INTRODUCTION
Tako Tsubo Syndrome is a new diagnostic entity that consist in an acute cardiomyopathy which mimics acute miocardical infarction, it is a disorder that is associated with transient left ventricular dysfunction, but without any evidence of obstructive coronary artery disease.
This Syndrome, also known as Stress Cardiomyopathy and Transient Apical Ballooning Syndrome, was named "Tako Tsubo" because of the acute apical left ventricle dilatation that characterize this condition, in fact this disorder gives to the heart the appearance of a tako-tsubo, the Japanese word for octopus trap, so it took this name for its shape.
Due to the fact that this weakening condition of the heart can be the result of severe emotional or physical stress, such as a sudden illness, the loss of a loved one, a constant rejection, a natural disaster or a break-up it is also called Broken-Heart-Syndrome.
Main symptoms include chest pain and dyspnea accompanied by electrocardiographic changes, such as ST-segment elevation and T-wave inversions, minimal elevation of cardiac enzyme levels and transient wall-motion abnormalities in the absence of substantial coronary artery obstruction.
EPIDEMIOLOGY
This disorder was first described in 1990 in Japan, and it is considered a benign and reversible cardiomyopathy, in fact most people recover rapidly with no long-term heart damage.
This is a rare disorder, and its precise incidence is unknown, although years of gender-based research have shown that this rare syndrome involves more often the female sex, and most commonly post-menopausal, it is believed that from 0.7% to 2.6% of all patients with an initial primary diagnosis of an acute coronary syndrome may have Tako Tsubo disease.
Patients are typically Asian or Caucasian. In a literature review of cases in which race was reported: 57.2% were Asian, 40% were Caucasian, and 2.8% were other races.
Research suggests that more than 90% of reported cases are in women, and at least 6% of women evaluated for a heart attack actually have this disorder.
Furthermore the mean age has ranged from 58 to 75 years, with <3% of the patients being <50 years.
Moreover, there is an other difference between Tako Tsubo cardiomyopathy and myocardial infarction in terms of circadian rhythms: Tako Tsubo patients refer that the symptoms occur during the daylight hours, between 6.00am to 6.00pm; and it is probably related to the association between physical and psychological stress and the Tako Tsubo cardiomyopathy.
ETIOPATHOGENESIS
The pathogenesis of this disorder remain unclear and the cause has not been established yet; although several pathological mechanism have been proposed as possible causes of this disorder, including: coronary artery vasospasm, microcirculation dysfunction, and transient obstruction of the left ventricular outflow tract.
Also catecholamine overload, in fact published data suggest that substantially elevated plasma catecholamine levels seen in stress cardiomyopathy patients could be particularly relevant, and result in catecholamine-related toxic effects.
A number of features of stress cardiomyopathy, including its association with physical or emotional stress suggest that this disorder may be caused by diffuse catecholamine-induced microvascular spasm or dysfunction, resulting in myocardial stunning, or by direct catecholamine-associated myocardial toxicity.
In some patients with stress cardiomyopathy, the only apparent stressor is exposure to catecholamine or beta-agonist drugs in routine clinical doses.
Support for a possible pathogenic role for catecholamines comes from studies in which plasma catecholamines were measured at presentation. Combining the results from these series, plasma norepinephrine levels were elevated in 26 of 35 patients (74%). Elevated catecholamine levels and reversible left ventricle ballooning have also been observed in a rat model of immobilization-induced stress.
The magnitude of catecholamine excess associated with this disorder was illustrated in a report that measured plasma catecholamine levels in 13 patients with stress cardiomyopathy and seven patients with a Killip class III MI. Plasma catecholamines were significantly higher in the patients with stress cardiomyopathy as compared to those with MI: epinephrine (1264 versus 376 pg/mL) and norepinephrine (2284 versus 1100 pg/mL). However, elevation in blood catecholamine levels is not uniformly present and some studies have reported normal levels.
It's also possible that some drugs , rarely, may cause broken heart syndrome by causing a surge of stress hormones. Drugs that may contribute to broken heart syndrome include: Epinephrine, which is used to treat severe allergic reactions or a severe asthma attack, Duloxetine (Cymbalta), a medication given to treat nerve problems in people with diabetes, or as a treatment for depression, Venlafaxine (Effexor XR), which is a treatment for depression, Levothyroxine (Synthroid, Levoxyl), a drug given to people whose thyroid glands don't work properly.
SYMPTOMS AND SIGNS
Chest pain and dyspnea(shortness of breath) are the most common presenting symptoms .
The chest pain often has the characteristics of angina, and it occurs after severe stress.
Cardiac arrest, syncope and arrhythmias have also been described.
In patients who are already critically ill with other medical conditions, a clue to the diagnosis may be clinical worsening, or may be incidentally discovered after noting ECG changes or biomarker elevations. The symptoms and signs are similar to those seen in other acute cardiac conditions characterized by acute myocardial ischemia or heart failure, such as acute coronary syndrome and myocarditis, and hence do not help in the differential diagnosis.
DIAGNOSIS
The diagnosis of Tako Tsubo Cardiomyopathy remains controversial. The diagnostic criteria most widely accepted were published by the Mayo Clinic in 2004. In 2008, a new criterion was added to them: a normal epicardial coronary artery. This disease was characterized by acute balloon-like dilation in the LV apex.
The are six main symptoms that are especially indicative of this syndrome: (1) acute onset and stressful inducement: One of the unique features of Tako Tsubo Cardiomyopathy is its relation with stressful emotional or physical events. Unlike acute coronary syndrome, with an onset peak early in the morning, Tako Tsubo presents in the afternoon in most cases when stressful inducible events are likely to occur; (2) electrocardiographic characteristics: Although the initial electrocardiogram (ECG) of patients with Tako Tsubo Cardiomyopathy is nonspecific, an ST segment elevation can be found mainly in the precordial leads in 50% of patients at onset. In addition, reciprocal ST-segment depression in the inferior wall leads is unlikely. In comparison with patients with base deformity, inverted T waves are more frequently observed in patients with apex balloon-like dilation and they resolve spontaneously within a few weeks to several months. Furthermore, this syndrome usually present abnormal Q waves in precordial leads. These Q waves are transient in most patients and generally resolve within a few days to several weeks; (3) cardiac enzymes: In most patients there is slight elevation in the cardiac enzyme level on admission. The enzyme levels decrease rapidly and do not seem to have prognostic significance; (4) absence of coronary lesion: It is characteristic that no specific coronary lesions are detected. Generally, patients with Tako Tsubo Cardiomyopathy have chest pain, changes in ECG, elevation of cardiac enzyme levels, and wall motion abnormalities. Therefore, coronary angiography has to be conducted to rule out acute coronary syndrome; (5) balloon-like dilation of the ventricle: In contrast with acute myocardial infarction, LV wall motion abnormalities are found beyond a single coronary artery perfusion area. Most patients show loss of motion or hypokinesia at the apex and an apical balloon-like dilation pattern associated with preservation of the base. However, cases of a Tako Tsubo Cardiomyopathy subtype without abnormalities of the apex were also been reported. This desease is essentially characterized by LV failure, although, approximately, one-third of patients also have abnormalities in the right ventricle. Cardiac magnetic resonance imaging is a suitable method to establish the diagnosis of Tako Tsubo Syndrome because this modality allows the accurate identification of reversible myocardium damage by visualization of wall motion abnormalities in each area, quantification of ventricular function, and assessment of inflammation and fibrosis. It could enable early treatment of acute symptoms, raise awareness, and improve clinical outcomes. Cardiac magnetic resonance is appropriate to evaluate wall motion abnormalities and LV ejection fraction. (6) recovery of cardiac function: One of the characteristics is that thorough recovery of cardiac function is achieved. In contrast to other serious wall motion abnormalities at onset, recovery of ventricular function is proven in follow-up evaluations. Most patients with Tako Tsubo Syndrome show significant improvement of systolic function within a week and achieve complete recovery by the end of third or fourth week after onset. Generally, another diagnosis should be considered in patients with suspected Tako Tsubo Cardiomyopathy whose systolic function is not normalized within 12 wk after onset.
The differential diagnosis of Tako Tsubo Cardiomyopaty includes the following: esophageal spasm, gastroesophageal reflux disease, myocardial infarction, myocardial ischemia, unstable angina, acute coronary syndrome, angina, aortic dissection, myocarditis, acute pericarditis, pneumothorax, cardiogenic pulmonary edema, pulmonary embolism, Boerhaave syndrome (spontaneous esophageal rupture), cardiac tamponade, cardiogenic shock, cocaine-induced cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, and coronary artery spasm.
As shown by these diagnostic criteria, the patients with Tako Tsubo Cardiomyopathy have non-specific or normal findings on physical examination; however, the clinical course resembles that of acute coronary syndrome or acute decompensated heart failure. The most common presenting symptoms listed in the diagnostic criteria are chest pain and dyspnea. In rare cases, patients developed palpitations, nausea, vomiting, syncope, or cardiogenic shock.
Cardiac Biomarkers
Consistent with the ECG findings, this syndrome is associated with only midly elevation in cardiac myonecrosis biomarkers such as CK and Troponin. This is not proportionate to the width of regional wall motion abnormalities seen on imaging tests: echocardiogram, left ventriculogram or cardiac magnetic resonance.
It was reported creatinine kinase elevation in 56% of the patients. Subsequent studies using cardiac troponin report almost universal elevations. The pattern of troponin elevation differs considerably from acute STEMI. Peak troponin T levels are modest, mean ~60-fold the upper limit of normal as opposed to >400-fold the ULN for acute STEMI similar to those seen in N-STEMI. This finding of modest elevation of troponin in patients with Tako Tsubo can be used as a criterion for differentiating with STEMI.
Plasma B-type natriuretic peptide (BNP) levels are usually higher in Tako Tsubo than in STEMI, and also the ratio of BNP to peak troponin levels may differentiate this two diseases. The levels of BNP (as well as NT-pro BNP) may correlate with the amount of myocardial dysfunction, but not hemodynamic parameters and can remain elevated for months following the acute event. These patterns of biomarker elevations are important, but there is not yet a threshold that has been identified that can be clinically meaningful or specificy to have a differential diagnosis between acute myocardial infarction and Tako Tsubo Cardiomyopaty.
Echocardiography
The typical finding is of apical ballooning of the left ventricle. This is due to akinesia, hypokinesia, or dyskinesia of the apical and middle segments of the LV and hyperkinesia of the basal segments. Some disturbances of contractility are similar to those that occur in systemic hypertension due to an increase in afterload. The LV Ejection Fraction is low or very low from the initial phase, with values below 30% in some cases and up to 75%. In the subacute phase, global and segmental systolic function and the electrocardiographic changes improve over a period of days, weeks, or a few months, until they stabilize with an LVEF above 50%. In general, echocardiography is normal at 1 year; the rate of recovery is more rapid in Asians than in whites.
The descriptions of diastolic function mainly use transmitral flow, and ignore information from the pulmonary veins or from tissue. Furthermore, little use has been made of intravenous echocardiographic contrast, which has enabled intraventricular thrombi and abnormalities of the coronary microcirculation to be detected, or dobutamine echocardiography, which can reveal underlying dysfunction.
Changes in the LVEF are initially similar to those seen in ischemic heart disease, although recovery is better in patients with Tako Tsubo. Functional valve disturbances can also develop, including: 1) mild-moderate tricuspid regurgitation (50%) associated with pulmonary hypertension (mean pulmonary arterial pressure 46.6±10.5 mmHg)in 33%; 2) mild-moderate aortic insufficiency (12.5%); and 3) mitral insufficiency of grade 2 or higher, present in 9.7–62.5%. Systolic anterior movement may be observed (6.67%) and a gradient in the LV outflow tract (43–100 mmHg) (20–35.71%). These findings are usually associated with a Killip III–IV infarct (50%) and higher levels of cardiac enzymes. Mitral insufficiency leads to a lower LVEF and a slow ventricular recovery (79%), with complete recovery of the syndrome occurring at around 6 months, although 8.1% continue to present mitral insufficiency of grade 2/4 or higher. Severe mitral insufficiency is a cause of death in 14.29%. Tricuspid insufficiency reverts and the pulmonary hypertension disappears in 13.33%.
ECG Findings
Although the initial electrocardiogram (ECG) may be non-specific or normal, the majority (11–100%) present elevation of the ST segment, particularly affecting the anterior wall (36–100%) and, more rarely, the inferior or lateral walls (4–50% and 5–70%, respectively) or in aVR. ST segment depression has been reported in 6–23%. These changes may be very dynamic. An absence of R-wave progression in the anterior wall may also be seen (7–32%). T wave inversion is very common (17–100%), and may be associated with a poorer prognosis; however, peaked T waves sometimes predominate (86%). A long QTc interval is seen in 50–100%. Pathological Q waves are observed in 20–63% and new bundle branch blocks develop in approximately 6–8%.
Racial differences exist in the electrocardiographic changes, with a higher frequency of inverted T waves in whites, and a higher incidence of ST elevation in Asians; in blacks the initial ECG is more commonly normal, with a rapid progression to T wave inversion and a prolonged QTc interval. The course of the changes usually shows ST elevation or depression for 1 to 2 days, and there may even be new intraventricular conduction disturbances. In the subacute phase, the ST changes normalise and disturbances of the QTc interval develop but disappear rapidly; T wave inversion develops in parallel with lengthening of the QTc interval but is of longer duration (1–4 months).
Pathological Q waves (myocardial stunning) may be observed in the chronic phase, but disappear more rapidly than in cardiac ischemia, although they may persist indefinitely in 10% of cases.
T wave inversion and the long QTc interval persist after normalisation of the echocardiographic images, whereas R wave progression normalises in parallel with the improvement in motility. All these electrocardiographic changes can usually resolve within 3 weeks to 1 year.
A case series from Mayo Clinic divided 105 retrospectively identified patients meeting the criteria for Tako Tsubo Cardiomyopaty into 3 groups according to the ECG at presentation. One group had ST segment elevation >1 mm in 2 contiguous leads or new left bundle branch block (ie, typical ST-segment elevation (STEMI) criteria); the second group had T-wave inversion >3 mm in 3 contiguous leads without significant ST shifts; and the third group had nonspecific ST-segment changes or a normal ECG.
Each group comprised approximately one-third of the overall cohort, with no discernable difference in clinical presentation or outcomes in the groups.
Another series from the Minneapolis Heart Institute evaluated 59 consecutive patients with Tako Tsubo Cardiomyopaty. ST-segment elevation was present in 56% of patients, predominantly in the precordial leads; 17% had widespread T-wave inversion, 10% had healed anterior myocardial infarction (abnormal Q waves or abnormal R wave progression in 2 or more contiguous anterior leads); 17% had either normal ECG or non-specific changes. When compared with patients presenting with Myocardial Infarction because of left anterior descending coronary artery occlusion, they found that the mean amplitude of ST-segment elevation was lower in the Tako Tsubo cardiomyopaty group than in the left anterior descending coronary artery occlusion group (1.4 vs. 2.4 mm), but there was significant overlap. There was no significant difference in the presence of abnormal anterior Q waves or 12-lead QRS amplitude between the groups.
Unfortunately, all the criteria don't have perfect diagnostic accuracy and do not allow for reliable differentiation between the 2 conditions in the emergency setting to guide the management.
In the subacute phase of Tako Tsubo, beyond the acute setting, the evolution of the ECG is often stereotypical. Following resolution of ST segment elevation, diffuse deep T-wave inversion develops. Q waves are uncommon and usually transient. QT prolongation is almost universally reported.
There was a study that aimed to clarify the phases of the ECG in 9 women with Tako Tsubo. They suggested 4 phases: initial ST elevation, followed by transient T-wave inversion (days 1–3) then T-wave recovery in some patients (days 2–6) followed by giant T-wave inversion associated with prominent QT prolongation, which persisted for up to at least 2 months. This evolution of findings may seem to be of some benefit in differential diagnosis, but any of these ECG patterns may be seen in myocardial ischemia caused by coronary artery disease. The deep T-wave inversions associated with QT prolongation, often described as the typical ECG of Tako Tsubo Cardiomyopaty.
PATHOPHYSIOLOGY
The exact pathogenesis of Tako Tsubo is unknown, but various hypotheses have been suggested and discussed, including coronary microvascular dysfunction, coronary artery spasm, catecholamine-induced myocardial stunning, reperfusion injury following acute coronary syndrome, myocardial microinfarction and abnormalities in cardiac fatty acid metabolism. Currently, catecholamine-induced cardiotoxicity and microvasculature dysfunction are the most supported theories.
Cathecolamine Theory
It was found that the serum catecholamine concentration was two to three times greater in patients with Tako Tsubo than that in patients with myocardial infarction, and described that serious emotional stress is a precipitating factor.
Catecholamine activation of alpha-adrenoceptors and beta-adrenoceptors is the primary trigger of Tako Tsubo changes. Catecholamine concentrates such as epinephrine and norepinephrine levels have been noted to be high during the acute phase of Tako Tsubo.
There is a theory, called: "stimulus trafficking” that could explain the decline of myocyte contractile function in patients with Tako Tsubo Cardiomyopaty: supraphysiological levels of catecholamines induce β2-coupling from Gs to Gi .
Therefore, the decline of myocyte contractile function is evidenced by hypokinesia in ECG. Involvement of the apex can be attributed to higher adrenoceptor density in the apex than in the base, it was also noted an increased beta-2 concentration gradient from apex to base. These observations support the hypothesis that, during times of stress when epinephrine is the main circulating catecholamine, regional differences in adrenaline sensitive b2-receptors could explain the myocardial response to the catecholamine surge.
The base of stimulus trafficking is that a switch to Gi occurs to protect the myocytes from the strong stimulation of Gs, which causes apoptosis. Slow increases in serum troponin level explain early minimal necrosis of the myocardial tissue. showed increased activity of the phosphatidyl inositol 3-kinase-protein kinase B (PI3K/AKT) signaling pathway, which has important anti-apoptosis functions and plays a role in the rapid recovery of myocytes. Thus, the transient LV dysfunction can be attributed to the PI3K/AKT pathway and inversely switching from Gi to Gs, associated with the homogeneous, prompt and clinically thorough recovery of systolic function observed in Tako Tsubo patients.
Furthermore, myocardial biopsy of patients with TCM showed regions with contraction band necrosis, inflammatory cell infiltration, and localized fibrosis. These changes were caused by direct catecholamine toxicity on cardiac muscle cells. C-reactive protein levels and white blood cell counts increased with the increase in norepinephrine levels in patients and it is possible that catecholamines produced more systemic inflammation with the induction of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6. Several studies have pointed out that the remarkable myocardial edema, occurs despite normal perfusion, which provides further evidence to support the inflammation theory. It was examined restraint stress in rats with Tako Tsubo Cardiomyopaty and reported that heme oxygenase 1 (HO-1) levels, a marker of oxidative stress that has cardioprotective properties, was increased significantly. Macrophages play an important main role in oxidative stress induction and expression of β- and α-adrenergic receptors. As a result of pretreatment with β- and α-antagonists, HO-1 expression and its altering gene expression, decreased.
Oestrogen Deficiency Theory
Also oestrogen deficency can be seen as a possible cause of Tako Tsubo disease, in fact more than 90% of patients presenting with Tako Tsubo syndrome are postmenopausal women. Animal models have demonstrated the cardioprotective properties of oestrogen. Experiments showed that when ovariectomised rats without oestradiol supplementation were exposed to immobilisation stress they demonstrated significantly greater increases in the heart rate and reduction in LV function in comparison to rats that had oestradiol supplementation. The myocytes are known to express oestrogen receptor-α and estrogen receptor-β. estrogen enhanced transcription of cardioprotective factors such as heat shock protein and atrial natriuretic peptide, and in turn, protected against the toxic effects of catecholamines, calcium overload and reduced oxidative stress. This evidence leads to the concept that postmenopausal women lose the protective effect of oestrogens, which may render them at risk of exaggerated response to circulating catecholamines.
RISK FACTORS
Furthermore there are some risk factors that can also be seen as candidates that may collaborate in causing Tako Tsubo Syndrome.
Lack of estrogen .
Infact, data says that about 90% of patients with Tako Tsubo Syndrome are post-menopausal women, and it can be related to the loss of the cardioprotective properties of estrogen that women have before the menopausal period.
Emotional or physical stress inducers.
It was also demonstrated that this syndrome often occur after an intense source of mental or physical stress. This stress can stimulate the cerebral cortex, that results in activation of sympathetic nervous system that cause an high secretion of cathecolamines. The cathecolamines have multiple effects: 1)Microvascular spasm that cause low myocardial pefusion; 2)Obstruction of left ventricle efflux tract; 3)Direct myocite damage; 4)Metabolic disorders. All the cathecolamines effects may finally cause the typical myocardial stunning of Tako Tsubo Disease.
Genetic Factors .
Certain polymorphisms of α- and β-adrenergic receptors are associated with neurogenic stunned myocardium that occurs as symptom of subarachnoid hemorrhage and has overlapping pathophysiology with Tako Tsubo Syndrome. Although adrenoceptor polymorphisms have not yet been identified in patients with TCM, patients with this disease showed L41Q polymorphism of G protein coupled receptor kinase (GRK5) more frequently compared with the control group. L41Q polymorphism of GRK5 responds to catecholamine stimulation and attenuates the response of β-adrenergic receptors. Under catecholamine stimulation, balloon dilation of the ventricle may occur either by negative inotropic effect by β-receptor decoupling or ischemia because of an imbalance between α1-adrenergic coronary artery vasoconstriction and β-adrenergic vasodilation. These reports suggest the very interesting possibility that the susceptibility to the apical balooning syndrome in individuals may be partially related to genetic factors.
TREATMENT
The most common presentation is chest pain with ST segment elevation in anterior leads mimicking anterior STEMI. Therefore the initial treatment is most likely to be based on suspicion of anterior STEMI. Therefore initial history such as emotional stress is important and Tako Tsubo should be suspected in all post-menopausal women who presents with anterior STEMI. The advantage of primary angioplasty is acute STEMI can be ruled out with angiography and the left ventriculogram may give the diagnosis of Tako Tsubo at an early stage.
The main management in patients with TCM during the acute phase is supportive and mainly symptomatic treatment. Intra-aortic balloon pump equipment is required for hemodynamically unstable patients in addition to cardiopulmonary circulatory support and continuous veno-venous hemofiltration. There is no consensus on pharmacological management of TCM and due to the rarity of this condition.
The use of b-blockers has been specifically advocated due to the possible abnormal response to excessive catecholamines. This is also supported by evidence from animal model studies which demonstrated that the resolution of ST segment elevation was successfully achieved by combined α and β adrenoceptor blockade. Furthermore α and β adrenoceptor blockers may have a role in prevention of stress induced cardiac dysfunction.
For patients with severe LV outflow tract obstruction with hemodynamic compromise, treatment with a β-blocker or α-adrenoceptor agonist such as phenylephrine and volume expansion should be considered. Calcium channel blockers can be used to decrease LV outflow tract pressure gradient. It is importat to avoid treatment with nitrites or inotropic drugs in these cases. For patients with suspected vasospasm, the use of calcium channel blockers such as verapamil or diltiazem is suggested.
Hemodynamically stable patients are often treated with diuretics, angiotensin-converting enzyme (ACE) inhibitors and β-blockers. To reduce the risk of thromboembolism, patients with loss of motion of the LV apex should be treated with anticoagulant therapy until the contractility of the apex is improved unless there is a definite contraindication.
There is no consensus regarding long-term management of TCM, although it is reasonable to treat patients with β-blockers and ACE inhibitors during the ventricular recovery period. However, no data support the continuous use of these drugs for the prevention of TCM recurrence or improvement of survival rate. After LV function normalizes, physicians may consider discontinuation of these drugs.
PROGNOSIS AND RECURRENCE
Patients with Tako Tsubo Cardiomyopathy usually have generally a good prognosis but a small subset has potentially life-threatening complications., and almost perfect recovery is observed in 96% of the cases.
Mortality rate in hospital vary at one to two percent. This syndrome was thought to follow a relatively benign course. However, approximately 5% of patients experienced cardiac arrest. While their long-term survival rate is the same as that in healthy subjects, patients with Tako Tsubo have a greater risk of death at the time of initial onset. The most frequent complaint was chest pain (30%) and that recurrence of the symptom occurred in 11% of patients after a 4-year follow-up. Some studies have been conducted to assess prognostic indicators such as ECG findings, signs of thrombolysis in myocardial infarction, grade of myocardial perfusion, and N-terminal pro-brain natriuretic peptide level. However, a definite outcome marker has not been established.
Furthermore in most cases, RWMA resolves spontaneously within a matter of days to a few weeks. However, there are cases of Tako Tsubo cardiomyopathy in which RWMA persisted for more than 3 months.
The precise reason remains unclear. In these cases, the patients require long-term management of heart failure or apical thrombosis.
CONCLUSION
A lot of attention has been focused on Tako Tsubo cardiomyopathy recently and this entity has been characterized as a transient left ventricle dysfunction with rapid recovery generally induced by a stressful emotional or physical event. The number of cases continues to increase. Because of close resemblance of its presentation and clinical course to acute myocardial infarction, Tako Tsubo should be included in one of the differential diagnosis for acute myocardial infarction. Although the cause of this disease has not been completely understood, some promising hypotheses have been suggested. The occurrence of this disease is attributed to the large-scale production of catecholamines that causes myocardial hypokinesia with direct cardiomyocyte toxicity and induction of coronary microvascular dysfunction. In order to that Tako Tsubo cardiomyopathy is an important disease that has to be differentiated from acute myocardial infarction promptly for appropriate management.
Its prognosis is generally favorable, but monitoring the clinical course is essential to prevent or treat acute complications.
It is necessary to clarify the pathophysiology for establishment of its optimal management. Further, the high prevalence of this syndrome in postmenopausal women suggests an important role of estrogen for myocardial protection. Another hypothesis includes oxidative/inflammatory stress-induced myocardial dysfunction. Although the treatment of Tako Tsubo remains controversial, adrenergic blockade is suggested as a reasonable therapy based on the presumptive pathophysiology of the disease.
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