Emergency stay triggered Tako-Tsubo syndrome: A case report and review of the literature

Transient apical ballooning of the left ventricle Tako-Tsubo Syndrome (TTS) or broken heart syndrome [1,2], is an acute cardiomyopathy associated with reversible kinetic disorders. These disorders mainly affect the middle and apical segments of the left ventricle in the absence of signifi cant lesions of the coronary arteries. The clinical appearance is similar myocardial infarction with a small increase in cardiac enzymes, which discord with the extent of left ventricular kinetic disorders, a crucial diagnostic criterion. This syndrome affects the menopausal woman often as a result of intense physicalemotional stress [2,3].


Introduction
Transient apical ballooning of the left ventricle Tako-Tsubo Syndrome (TTS) or broken heart syndrome [1,2], is an acute cardiomyopathy associated with reversible kinetic disorders. An episode of intense emotional of physical stress is reported in many cases prior to presentation. The pathophysiology remains unknown, but high levels of circulating catecholamine are presumed to be the triggering factor and the most favored explanation for this primary acquired cardiomyopathy.
We describe the case of 48-year-old women presenting Tako-Tsubo Cardiomyopathy (CTM), triggered 4 hours later during her stay in the emergency department to manage a hypertensive emergency.  in the Liepiecki, et al., [8] and 71±11 years in the Bybee, et al., [4]. We often fi nd stress triggering this cardiomyopathy. In the series of Tsuchihashi, et al., [6] (n=88), a possible trigger factor is found in 65% of cases, most commonly surgery. In Western series, the share of emotional stress seems more important.
Thus, the triggering factors of the Wittstein, et al., [10] and Sharkey, et al., [11] are exclusively of this order (Table 1).  and 100% [8]. The average age is high. He was 66±15 years old In our case, the triggering factor was probably the stress of stay in the emergency department responsible for an elevation of catecholamines which is incriminated in the occurrence of this pathology.
It has been shown that emotional stress from increased catecholamine levels can sometimes result in impaired left ventricular ejection fraction [15]. Pheochromocytoma and subarachnoid hemorrhage may also cause abnormalities of left ventricular contractility similar to the disorders found in Tako Tsubo Cardiomyopathy (TTC), and the pathophysiological mechanism of this left ventricular dysfunction is clearly the major elevation of catecholamines or intense sympathetic stimulation [16]. In Tako-Tsubo cardiomyopathy, catecholamine levels are also signifi cantly higher in the acute phase compared to those found in patients with myocardial infarction [10] and endomyocardial biopsies were found in patients with cardiomyopathy. Stress stigmas of toxicity of catecholamines. Coronary spasms, including coronary microcirculation, have also been suggested. The spastic hypothesis of large coronary trunks was quickly ruled out, whereas the fi rst Japanese studies initially favored this hypothesis (spasm caused only in 14% of cases) [6]. Anomalies of microcirculation have also been reported during the acute phase of Tako-Tsubo Cardiomyopathy (TTC) [17]. However, these perfusion abnormalities are probably a consequence of myocardial related to catecholergic discharges. Finally, an infectious origin (myocarditis) has been mentioned because left ventricular dysfunction does not correspond to a systemized territory of a coronary artery. However, the anatomopathological and magnetic resonance study of Tako-Tsubo cardiomyopathy (TTC) did not fi nd any signs of myocarditis, making it possible to eliminate this physio pathological hypothesis [12,18,19]. The prescription of long-term beta-blockers is not currently justifi ed, as no study has demonstrated its usefulness, in order to reduce the risk of recurrence.
Finally, it is important to make the diagnosis of Tako-Tsubo cardiomyopathy, because the similar clinical presentation of an acute coronary syndrome, the diagnosis is not easy made, it may delay diagnosis and must be known in order to provide the best chance at early detection and avoid a long-term treatment of ischemic heart disease. Thus, the patient will be exposed to a risk of unjustifi ed haemorrhage, given the prescription of dual antiplatelet therapy for one year.

Conclusion
Tako-Tsubo cardiomyopathy is a new cardiomyopathy  • Achievement of the more average apical portions of all the walls with normo or hyperkinesia of the basal segments.

Median form (25%):
• Achievement of the medial segments with respect to the apex and the basal collar. Takotsubo cardiomyopathy (TTC) and ischemic heart disease, or even myocarditis. The true limit of magnetic resonance imaging is its poor availability, with most often the completion of the examination several days after the acute phase.
Serious complications can occur in the acute phase and are mainly: cardiogenic shock, heart failure, mitral insuffi ciency, left intraventricular gradient, associated right ventricular dysfunction, left intraventricular thrombus formation (with its complications thromboembolic) and exceptionally left ventricular arrhythmias [9,18].
In the acute phase, the management of Tako-Tsubo Cardiomyopathy (TTC) should be from acute coronary syndrome to removal of coronary lesions from coronary angiography. Once the diagnosis of Tako-Tsubo cardiomyopathy is made, there is currently no formal recommendation. However, because of this left ventricular dysfunction, the prescription of the converting enzyme inhibitor and beta-blocker is advocated, at least until the recovery of the LVEF. In cases of cardiogenic shock, the intra-aortic counter-pulse balloon may be used, preferentially than pressurized amines, which may further aggravate a left intraventricular gradient, if he is present.