ReviewTakotsubo cardiomyopathy systematic review: Pathophysiologic process, clinical presentation and diagnostic approach to Takotsubo cardiomyopathy
Section snippets
Definition
In 1990, takotsubo cardiomyopathy (TTC) was initially reported by Sato et al. in Japan [1], [2]. “Takotsubo” is named after Japanese octopus trap, whose shape is similar to the appearance of the patient's left ventricle in systole. (Fig. 1) TTC is described as a transient reversible cardiomyopathy, which typically occurs in older women after emotional or physical stress [3], [4], [5]. The presenting features of TTC are similar to those of myocardial ischemia after acute plaque rupture, but the
Epidemiology
One study in the United States results show there were 6837 patients diagnosed with TTC in the Nationwide Inpatient Sample database of 2008 and women were found to have higher odds of developing TTC (odd ratio 8.8). In absolute number of admissions, 6178 (90.4%) were women, and 660 (9.6%) were men. Patients aged from 18 to 34 were 127 (1.9%), patients aged from 35 to 49 were 581 (8.5%), patients aged from 50 to 64 were 1975 (28.9%), patients aged from 65 to 79 were 2952 (43.2%), and patients ≥ 80
Pathophysiology
The pathophysiology of TTC is not well established, but several possible theories on mechanisms with this disorder have been proposed [5], [12], [13].
Clinical presentation
TTC represents an estimated 1% to 2% of patients who present with an acute coronary syndrome [6], [36], [37]. Of 1750 patients with TTC, 89.8% were women and the mean age was 66.4 ± 13.1 years. Emotional triggers were not as common as physical triggers (27.7% vs. 36.0%), and 28.5% of patients had no evident trigger [38]. In the acute phase, the clinical presentation, electrocardiographic findings, and biomarker profiles are often similar to those of an acute coronary syndrome [3], [4], [6], [38],
Diagnosis
There is no single universally accepted diagnostic definition of TTC. TTC is a very common illness, often undetected. Current diagnostic criteria are restrictive, and thus they need to be “liberalized”. We follow the opinion of John Madias that there are many atypical and mild forms of TTC and that many patients have a “takotsubo component” as comorbidity to an acute coronary syndrome [44]. Under this condition, we would like to introduce the fact that several diagnostic criteria have been
Differential diagnosis
As we already mentioned in the above diagnostic criteria, the following conditions must be excluded in the diagnosis of TTC.
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 [10], [49], [18]. (Fig. 2) Furthermore, the additional presence of right ventricular apical akinesia during echocardiographic examination makes the diagnosis of this syndrome very likely [71].
The median left ventricular ejection fraction on the initial echocardiogram was 20% (interquartile range,
Catecholamine
TTC may be caused by catecholamine-induced microvascular spasm or by direct catecholamine-associated myocardial toxicity [5]. Recent evidence suggests that the pathophysiology of TTC may lie in changes in β-adrenergic receptor signaling [19]. Wittstein et al. compared admission plasma catecholamine concentrations between a group of 13 patients with stress cardiopathy who had transient apical ballooning and a group of 7 patients hospitalized for acute myocardial infarction (Killip class III).
Treatment
Since the initial presentation mimics AMI, initial management should be directed toward the treatment of myocardial ischemia with oxygen inhalation, intravenous heparin, aspirin (the treatment of myocardial infarction imply double platelet antiaggregation) and β-blockers. After confirmation of TTC, aspirin (antiaggregation) can be discontinued if there is no incidental coronary artery disease. Thrombolytic agents should not be administered because they have no benefit in TTC, and can give rise
Prognosis
Prognosis is generally favorable, but a small subset has potentially life-threatening complications [82]. The in-hospital death rate ranges from 0% to within 10% [3], [8], [49], [84], [85]. One study of the national inpatient sample 2008 to 2009 with a total of 24,701 TTC patients notes in-hospital mortality was 1027 (4.2%). Of 24,701 patients with TTC, 8640 (34.5%) patients have acute cardiac complications such as acute CHF, cardiac shock, respiratory failure with CHF, cardiac arrest, etc. and
Conflict of interest
The authors report no relationships that could be construed as a conflict of interest.
Acknowledgment
The authors thank Prof. Yoshio Kobayashi , Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, for his permission of several clinical images.
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