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Takotsubo cardiomyopathy

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Last Updated: 02 July 2021

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Takotsubo cardiomyopathy

Other namesTransient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced cardiomyopathy, broken-heart syndrome
SpecialtyCardiology

Ever hear of someone dying from a broken heart? Broken heart syndrome, also known as Takotsubo cardiomyopathy, or stress induced cardiomyopathy, or apical ballooning syndrome, has been increasingly recognized over the past 2 decades as a real entity. While not usually life - threatening, incidence of sudden cardiac death is difficult to measure. A sudden emotional upset can suddenly trigger a cascade of events, resulting in acute systolic heart failure with characteristic regional wall motion pattern causing severe hypokinesis of mid and apical myocardial segments with preservation of basal segments. This results in apical ballooning of the left ventricle. The Japanese word Takotsubo refers to an octopus trap with a similar shape. The Octopus can get in, but is not able to maneuver itself to turn around and get out. The actual pathophysiology behind this unusual phenomenon remains unclear, but it has been hypothesized that sudden catecholamine surge is the cause. Interestingly, similar acute leave ventricular dysfunction pattern can occur with cocaine intoxication. It is well known that cocaine causes a significant increase in the sympathetic nervous system. The difficult part about making a clinical diagnosis of stress - induced cardiomyopathy is the major overlap in symptoms between this disorder and acute coronary syndrome. Typical presentation is chest pains, acute shortness of breath and generalized weakness. Rhythm disturbances and hypotension can cause syncope, as well. Diaphoresis, palpitations and nausea are common. Sounds just like acute MI, doesnt it? I ca tell you how many times I have explained to patients that they are having a heart attack from thrombus in the coronary artery and we need to do angiogram to open vessels and restore blood flow, just to be eating my words later asking them to forget everything I previously say because their coronary arteries were normal on angiogram. They have Takotsubo cardiomyopathy!

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Signs and symptoms

Many people seek medical help because it feel like they are having a heart attack. Most people are initially treated for heart attack until tests can diagnose the true cause. Others may see their doctor because they are experiencing shortness of breath, and few because they lose consciousness. Representation of the shape of the left ventricle in the heart with Takotsubo cardiomyopathy and Japanese Octopus trap. Typically, symptoms start just after a stressful event, and can include any of the following: sudden, intense chest pain; Shortness of breath - caused by the heart not being able to pump properly, which causes fluid to build up in the lungs; and arrhythmia - where the heart beats either too fast or too slow, or may beat irregularly.

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Pathophysiology

A normal myocardium utilizes approximately 90% of its energy from fatty acid metabolism at rest and with aerobic activity. During ischemia, this pathway is suppress, and glucose is largely utilized instead, which results in impaired cardiac function. Patients with Takotsubo cardiomyopathy are found to have shifted toward glucose pathway despite relatively normal myocardial perfusion and lack of ischemia in left ventricular segments. The most commonly discussed possible mechanism for Takotsubo cardiomyopathy is stress - induced catecholamine release, with toxicity to and subsequent stunning of the myocardium. Endomyocardial biopsy of patients with Takotsubo cardiomyopathy demonstrates reversible focal myocytolysis, mononuclear infiltrates, and contraction band necrosis. The Sympathetic / catecholamine theory is gaining momentum, because Takotsubo cardiomyopathy was induced in rats exposed to physical stress and, in some instances, was prevented by pretreatment with alpha blocker or beta blocker. Other evidence for this theory has been demonstrated through myocardial imaging studies using catecholamine analogues that evaluate 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 characteristic LV wall - motion abnormality of Takotsubo cardiomyopathy. Whether this is triggered by multivessel spasm, thrombosis, epicardial vessel occlusion, or direct myocardial toxicity remains to be see. These authors point out that wall - motion abnormality of Takotsubo cardiomyopathy can be seen in other conditions, including those with certain left anterior descending lesions, making wall motion alone insufficient for diagnosis of Takotsubo cardiomyopathy. Cases of Takotsubo cardiomyopathy have been reported in literature following cocaine, methamphetamine, and excessive phenylephrine use. Exercise stress testing, which is known to cause increased levels of catecholamines, has resulted in false positives attributable to Takotsubo cardiomyopathy. Studies have found that patients with Takotsubo cardiomyopathy have, by a statistically significant margin, higher levels of serum catecholamines than do patients with myocardial Infarction. Apical portions of LV have the highest concentration of sympathetic innervation found in the heart and may explain why excess catecholamines seem to selectively affect its function. Underlying Coronary endothelial dysfunction may also play a role in Takotsubo cardiomyopathy, wherein abnormal tendency toward spasticity in Coronary tree can manifest as angina and as Takotsubo cardiomyopathy. One theory indicates that substantially increased coronary spasticity may lead to diffuse, transient spastic obliteration of coronary arteries and to critical ischemia, which can be reproduced by acetylcholine testing early after an episode of Takotsubo cardiomyopathy.


Introduction & Background

Since 1990, after describing the term tako - tsubo - like leave ventricular dysfunction, several concepts have been put forth to individually explain unique contractile dysfunction seen in Takotsubo cardiomyopathy. In particular, microcirculatory dysfunction theory is a widely accepted explanation for the genesis of TCM. Rivero et al., In a small group of women, angiographically assessed index microcirculatory resistance as marker of microvascular dysfunction and demonstrated inverse correlation between extent of microvascular dysfunction and time of symptom onset, adding to existing evidence towards significant association between existence of microcirculation dysfunction and TCM pathophysiology. Additionally, there is increasing evidence of microcirculatory dysfunction occurring predominantly during the acute phase of TCM; as demonstrated in a small study group, administering intravenous adenosine among TCM patients during the acute phase has shown significant immediate improvement in myocardial perfusion and leave ventricular ejection fraction, suggesting intense microvascular constriction playing an important role in pathophysiology of acute TCM. Microcirculation dysfunction is often demonstrated in the presence of normal macrovascular coronary blood flow, as assessed using coronary angiography, in - spite of 12 - lead electrocardiogram demonstrating - segment elevation. Therefore, providing evidence towards altering blood flow at a certain level, likely in microcirculation. Microcirculation dysfunction theory, in addition to few notable pathophysiological mechanisms like; multi - vessel epicardial spasm, transient ischemia due to coronary plaque rupture, and cardiotoxicity from catecholamine surge would explain the pathophysiology of TCM, but fails to provide evidence towards selective involvement of LV apex. Therefore, in this brief scientific review, we generate a hypothesis of differential distribution of adrenergic nerve and cholinergic nerve to not only understand the pathophysiology of TCM but also to learn its selective involvement of LV apex.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Diagnosis

Since its first description in Japan in 1990, Takotsubo Syndrome, also know as Stress Cardiomyopathy, broken Heart Syndrome, or apical ballooning Syndrome, has emerged as an important form of acute reversible myocardial injury characterized by transient regional systolic leave ventricular dysfunction. Takotsubo refers to the classic apical ballooning shape seen in the majority of cases that resembles octopus trap used in Japan. Initially considered a rare event, with greater awareness and recognition, prevalence is currently estimated at 1% to 2% of patients with suspected acute coronary Syndrome. Although it was originally believed to represent benign syndrome due to its self - limiting clinical course and absence of significant coronary artery disease, there is substantial risk of mortality, not dissimilar to that of ACS. Complications of Stress Cardiomyopathy, such as acute Heart Failure, leave ventricular outflow tract obstruction, and mitral regurgitation, leading to cardiogenic shock are not infrequent. The purpose of this review is to provide a practical approach to diagnosis and treatment of Patients With Stress Cardiomyopathy and to highlight potential challenges and unresolved questions. Receive May 15, 2018. Revision received July 5 2018. Accept July 6 2018. 2018 American College of Cardiology Foundation in predisposed individual,ss who may have enrichment in NPY / norepinephrine granules and Risk Factors for endothelial dysfunction, intense stimulation for adrenergic stimulation may be sufficient to trigger Stress Cardiomyopathy in response to emotional or physical Stress. Stress - relate neuropeptides stored in pre - synaptic terminations of postganglionic neurons at level of CANS may suddenly spill at myocardial level, and through direct catecholamine toxicity and / or microvascular dysfunction, explain prevailing theory of neurogenic - mediate mechanism of myocardial stunning. Diagnosis of Stress Cardiomyopathy is based on demonstration of regional LV wall motion abnormality beyond territory perfused by single epicardial coronary artery that is reversible in nature and is often associated with emotional or physical stress. As such, definite diagnosis cannot be established at presentation because of the need to demonstrate the reversible nature of the condition, although some clinical features are highly predictive of Stress Cardiomyopathy. Acute Treatment of Patients With Stress Cardiomyopathy and Hemodynamic Compromise in Patients With no Hemodynamic instability and pulmonary congestion, Treatment is direct to relieve congestion with diuretic agent and vasodilators. Arterial vasodilators and - adrenergic blockers are useful, especially if hypertension is present. For patients with Hemodynamic instability, treatment depends on the presence of LVOTO obstruction. In the absence of LVOTO, inotropic agents, and if not sufficient, mechanical leave ventricular assist devices should be consider. In presence of LVOTO, intravenous fluids and low dose of short - acting - adrenergic blockers may be used with caution to reduce LVOTO or peripherally active vasopressor drugs to maintain adequate perfusion pressure as temporizing solution to LVOTO resolution or mechanical support. Extracorporeal membrane oxygenation is used as a mechanical cardiac assist device for refractory cases of Stress Cardiomyopathy With LVOTO or biventricular Failure.

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* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Treatment

Treatment of takotsubo cardiomyopathy is generally supportive in nature, because it is considered a transient disorder. Treatment is dependent on whether patients experience heart failure or acute hypotension and shock. In many individuals, left ventricular function normalizes within two months. Aspirin and other heart drugs also appear to help in the treatment of this disease, even in extreme cases. After a patient has been diagnose, and myocardial infarction ruled out, aspirin regimen may be discontinue, and treatment becomes that of supporting patient. There is currently no internationally agreed protocol for treatment of this condition. While medical treatments are important to address acute symptoms of takotsubo cardiomyopathy, further treatment includes lifestyle changes. It is important that individuals stay physically healthy while learning and maintaining methods to manage stress, and to cope with future difficult situations. Although 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 treat. 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.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Prognosis

Recently, increasing research efforts have been directed to prognosis of patients with Takotsubo cardiomyopathy. Several study groups have published outcome data during last year. A Swedish Registry study found a 30 - day mortality of 4. 1% in 302 patients with TTC. The Large International Takotsubo Registry includes 1 750 patients, and it reports 5. 9% mortality after 30 days. The rate of death during long - term follow - up was 5. 6% per patient - year. Furthermore, our bicentric study of 286 prospectively identified TTC patients revealed 28 - day, 1 - year, and long - term mortality rates of 5. 5%, 12. 5%, and 24. 7%, respectively. Of note, all these trials compare mortality in TTC with matched cohorts of patients with acute myocardial infarction or acute coronary syndrome, and find similar risk of death. Long - term mortality in TTC even exceeded that of patients presented with with - segment elevation myocardial infarction in 1 study. These findings challenge initial opinion of favorable prognosis in TTC patients due to complete recovery of left ventricular dysfunction within days to weeks. Murugiah et al. Examine the United States Medicare database and report 30 - day and 1 - year mortality rates of 2. 5% and 6. 9% for patients with principal TTC and 4. 7% and 11. 4% for patients with secondary TTC, respectively. These results illustrate indisputable prognostic difference between principal and secondary TTC, which has also been demonstrated previously. However, observed mortality in the overall TTC population is comparable to aforementioned trials in unselected TTC patients, albeit at the lower end of reported rates. Considering these novel insights, we think that prognosis of TTC should no longer be referred to as favorable for patients with principal TTC. During acute and subacute phases of disease, patients are prone to severe complications, including heart failure, cardiogenic shock, or life - threatening arrhythmias. Therefore, we suggest close monitoring in coronary care units, in similar fashion as recommended for patients with acute coronary syndrome. Recovery of left ventricular function and electrocardiographic changes should be documented during regular follow - up visits after hospital discharge. Future research efforts should be direct to determining detailed causes of death, and particularly, impact of underlying noncardiovascular diseases in patients with secondary TTC. Furthermore, development of evidence - base treatment approaches is desirable. It is necessary to enhance awareness of substantial mortality rates in TTC and to avoid trivializing disease to ensure adequate management strategies and to achieve scientific progress. American College of Cardiology Foundation

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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Epidemiology

Computer - assisted SCOPUS or MEDLINE searches of literature for terms apical ballooning, ampulla cardiomyopathy, tako - tsubo cardiomyopathy, and Takotsubo cardiomyopathy between 1989 and December 2007 demonstrate an exponentially increasing frequency of publications. Until 2000, few case reports were publish, but presentation of Takotsubo cardiomyopathy has increased gradually since 2001. The number of publications has increased rapidly; Takotsubo cardiomyopathy has probably gained broad attention in the field of cardiology among US and European physicians. On basis of recent analysis reports from several countries, this condition probably accounts for 1% to 2% of all cases of suspected acute myocardial infarction.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

History

Takotsubo cardiomyopathy is also called stress - induce cardiomyopathy. It is novel condition first identified in Japan, and is also known as stress cardiomyopathy. It has presentation akin to acute coronary syndrome, but is non - ischemic in etiology. Takotsubo syndrome is named after a type of octopus - trapping pot used by Japanese fishermen. It refers to the occurrence of sudden stress - related cardiac weakening. The stressor may be physical, as occurs in almost 40% of cases, or emotional, in about a quarter of patients. Stressor may be chronic in some cases, with patients reporting constant but high - level anxiety preceding attack. It almost always affects postmenopausal women and follow intense stress.


The exploration of Takotsubo pathophysiology

Echocardiogram and sometimes magnetic resonance imaging studies are performed to evaluate the heart's pumping ability. Patients are in the intensive care unit for at least 24 hours, during which time vital signs are monitored and blood is tested for troponin. Commonly used medications include - blockers and angiotensin - converting enzyme inhibitor drugs, both of which promote recovery of heart muscle. Drugs that interfere with blood clotting may be administered briefly to avoid stroke caused by blood clot traveling from heart to brain. Major life - threatening complications are infrequent. Low blood pressure requires administration of intravenous drugs or, in extreme cases, temporary internal blood pressure support device. Fluid buildup in lungs necessitates drugs to promote urine production or occasionally temporary use of breathing support device. Chaotic heart rhythm may require rhythm - stabilizing drugs or rarely electric shock. Fortunately, with timely recognition and supportive therapy, Takotsubo events are reversible, and recovery is usually rapid and complete. Heart function gradually improves over several days and is usually normal by hospital discharge. The term stun heart muscle is commonly used to indicate that injury in Takotsubo, although initially profound, is only temporary. Drugs are discontinued once heart contraction has returned to normal.


Inverted Takotsubo syndrome

Tts IS poorly recognized heart disease that was initially regarded as a benign condition. Recently, it has been shown that TTS may be associated with severe clinical complications, including death, and that its prevalence IS probably underestimated. Tts derives its name from the Japanese word for octopus trap, because of the shape of the left ventricle at the end of the systole. It has been described under a remarkable number of different names in literature, including broken Heart Syndrome, Stress cardiomyopathy and apical ballooning Syndrome. The most common symptoms of TTS are acute chest pain, dyspnea or syncope. Thus, it IS indistinguishable from Acute myocardial infarction at first glance. Tts IS estimated to represent approximately 1 - 3 percent of all patients and 5 - 6 percent of female patients presenting with suspected STEMI. Diagnosis of TTS is IS is often challenging because its clinical phenotype may closely resemble AMI regarding electrocardiographic abnormalities and biomarkers. While widely established noninvasive tool allowing rapid and reliable diagnosis of TTS IS currently lacking, Coronary Angiography with left ventriculography IS considered the gold standard diagnostic tool to exclude or confirm TTS. Precise pathophysiological mechanisms of TTS are incompletely understood, but there IS considerable evidence that sympathetic stimulation IS central to its pathogenesis. Identifiable emotionally or physically triggering events precipitate Syndrome in most cases. Tts have been associated with conditions of catecholamine excess and activates specific cerebral regions. Physical triggers are more common than emotional stress factors. Of note, male patients are more often affected by physical stressful event,sss while in women, emotional triggers can be observed more frequently. Current evidence suggests that TTS IS caused by acute release of catecholamines from either sympathetic nerves, adrenal medulla or as drug therapy, and occurs primarily in patients with increased susceptibility of Coronary microcirculation and of Cardiac myocytes to Stress hormones leading to prolonged but transient leave Ventricular dysfunction with secondary myocardial inflammation. Although several anatomical TTS variants have been describe, four major types can be differentiated based on distribution of regional wall motion abnormalities. The most common TTS type and widely recognized form is IS apical ballooning type, also know as typical TTS form, which occurs in the majority of cases. Over past years, atypical TTS types have been increasingly recognize. These include midventricular, basal and focal wall motion patterns. A growing body of evidence reveals that acute cardiovascular events are not distributed randomly over time, but instead depend on time of day, day of week and months / season of year. Most conducted studies report summer preference for TTS, while one study reported winter peak.

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Takotsubo cardiomyopathy (broken-heart syndrome)

Years of gender - base research have shown that in matters of heart, sex differences abound. One striking example is temporary heart condition know as Takotsubo cardiomyopathy, also know as broken - Heart syndrome, first described in 1990 in Japan. More than 90% of Report cases are in women ages 58 to 75. Research suggests that up to 5% of women suspected of having a heart attack actually have this disorder. Most people recover with no long - term heart damage. Takotsubo cardiomyopathy is weakening of the left ventricle, heart's main pumping chamber, usually as result of severe emotional or physical stress, such as sudden illness, loss of loved one, serious accident, or natural disaster such as an earthquake. That's why the condition is also called stress - induce cardiomyopathy, or broken - Heart syndrome. The main symptoms are chest pain and shortness of breath. The precise cause isn't know, but experts think that surging stress hormones essentially stun the heart, triggering changes in heart muscle cells or coronary blood vessels that prevent the left ventricle from contracting effectively. Broken - Heart syndrome occurs more often in women than in men, especially after menopause. Takotsubo's symptoms are indistinguishable from those of heart attack. And electrocardiogram may show abnormalities similar to those found in some heart attacks in particular, changes known as - segment elevation. Consequently, imaging studies and other measures are needed to rule out heart attack. To get definitive diagnosis, clinicians look for the following: no evidence on angiogram of blockages in coronary arteries, most common cause of heart attacks. Rapid but small rise in Cardiac biomarkers. In heart attack, cardiac biomarkers take longer to rise but peak higher. Echocardiogram or other imaging technique that show abnormal movements in walls of the left ventricle. The most common abnormality in Takotsubo cardiomyopathy one that gives the disorder its name, is ballooning of the lower part of the left ventricle. During contraction, this bulging ventricle resembles tako - tsubo, pot used by Japanese fishermen to trap octopuses. Another term for disorder is apical ballooning syndrome. There is no standard treatment for broken - heart syndrome. It depends on the severity of symptoms, and whether person has low blood pressure or evidence of fluid backing up into the lungs. Clinicians often recommend standard Heart Failure medications such as beta blockers, ACE inhibitors, and diuretics. They may give aspirin to patients who also have atherosclerosis. Although there's little evidence for long - term therapy, beta blockers may be continue indefinitely to help prevent recurrence by reducing the effects of adrenaline and other stress hormones. It's also important to alleviate any physical or emotional stress that may have played a role in triggering the disorder. Most abnormalities in systolic function and ventricle wall movement clear up in one to four weeks, and most patients recover fully within two months. Death is rare, but Heart Failure occurs in about 20% of patients.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Case Reports

Table

AuthorAffiliation
Kristin Meigh, BSWest Virginia University School of Medicine, Morgantown, West Virginia
Madison Caja, BSWest Virginia University School of Medicine, Morgantown, West Virginia
Melinda Sharon, MPHWest Virginia University, Department of Emergency Medicine, Morgantown, West Virginia
Allison Tadros, MDWest Virginia University, Department of Emergency Medicine, Morgantown, West Virginia
Shane Dragan, MDWest Virginia University, Department of Emergency Medicine, Morgantown, West Virginia
David Henkel, MDWest Virginia University, Department of Emergency Medicine, Morgantown, West Virginia
Joseph Minardi, MDWest Virginia University, Department of Emergency Medicine, Morgantown, West Virginia; West Virginia University, Department of Medical Education, Morgantown, West Virginia

A 70 - year - old woman had to ED with chest pain and nausea. Symptoms start after receiving news about family members ' critical illness. Chest pain was described as heavy with radiation to her right upper extremity and was associated with dyspnea. No other symptoms were associated with chest pain. She had no history of previous cardiac disease. She was a smoker and her past medical history was significant for hyperlipidemia. Her vital signs were unremarkable, with a heart rate of 84 beats per minute, respiratory rate of 18 breaths per minute, blood pressure of 124 / 84 mmHg, and a temperature of 36. 7 Celsius. Her physical examination was also unremarkable. The initial ECG demonstrates normal sinus rhythm. Chest radiograph show hyperexpanded lungs with chronic obstructive changes but reveal no acute process. Focus performed by general EP without fellowship training or special interest in ultrasound revealed severely reduced leave ventricular systolic function with mid to apical hypokinesis and preservation of basal segments. Apical 4 - chamber and parasternal long axis FOCUS findings can be observed in Images 1 and 2, respectively. Takotsubo cardiomyopathy was strongly suspected based on these findings and patients presentation. She was treated with aspirin and typical measures for acute coronary syndrome and admitted to the cardiology service. Her troponin return at 595 ng / L and subsequent ECG showed lateral T - wave inversions. There were no significant changes in vital signs from time of presentation. She underwent a comprehensive echocardiogram that confirmed FOCUS findings. Because her troponins continued to rise, she underwent cardiac catheterization the following day, which revealed clean coronary arteries and supported diagnosis of TCM. Other than development of atrial fibrillation, her hospital course was unremarkable and she was discharged a few days later. A Follow - up echocardiogram seven weeks later demonstrate normal left ventricular function. She was no longer in atrial fibrillation, and the patient reported her symptoms had resolve.


Discussion and conclusions

Tcm represents approximately 1. 2% of troponin - positive acute Coronary syndromes. 6 term Takotsubo comes from the Japanese word for octopus pot, which appearance of affected Patients heart resembles, typically showing hypokinesis or ballooning of apical segments and hyperkinesis of basal segments. 7 This description matches the most common form of TCM, know as apical TCM. According to the International Takotsubo Registry, rare variants of TCM know as basal or reverse Takotsubo, occur in approximately 2. 2% of TCM Patients. 1 in this form, opposite presentation is see, with hypokinesis of basal heart and hyperkinesis of apical segments. 1 Two other variants, focal and midventricular TCM, have also been describe.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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Causes

The mechanism by which takotsubo cardiomyopathy develops is not entirely understood. In about 2 / 3 of cases, disease is preceded by intense emotional stress or physical stress. The hypothesis is that these stressors lead to release of large amounts of adrenaline and other stress - related hormones collectively know as catecholamines. This surge of hormones might lead to spasms of blood vessels and disruption of the ventricles of the heart, which would be responsible for ventricular dysfunction and ballooning seen in takotsubo cardiomyopathy.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

What causes takotsubo cardiomyopathy?

Medical experts do not know the exact cause of takotsubo cardiomyopathy. However, it is thought that about a third of cases are triggered by physical stress and about third are triggered by emotional stress. Car accident or other extreme physical event, asthma attack surgery, acute illness, death of loved one, marriage breakup, frightening medical diagnosis, job loss, sudden loss of money, domestic abuse. Sometimes takotsubo can occur after extremely happy event, such as winning a large sum of money or a family reunion. In about a third of cases, people are unable to identify any kind of stress that might have triggered their event. It is not an inherited condition like other cardiomyopathies, such as hypertrophic cardiomyopathy. You are more likely to experience takotsubo if youre female and have been through menopause. According to the international registry of people with takotsubo, approximately 90 percent of people who experience it are women, with an average age of 66.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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