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Takotsubo cardiomyopathy, also known as transient apical ballooning, stress-induced cardiomyopathy and simply stress cardiomyopathy, is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium (the muscle of the heart). Because this weakening can be triggered by emotional stress, such as the death of a loved one, the condition is also known as broken heart syndrome .
The typical presentation of someone with takotsubo cardiomyopathy is a sudden onset of congestive heart failure or chest pain associated with EKG changes suggestive of an anterior wall heart attack. During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted. It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name "tako tsubo", or octopus trap in Japan, where it was first described. The etiology (cause) appears to involve high circulating levels of catecholamines (ie, adrenaline). Evaluation of individuals with takotsubo cardiomyopathy typically include a coronary angiogram, which will not reveal any significant blockages that would cause the left ventricular dysfunction. Provided that the individual survives their initial presentation, the left ventricular function improves within 2 months. Takotsubo cardiomyopathy is more commonly seen in post-menopausal women. Often there is a history of a recent severe emotional or physical stress.
Additional recommended knowledge
The etiology of takotsubo cardiomyopathy is not fully understood, but several mechanisms have been proposed.
It is likely that there are multiple factors at play which could include some amount of vasospasm, failure of the microvasculature, and an abnormal response to catecholamines (such as epinephrine and norepinephrine, released in response to stress).
Case series looking at large groups of patients report that some patients develop takotsubo after an emotional stressor, while others have a preceding clinical stressor (such as an asthma attack or sudden illness). Roughly one third of patients have no preceding stressful event .
While the original case reports reported on individuals in Japan, takotsubo cardiomyopathy has been noted more recently in the United States and Western Europe. It is likely that the syndrome went previously undiagnosed before it was described in detail in the Japanese literature.
The diagnosis is made by the pathognomic wall motion abnormalities, in which the base of the left ventricle is contracting normally or are hyperkinetic while the remainder of the left ventricle is akinetic or dyskinetic. This is accompanied by the lack of significant coronary artery disease that would explain the wall motion abnormalities.
Focal myocytolysis is reported as an origin of this cardiomyopathy. No microbiological agent has been associated so far with Takotsubo cardiomyopathy. Kloner et al reported that a pathologic change in the myocardium was not demonstrated in the stunned myocardium.Infiltration of small mononuclear cells has been documented in some cases; these pathologic findings suggest that this cardiomyopathy is a kind of inflammatory heart disease, but not a coronary heart disease. There is also a report describing histologic myocardial damage without coronary heart disease.
The treatment of takotsubo cardiomyopathy is generally supportive in nature. In individuals with hypotension, support with inotropic agents or an intra-aortic balloon pump have been used. In many individuals, left ventricular function normalizes within 2 months.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Takotsubo_cardiomyopathy". A list of authors is available in Wikipedia.|