|

External resources|

* eMedicine: article/1513631

* v
* t
* e

Cardiovascular disease (heart)

Ischaemic|

| Coronary disease|

* Coronary artery disease (CAD)
* Coronary artery aneurysm
* Spontaneous coronary artery dissection (SCAD)
* Coronary thrombosis
* Coronary vasospasm
* Myocardial bridge

|

Active ischemia|

* Angina pectoris
* Prinzmetal's angina
* Stable angina
* Acute coronary syndrome
* Myocardial infarction
* Unstable angina

Sequelae|

* hours
* Hibernating myocardium
* Myocardial stunning
* days
* Myocardial rupture
* weeks
* Ventricular aneurysm
* Dressler syndrome

Layers|

| Pericardium|

* Pericarditis
* Acute
* Chronic / Constrictive
* Pericardial effusion
* Cardiac tamponade
* Hemopericardium

|

Myocardium|

* Myocarditis
* Chagas disease
* Cardiomyopathy
* Dilated
* Alcoholic
* Hypertrophic
* Tachycardia-induced
* Restrictive
* Loeffler endocarditis
* Cardiac amyloidosis
* Endocardial fibroelastosis
* Arrhythmogenic right ventricular dysplasia

Endocardium /
valves|

| Endocarditis|

* infective endocarditis
* Subacute bacterial endocarditis
* non-infective endocarditis
* Libman–Sacks endocarditis
* Nonbacterial thrombotic endocarditis

|

Valves|

* mitral
* regurgitation
* prolapse
* stenosis
* aortic
* stenosis
* insufficiency
* tricuspid
* stenosis
* insufficiency
* pulmonary
* stenosis
* insufficiency

Conduction /
arrhythmia|

| Bradycardia|

* Sinus bradycardia
* Sick sinus syndrome
* Heart block: Sinoatrial
* AV
* 1°
* 2°
* 3°
* Intraventricular
* Bundle branch block
* Right
* Left
* Left anterior fascicle
* Left posterior fascicle
* Bifascicular
* Trifascicular
* Adams–Stokes syndrome

|

Tachycardia
(paroxysmal and sinus)|

| Supraventricular|

* Atrial
* Multifocal
* Junctional
* AV nodal reentrant
* Junctional ectopic

|

Ventricular|

* Accelerated idioventricular rhythm
* Catecholaminergic polymorphic
* Torsades de pointes

Premature contraction|

* Atrial
* Junctional
* Ventricular

Pre-excitation syndrome|

* Lown–Ganong–Levine
* Wolff–Parkinson–White

Flutter / fibrillation|

* Atrial flutter
* Ventricular flutter
* Atrial fibrillation
* Familial
* Ventricular fibrillation

Pacemaker|

* Ectopic pacemaker / Ectopic beat
* Multifocal atrial tachycardia
* Pacemaker syndrome
* Parasystole
* Wandering atrial pacemaker

Long QT syndrome|

* Andersen–Tawil
* Jervell and Lange-Nielsen
* Romano–Ward

Cardiac arrest|

* Sudden cardiac death
* Asystole
* Pulseless electrical activity
* Sinoatrial arrest

Other / ungrouped|

* hexaxial reference system
* Right axis deviation
* Left axis deviation
* QT
* Short QT syndrome
* T
* T wave alternans
* ST
* Osborn wave
* ST elevation
* ST depression
* Strain pattern

Cardiomegaly|

* Ventricular hypertrophy
* Left
* Right / Cor pulmonale
* Atrial enlargement
* Left
* Right
* Athletic heart syndrome

Other|

* Cardiac fibrosis
* Heart failure
* Diastolic heart failure
* Cardiac asthma
* Rheumatic fever

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