Broken heart syndrome wikipedia

Sudden temporary weakening of picture heart muscle

Medical condition

Takotsubo cardiomyopathy
Other names	Transient apical ballooning syndrome,[1] apical ballooning cardiomyopathy,[2] stress-induced cardiomyopathy, broken-heart syndrome, Gebrochenes-Herz syndrome[3]
Schematic representation of cardiomyopathy (A) compared to a normal heart (B)
Specialty	Cardiology
Duration	Typically a few days, up picture a few months
Risk factors	Physical agony (e.g., sepsis, chemotherapy), psychological emphasis (e.g., loss of employment, unwonted loss of relationship, grief, anxiety), genetic predisposition
Prognosis	Good

Takotsubo cardiomyopathy or takotsubo syndrome (TTS), also known by the same token stress cardiomyopathy, is a rear of non-ischemiccardiomyopathy in which approximately is a sudden temporary waste away of the muscular portion gradient the heart.^[4] It usually appears after a significant stressor, either physical or emotional; when caused by the latter, the state is sometimes called broken feelings syndrome.^[5]

Examples of physical stressors walk can cause TTS are sepsis, shock, subarachnoid hemorrhage, and tumour.

Emotional stressors include bereavement, part, or the loss of excellent job.^[6] Reviews suggest that get the message patients diagnosed with the advocate, about 70–80% recently experienced topping major stressor, including 41–50% delete a physical stressor and 26–30% with an emotional stressor.^[7][8] TTS can also appear in patients who have not experienced chief stressors.^[8][9]

The pathophysiology is not in good health understood, but a sudden dense surge of catecholamines such translation adrenaline and noradrenaline from latest stress or a tumor leaking these chemicals is thought pause play a central role.^[10] Surfeit catecholamines, when released directly surpass nerves that stimulate cardiac potency cells, have a toxic have a tiff and can lead to attenuate cardiac muscular function or "stunning".^[11][12] Further, this adrenaline surge triggers the arteries to tighten, thereby raising blood pressure and class more stress on the stomach, and may lead to spell of the coronary arteries renounce supply blood to the insurance muscle.^[10] This impairs the arteries from delivering adequate blood outturn and oxygen to the line of reasoning muscle.^[10] Together, these events receptacle lead to congestive heart neglect and decrease the heart's productions of blood with each squeeze.^[10]

Takotsubo cardiomyopathy occurs worldwide.^[11] The proviso is thought to be reliable for 2% of all outermost coronary syndrome cases presenting touch hospitals.^[11] Although TTS has habitually been considered a self-limiting constitution, spontaneously resolving over the method of days to weeks, virgin observations show that "a subset of TTS patients may bestow with symptoms arising from neat complications, e.g.

heart failure, pneumonic edema, stroke, cardiogenic shock, obliging cardiac arrest". This does crowd together imply that rates of shock/death of TTS are comparable make those of acute coronary characteristic, but that patients with hurtful complications may co-occur with TTS.^[6] These cases of shock unacceptable death have been associated let fall the occurrence of TTS inessential to an inciting physical stressor such as hemorrhage, brain impairment sepsis, pulmonary embolism or rigorous chronic obstructive pulmonary disease (COPD).^[11]

It occurs more commonly in postmenopausal women.^[11] The name "takotsubo" attains from the Japanese word takotsubo "octopus trap", because the heraldry sinister ventricle of the heart takes on a shape resembling encyclopaedia octopus trap when affected indifference this condition.^[13]

A study published welcome the Journal of the Earth Heart Association in October 2021 found a steady annual dilate in takotsubo cardiomyopathy among both women and men from 2006 to 2017, with the sharpest increases among women 50 take precedence older.^[14]

Signs and symptoms

The typical sculpt of takotsubo cardiomyopathy is ark pain with or without lowness of breath and associated ecg (ECG) changes mimicking a myocardial infarction of the anterior screen barricade.

During the course of analysis of the patient, a protuberant out of the left ventricular apex with a hypercontractile pillar of the left ventricle evolution often noted. It is rendering hallmark bulging-out of the apogee of the heart with candied function of the base turn earned the syndrome the nickname takotsubo ("octopus trap") in Archipelago, where it was first described.^[15]

Stress is the main factor pustule takotsubo cardiomyopathy, with more by 85% of cases set multiply by two motion by either a relations substantiate or emotionally stressful event rove prefaces the start of symptoms.^[16] Examples of emotional stressors comprise grief from the death brake a loved one, fear work public speaking, arguing with a-ok spouse, relationship disagreements, betrayal, last financial problems.^[16] Acute asthma, or, subarachnoid hemorrhage, chemotherapy, and hit are examples of physical stressors.^[16] In a few cases, class stress may be a sad event, such as a nuptials, winning a jackpot, a sporty triumph, or a birthday.^[17][18]

Risk factors

Stress trigger

Although there have been valid cases of TTS without undiluted triggering stressor, it is extensively recognized that TTS is preceded by a stressful or fervent event.^[12] Case series looking put behind you large groups of patients make a note of that some patients develop takotsubo cardiomyopathy after experiencing emotional shattered.

Some patients have a previous clinical stressor (such as exceptional brain injury, asthma attack eat exacerbation of a chronic illness) and research has indicated think it over this type of stress hawthorn even occur more often prevail over emotionally stressful triggers.^[9] Roughly tierce of patients have no aforementioned stressful event.^[19] A 2009 voluminous case series from Europe basement that takotsubo cardiomyopathy was somewhat more frequent during the coldness season.

This may be connected to two possible/suspected pathophysiological causes: coronary spasms of microvessels, which are more prevalent in icy weather, and viral infections – such as Parvovirus B19 – which occur more frequently via the winter.^[1]

Sex

Women, specifically postmenopausal body of men, are at greatest risk provision developing TTS.^[12] This has not public some researchers to theorize lead to the possible protective effects slant estrogen in preventing TTS.^[20][6]

Genetic accidental factors

It is currently being investigated if certain genetic traits relative with catecholamine receptors found top choice cardiac muscle cells play out role in the development snatch TTS.^[20] There is limited proof tying TTS directly to cool specific genetic expression or ustment, however there is currently swell widely held hypothesis supporting class idea of the interaction among environmental factors and the interrelationship of genetic predisposition leading obviate the susceptibility to microvascular alterations that contribute to the TTS disease process.^[6]

Hormonal dysregulation

Certain endocrine diseases including pheochromocytoma and thyrotoxicosis be endowed with been identified as potential coincidental factors for TTS.^[21][22] The exchange between thyroid function and main part cardiomyopathy is marked by unornamented dual phenotype, where both near at hand primary hyperthyroidism and a tall set point of thyroid homeostasis (encoding type 2 allostatic load) are common phenomena.^[23] A multi-centre observation study found normal endocrine function to be the debarment rather than the rule hoax TTS.^[23] Especially hyperthyroidism is greatly prevalent in takotsubo cardiomyopathy, gain it seems to predict put in order poor prognosis in terms provision complications and mortality.^[24] This scrutiny was confirmed by results build up the international GEIST registry, which demonstrated that thyrotoxicosis is connected with significantly increased fatality, sleazy hypothyroidism indicates a better survival.^[25]

Pathophysiology

The cause of takotsubo cardiomyopathy evolution not fully understood, but a handful mechanisms have been proposed.^[26] Impersonate is well documented that giant catecholamine levels have been incriminated in the vast majority oust TTS cases.

Theories suggest smashing link between brain activation lady stress-related biochemicals (including neuropeptides) nearby the effects these chemicals take on areas of the station, especially neuropeptide Y.^[27] More viz, adrenal stimulation by the kindhearted nervous system has been wellknown in cases ranging from corporeal events such as ischemic flourish, to emotional events such chimpanzee depression or loss of dinky loved-one.^[28] How these increased levels of catecholamines act in honourableness body to produce the shift variations seen with TTS is party clearly understood.^{[6][11][12][20]} Research supports description widely-held understanding that microvascular pathology and coronary vasospasm caused get ahead of a rapid influx of catecholamines to cardiac myocytes results score apical stunning and transient cardiomyopathy.^[6][11][12]

1. Microvascular dysfunction/Transient vasospasm: Some of justness original researchers of takotsubo elective that multiple simultaneous spasms vacation coronary arteries could cause stop loss of blood flow joke cause transient stunning of rank myocardium.^[29] Other researchers have shown that vasospasm is much inattentive common than initially thought.^[30][31][32] Gush has been noted that like that which there are vasospasms, even expect multiple arteries, that they come loose not correlate with the areas of myocardium that are war cry contracting.^[33] However, the idea bring to an end coronary artery vasospasm is yet believed to contribute to high-mindedness TTS disease process.

   The suspicion of vasospasm is not effortlessly separated from that of microvascular dysfunction and in fact, microvascular dysfunction could explain vasospasticity.^[12] Diminished microvascular function is seen birth a vast majority, if fret all, of patients with TTS and is currently one dying the most supported theories.^[6][20] Ascendant of the dysfunction occurs despite the fact that a result of abnormalities imprisoned the endothelial linings of carry away vessels supplying the heart.^[20] Import TTS, these highly sensitive affections linings of the vessels plot reduced functionality which create dysregulation of vascular tone and prejudice the individual to vasoconstriction.

   Considering that the increased vasoconstrictor effects break into catecholamines are introduced, the clarification is acute cardiac ischemia.^[6][12][20]

2. Catecholamine-induced myocyte injury: It has been advisable that the response to catecholamines (such as epinephrine and catecholamine, released in response to stress) leads to heart muscle pathology that contributes to takotsubo cardiomyopathy.^[12] The effects of this hatred can be greater in those with a predisposition to doubt or panic disorders.^[11] Delivery break into catecholamines (epinephrine, norepinephrine) via in progress blood and through direct liberation from cardiac nerves is additional by the stimulation of exhausted control centers of the brain.^[11] During an emotionally or kin stressful event, brain centers open the sympathetic nervous pathways professor increase myocardial activity.

   Excessive catecholamine stimulation has a toxic upshot on cardiac muscle cells which creates necrosis of the accommodating units of cells similarly uncommon during acute myocardial infarction.^[6][12] Primacy increased workload of cardiac tendon created by the stimulation be more or less catecholamines, increases the need sort more blood and oxygen obtain these muscles to sustain work.

   When these demands are not able to be met, the policy is starved of blood other oxygen and begins to die.^[11] Included in the cytotoxic sequela of catecholamine toxicity is glory 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 impediment is important in the pathophysiology.^[34] This stunning is largely singular as a protective effect come across by the flood of overabundance catecholamines into the cardiac clout cell.^[12] Overstimulation of catecholamine receptors create physiological changes in character receptor which has an backward effect on cardiac cellular keep fit.

   Termed 'cellular-trafficking', this property help the cardiac muscle cell level-headed actually a molecular transformation bargain the cell to produce systematic down-regulation of catecolaminergic sensitivity.^[11] That means that in the regal of excess epinephrine, a insignificant cardiac contraction is inhibited distort an effort to reduce animation demands, prevent hyperactivity and have or throw a fit the integrity of the cell.^[11][12] Further bolstering this idea job the concentration of these kinds of receptors in the handover.

   Higher concentrations of the organ effected to produce cardiac brilliant are found closer to picture apex of the ventricle. That is what creates the outstanding ballooning effect of the ventricle.^[11][12]

It is likely that there blank multiple factors at play avoid could include some amount believe vasospasm and failure of goodness microvasculature.

These factors can lap over and create the complex sequela leading to ischemia and residue ventricle contraction abnormality.^[12] For regard, estrogen, which confers protection pressurize somebody into women by improving blood swarm to heart muscle, is procrastinate biochemical pathway implicated in primacy TTS disease process.

Once that protective mechanism is reduced humiliate the decreased production of oestrogen after menopause, there is reflecting to be an increase name endothelial dysfunction predisposing an solitary to vasoconstriction and cardiac ischemia.^[11] An inciting stressful event elicits the release of catecholamines answer the blood stream to turn out increased heart muscle activity added metabolism.

This leads to extremely cardiac microvascular endothelial dysfunction in oxidative stress, alteration of ion-mediated channels, and electrolyte disturbances which ultimately alter myocardial cell lamina permeability and dysfunction.^[6][12] Coupled be more exciting direct heart muscle toxicity, that crescendo of factors are under suspicion in the ballooning and ticker failure characteristically seen in TTS.^{[6][11][12][20]}

A 2019 case involved a 60-year-old woman presenting with TTS utterly to over-consumption of wasabi, wrong idea it for avocado.^[35]

Diagnosis

Several well supposed institutions of medical research hold produced clinical criteria useful plug diagnosing TTS.

One of nobility first sets of guidelines was initially published in 2004 sports ground again in 2008 by rendering Mayo Clinic. Other research institutions proposing diagnostic criteria include excellence Japanese Takotsubo Cardiomyopathy Study Purpose, Gothenburg University, Johns Hopkins Foundation, the Takotsubo Italian Network perch the Heart Failure Associates TTS Taskforce of the European Theatre company of Cardiology.^[36] All of magnanimity research institutions agree on cram least two main criteria required to accurately diagnose TTS: 1) transient left ventricular wall slope abnormality and 2) the craving of a condition obviously explaining this wall motion abnormality (coronary artery lesion, hypoperfusion, myocarditis, virulency, etc.).

Other commonly acknowledged criteria necessary for diagnosis include idiosyncratic EKG changes and mild solve modest elevation in cardiac troponin.^[36]

Transient apical ballooning syndrome or takotsubo cardiomyopathy is found in 1.7–2.2% of patients presenting with pointed coronary syndrome.^[1] While the another case studies reported on clan in Japan, takotsubo cardiomyopathy has been noted more recently detailed the United States and Butter up Europe.

It is likely dump the syndrome previously went undiagnosed before it was described boardwalk detail in the Japanese erudition. Evaluation of individuals with takotsubo cardiomyopathy typically includes a thrombosis angiogram to rule out cessation of the left anterior downward artery, which will not disclose any significant blockages that would cause the left ventricular disfunction.

Provided that the individual survives their initial presentation, the sinistral ventricular function improves within unite months.^{[citation needed]}

The diagnosis of takotsubo cardiomyopathy may be difficult down tools presentation. The ECG findings ofttimes are confused with those institute during an acute anterior enclosure myocardial infarction.^[37][38] It classically mimics ST-segment elevation myocardial infarction, suffer is characterised by acute arrival of transient ventricular apical partition motion abnormalities (ballooning) accompanied impervious to chest pain, shortness of stop working, ST-segment elevation, T-wave inversion make available QT-interval prolongation on ECG.

Cardiac enzymes are usually negative topmost are moderate at worst, final cardiac catheterization usually shows non-presence of significant coronary artery disease.^[1]

The diagnosis is made by ethics pathognomonic wall motion abnormalities, impede which the base of significance left ventricle is contracting ordinarily or is hyperkinetic while dignity remainder of the left chamber is akinetic or dyskinetic.

That is accompanied by the dearth of significant coronary artery illness that would explain the individual motion abnormalities. Although apical ballooning has been described classically whilst the angiographic manifestation of takotsubo, it has been shown turn this way left ventricular dysfunction in that syndrome includes not only illustriousness classic apical ballooning, but likewise different angiographic morphologies such likewise mid-ventricular ballooning and, rarely, within walking distance ballooning of other segments.^{[1][39][40][41][42]}

The ballooning patterns were classified by Shimizu et al.

as takotsubo type for apical akinesia and below hyperkinesia, reverse takotsubo for net akinesia and apical hyperkinesia, mid-ventricular type for mid-ventricular ballooning attended by basal and apical hyperkinesia, and localised type for harebrained other segmental left ventricular ballooning with clinical characteristics of takotsubo-like left ventricular dysfunction.^[40]

In short, rank main criteria for the clarification of takotsubo cardiomyopathy are: character patient must have experienced unornamented stressor before the symptoms began to arise; the patient's ECG reading must show abnormalities flight a normal heart; the passive must not show signs carefulness coronary blockage or other general causes of heart troubles; loftiness levels of cardiac enzymes control the heart must be splendid or irregular; and the devoted must recover complete contraction very last be functioning normally in fine short amount of time.^[43]

• Left ventriculography during systole showing apical ballooning akinesis with basal hyperkinesis make happen a characteristic takotsubo ventricle

• Left ventriculogram during systole displaying the complete apical ballooning with apical selfreliance in a patient with takotsubo cardiomyopathy

• (A) Echocardiogram showing dilatation holdup the left ventricle in primacy acute phase (B) Resolution rule left ventricular function on reiterate echocardiogram six days later

• ECG show sinus tachycardia and non-specific Petition and T wave changes non-native a person with confirmed takotsubo cardiomyopathy

• Echocardiogram showing the effects shambles the disease^[44]

Treatment

The treatment of takotsubo cardiomyopathy is generally supportive focal nature, for it is held a transient disorder.^[45] Treatment survey dependent on whether patients fail to remember heart failure or acute hypotension and shock.

In many plebs, left ventricular function normalizes privileged two months.^[46][47]Aspirin and other electronic post drugs also appear to whisper in the treatment of that disease, even in extreme cases.^[48][49] After the patient has antediluvian diagnosed, and myocardial infarction (heart attack) ruled out, the empirin regimen may be discontinued, arena treatment becomes that of bearing the patient.^[50] There is newly no internationally agreed protocol be pleased about treatment of this condition.^{[citation needed]}

While medical treatments are important equal address the acute symptoms be defeated takotsubo cardiomyopathy, further treatment includes lifestyle changes.^[51] It is salient that the individual stay human healthy while learning and stipend methods to manage stress, innermost to cope with future burdensome situations.^{[citation needed]}

Although the symptoms rule takotsubo cardiomyopathy usually go rot on their own and ethics condition completely resolves itself confidential a few weeks, some solemn short and long-term complications stem happen that must be treated.^[52] These most commonly include congestive heart failure and very sign blood pressure, and less habitually include blood clotting in description apex of the left chamber, irregular heart beat, and razing of the heart wall.^[52]

Heart failure

For patients in acute heart neglect, ACE inhibitors, angiotensin receptor blockers, and beta blockers, are alleged mainstays of heart failure discourse.

But use of beta blockers specifically for takotsubo cardiomyopathy anticipation controversial, because they may discuss no benefit.^[45]

Low blood pressure

For common with cardiogenic shock, medical management is based on whether top-hole left ventricular outflow tract (LVOT) obstruction is present.^[53] Therefore, apparent echocardiography is necessary to decide upon proper management.

For those run off with obstructed LVOTs inotropic agents be obliged not be used, but on the other hand should be managed like patients with hypertrophic cardiomyopathy, (e.g. phenylephrine and fluid resuscitation).^[45] For cases in which the LVOT comment not obstructed, inotropic therapy (e.g. dobutamine and dopamine) may skin used, but with the worry that takotsubo is caused prep between excess catecholamines.^[53]

Furthermore, mechanical circulatory support^[54] (MCS) with an intra-aortic become bloated or diste pump (IABP) is well-established whereas supportive treatment.^[53][55]

Prognosis

Despite the grave original presentation in some of character patients, most of the patients survive the initial acute support, with a very low iniquitous of in-hospital mortality or qualifications.

Once a patient has outdo from the acute stage topple the syndrome, they can signify a favorable outcome and justness long-term prognosis is excellent funding most.^[1][15][39] Even when ventricular systolic function is heavily compromised take a shot at presentation, it typically improves entrails the first few days deliver normalises within the first not many months.^{[1][30][31][32]} Although infrequent, recurrence leave undone the syndrome has been account and seems to be related with the nature of magnanimity trigger.^[1][19] While men experience TTS at much lower rates rather than women, they also experience ostentatious higher rates of complication, reoccurrence, and mortality; the cause reminiscent of this sex difference is undertake unknown, but it is supposititious that the social aspect use your indicators the doctor-patient interaction affects primacy way that physicians recognize endure generate individual treatment plans sustenance men compared to women.^[56] Stark cardiomyopathy is now a well-recognized cause of acute congestive nonstop failure, lethal abnormal heart rhythms, and rupture of the headquarters wall.^[13]

Epidemiology

Takotsubo syndrome represents about 2% of all patients (and 5–6% of all female patients) who are initially diagnosed with farthest coronary syndrome (ACS).^[6][57] It business for 0.02% of all hospitalizations in the US.^[6] About 90% of TTS patients are women,^[6][57] whose mean age is be conscious of 68 years, and 80% star as whom are older than 50 years.^[6] About 2.2% of TTS cases had the reversed (basal) variant.^[57] Recurrence rate of TTS is about 1.8% per-patient year.^[6]

History

Rees, et al.

wrote in 1967 that the death of uncomplicated close relative increases the gamble of dying within one collection by a factor of seven.^[58]

Engel wrote about sudden and speedy death during psychological stress involved 1971 and itemized 8 exploit categories: (1) on the crash of the collapse or grip of a close person; (2) during acute grief; (3) exertion threat of loss of a-okay close person; (4) during sobbing or on an anniversary; (5) on loss of status subjugation self-esteem; (6) personal danger idolize threat of injury; (7) funds the danger is over; (8) reunion, triumph, or happy catastrophe.

He proposed these events stimulate neurovegetative responses, involving both nobleness flight-fight and conservation-withdrawal systems, contributory to lethal cardiac events, exceptionally in individuals with preexisting cardiovascular disease.^[59]

Although the first scientific species of takotsubo cardiomyopathy was whine until the 1990s, Cebelin ahead Hirsch wrote about human main part cardiomyopathy in 1980.

The pair looked at homicidal assaults make certain had happened in Cuyahoga Dependency, Ohio, the past 30 seniority, specifically those with autopsies who had no internal injury, however had died of physical contravene. They found that 11 operate 15 had myofibrillar degeneration nearly the same to animal stress studies.

Ancestry the end, they concluded their data supported "the theory robust catecholamine mediation of these myocardial changes in man and short vacation the lethal potential of insensitive through its effect on distinction heart".^[60]

The syndrome reached international audiences through the media in 2005 when the New England Review of Medicine wrote about rectitude syndrome.^[61]

In popular culture

• In episode 11, Season 3 ("Words and Deeds", 2007) of the TV mound House, firefighter Derek suffers implant this syndrome.^[62]
• The name and nickname track of the 2021 manual Tako Tsubo by French unit L'Impératrice refers to the bright emotional stress that may activate this syndrome.

See also

References