Síndrome de Takotsubo / Takotsubo syndrome

El síndrome de Takotsubo es una miocardiopatía aguda con una clínica similar a la protagonizada por un síndrome coronario agudo, y que se caracteriza por insuficiencia cardiaca aguda y alteraciones reversibles de la función ventricular, en ausencia de enfermedad coronaria que las justifique. Este documento ofrece una revisión exhaustiva de las diversas hipótesis propuestas que intentan explicar la fisiopatología de esta enfermedad, y proporciona una revisión actualizada de las distintas clasificaciones surgidas en los últimos años. Además, describimos las principales características clínicas que estos pacientes presentan, las pruebas diagnósticas que se deben realizar y el tratamiento más adecuado

Takotsubo syndrome is an acute cardiomyopathy that mimics acute coronary syndrome and is characterized by acute heart failure with reversible ventricular motion abnormalities, in the absence of justifying coronary artery disease. This document offers an exhaustive review of various proposed hypotheses that attempt to explain the pathophysiology of this disease and provides an updated review of the different classifications that have emerged in recent years. In addition, we describe the main clinical characteristics of these patients, the diagnostic tests that must be performed and the most appropriate treatment

Clinical frailty and triggers in Takotsubo syndrome: the notable role of a new classification.

AIMS: Takotsubo syndrome (TTS) is a mainly transient and acute heart failure mimicking an acute coronary syndrome. Originally described in postmenopausal women, over time TTS has been associated with an increasingly advanced age. Emotional and physical triggers precipitating TTS have been correlated in most cases. The aim of our work was to detect differences between patients with or without recognizable triggers preceding the onset of symptoms. METHODS: We enrolled 22 consecutive patients. They were all women with an average age of 71 ±â€Š12 (range 40-90) years. Twelve patients correlated the onset of TTS symptoms with a trigger (group 1) and 10 patients (group 2) denied any correlation with stressful events. RESULTS: Patients in group 1 showed a higher average age than group 2 (76 ±â€Š10 vs. 64 ±â€Š12 years; P = 0.023), a longer hospitalization period (22 ±â€Š12 vs. 11 ±â€Š10 days; P = 0.01) and greater value of frailty score (P = 0.004). Despite a decrease and subsequent recovery of systolic function, there was no significant difference between groups. Group 1 showed a longer corrected QT (QTc) (505 ±â€Š53 vs. 453 ±â€Š42 ms, P = 0.03), a greater decrease in QTc at discharge (-57 ±â€Š44 vs. 0.3 ±â€Š39 ms; P = 0.004), with the result that at discharge both groups showed a comparable QTc. CONCLUSION: Our results emphasized that typical TTS female patients with precipitating triggers have advanced age, clinical frailty and QTc abnormalities.

Takotsubo is not a cardiomyopathy.

Unraveling the mechanisms underlying Takotsubo (TTS) leads to question the current inclusion of the condition within the spectrum of cardiomyopathies. Indeed, the clinical presentation and pathophysiology of TTS clearly differ from cardiomyopathies, i.e. diseases of heart muscle unexplained by abnormal loading conditions or coronary artery disease, which cannot recover spontaneously and may cause sudden death often in minimally symptomatic individuals or result in a gradual deterioration in ventricular function and end-stage heart failure. Furthermore, the term 'cardiomyopathy' can no longer be applied when functional or morphologic abnormalities of the coronary arteries leading to acute myocardial ischemia are deemed responsible for left ventricular (LV) systolic dysfunction. After 27years of investigation, time has come to recognize that patients with TTS do suffer from severe myocardial ischemia and fulfill all criteria of acute coronary syndromes, i.e. acute chest pain, typical electrocardiographic changes, cardiac troponin rise, as well as LV wall motion abnormalities. Accordingly, we propose that TTS should be labeled as an acute 'syndrome' to be included more appropriately within the spectrum of ischemic heart disease. With regard to the term 'stress', it may imply that the catecholamine surge is essential to produce the typical transient myocardial injury. Thus, the terminology 'Takotsubo (stress) syndrome' would more accurately reflect recent advances in the pathophysiology.

Stress cardiomyopathy: Is it limited to Takotsubo syndrome? Problems of definition.

In 2006, Takotsubo syndrome (TTC) was described as a distinct type of stress-induced cardiomyopathy (stress cardiomyopathy). However, when thinking about Takotsubo cardiomyopathy from the viewpoints of the AHA and ESC classifications, 2 possible problems may arise. The first potential problem is that a forecast of disease outcome is lacking in the ESC classification, whereas the AHA only states that 'outcome is favorable with appropriate medical therapy'. However, based on the literature data, one can make a general conclusion that occurrence of myocardial lesions in TTC (i.e., myocardial fibrosis and contraction-band necrosis) causes the same effects as in other diseases with similar levels of myocardial damage and should not be considered to have a lesser impact on mortality. To summarise, TTC can cause not only severe complications such as pulmonary oedema, cardiogenic shock, and dangerous ventricular arrhythmias, but also damage to the myocardium, which can result in the development of potentially fatal conditions even after the disappearance of LV apical ballooning. The second potential problem arises from the definition of TTC as a stress cardiomyopathy in the AHA classification. In fact, the main factors leading to TTC are stress and microvascular anginas, since, as has been already discussed, coronary spasm can cause myocardium stunning, resulting in persistent apical ballooning. Thus, based on this review, 3 distinct types of stress cardiomyopathies exist (variant angina, microvascular angina, and TTC), with poor prognosis. Adding these diseases to the classification of cardiomyopathies will facilitate diagnosis and preventive prolonged treatment, which should include intensive anti-stress therapy.

Comparison and outcome analysis of patients with apical and non-apical takotsubo cardiomyopathy.

BACKGROUND: Takotsubo cardiomyopathy (TTC) is a relevant differential diagnosis in patients presenting with signs of an acute coronary syndrome. Although recent literature has highlighted some salient features of this disorder, there has been little information elucidating the differences in clinical features, electrocardiographic findings, echocardiographic data and TTC-related complications associated with the different variants of TTC. METHODS AND RESULTS: Our institutional database constituted a collective of 114 patients diagnosed with TTC between 2003 and 2015 and these patients were subsequently divided into two groups based on the presence (n = 82, 72%) or absence (n = 32, 28%) of the apical form of TTC. The protocol for our proposed study was approved by the Ethics Committee of the University Medical Centre in Mannheim. It was noticed that the patients presenting with the apical form of TTC belonged to an older age group as compared to those presenting with the non-apical form (61.1 ± 8.9 years vs. 69.5 ± 11.2; P < 0.01). The QTc interval prolongation at index-event was observed to be quantifiably greater in the 'apical variant' patients group (484.8 ± 57 ms vs. 464 ± 34.1 ms; P = 0.06). With respect to cardiovascular risk factors, patients with arterial hypertension did have a higher predilection to present with the apical form (63.4% vs. 43.7%; P = 0.06), however, the impact of smoking was less pronounced in this patient group (24.4% vs. 50%, P = 0.01). Furthermore, our study highlighted a significant impact on ejection fraction (EF), with a compromised left ventricular function (36 ± 9% vs. 42.4 ± 9.7%, P < 0.01) and greater involvement of the right ventricle in the apical variant patients group (23% vs. 3%, P = 0.04). Patients with the apical form also showed a greater tendency to develop TTC-related complications such as cardiogenic shock and required longer monitoring and care in comparison. CONCLUSIONS: The apical and non-apical variants of TTC are manifestations of the same syndrome. They differ significantly, however, in their clinical presentation, related complications and prognosis.

[ECG in patients with tako tsubo cardiomyopathy]. / EKG bei Patienten mit Tako-Tsubo-Kardiomyopathie.

Takotsubo cardiomyopathy, also known as transient left ventricular ballooning and stress myocardiopathy, has been diagnosed increasingly more over the last decade. The takotsubo syndrome mimics acute myocardial infarction in symptoms and in electrocardiographic findings. There are two major types of takotsubo cardiomyopathy: the classical type with left ventricular apical ballooning and a type with midventricular ballooning. Both types show different electrocardiographic patterns at presentation. The present article describes classical electrocardiographic findings of the acute and subacute phases of takotsubo cardiomyopathy.

Unclassified cardiomyopathies in neuromuscular disorders.

OBJECTIVES: Unclassified cardiomyopathies (CMPs) include left ventricular hypertrabeculation or noncompaction (LVHT) and Takotsubo syndrome (TTS). Unclassified CMPs are frequently associated with noncardiac disease, including neuromuscular disorders (NMDs). This review aims at summarizing and discussing recent findings concerning the association of NMDs with unclassified CMPs. METHODS: Literature search using the database PubMed from 1966 to June 2013 was performed. RESULTS: LVHT has been described in association with dystrophinopathies, myotonic dystrophies, zaspopathies, laminopathies, dystrobrevinopathies, oculopharyngeal muscular dystrophy, tropomyosin-1 mutations, multiminicore disease, Danon disease, mitochondrial disorders, myoadenylate deaminase deficiency, Pompe's disease, glycogen storage disease-IV, fatty acid oxidation disorder, Barth syndrome, ryanodine receptor mutation, inclusion body myopathy, dystrophic epidermolysis bullosa, Charcot-Marie-Tooth neuropathy, hereditary cobolamine deficiency, beta-thalassemia, poliomyelitis, and Friedreich ataxia. Takotsubo syndrome has been described in association with myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barre syndrome, rhabdomyolysis, mitochondrial disorder, hypokalemia-related myopathy, syndrome malin, hereditary sensorimotor neuropathy, Beals syndrome, polymyalgia rheumatica, and unclassified myopathy. It is important for treating physicians to know about these associations because treatment and outcome of LVHT, including artificial ventilation, are determined by the presence or absence of an NMD. There are also indications that LVHT in NMDs favors the development of TTS. CONCLUSIONS: LVHT and TTS may be associated with NMDs. The pathogenetic link between unclassified CMPs and NMDs remains elusive. Outcome of LVHT and treatment of TTS are additionally determined by the presence or absence of an NMD.

Tako-tsubo, hypertrophic obstructive cardiomyopathy & muscle bridging--separate disease entities or a single condition?

We report a case of an apical ballooning syndrome using classical and high quality imagery. Co-existing features of asymmetrical septal hypertrophy, outflow tract obstruction, systolic anterior mitral valve motion and LAD myocardial bridging make the underlying patho-physiology difficult to ascertain. In conclusion we believe that this single case will promote discussion and add to an expanding literature base of the tako-tsubo cardiomyopathy syndrome.