Takotsubo cardiomyopathy

Takotsubo cardiomyopathy. Also known as Broken Heart Syndrome or Transient Apical Dysfunction, it is a type of nonischemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium .


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  • 1 Presentation
  • 2 Etiology
  • 3 Histology
  • 4 signs and symptoms
  • 5 Clinical manifestations
  • 6 Diagnosis
  • 7 Treatment
  • 8 Prevention
  • 9 Sources


The typical presentation of a person with Takotsubo Cardiomyopathy is a sudden onset of congestive heart failure or chest pain associated with abnormalities on the electrocardiogram that suggest an acute myocardial infarction of the anterior wall.

During the course of patient evaluation, a bulge of the tip of the left ventricle is frequently observed with hypercontractility of the base of the left ventricle. It is this feature that gave the syndrome the name “tako tsubo”, or octopus trap in Japan , where it was first described.

The cause appears to involve high levels of circulating catecholamines (primarily epinephrine / epinephrine ). Assessment of people with Takotsubo Cardiomyopathy typically includes coronary angiography , which may not reveal some significant obstructions that may cause left ventricular dysfunction.

When the person survives their initial presentation, left ventricular function improves within 2 months. Takotsubo cardiomyopathy is more frequent in postmenopausal women. It usually presents a story with recent severe physical or emotional stress .


The etiology of Takotsubo Cardiomyopathy has not yet been fully explained, however, various mechanisms have been proposed.

Case series to large patient groups report that some patients develop Takotsubo cardiomyopathy after emotional stress, while others have a prior clinical stressor (such as an asthma attack or sudden illness).

Approximately one third of patients have no history of previous stressful events.


Focal myocytolysis has been reported as a source of this cardiomyopathy . Until now, no microbiological agent has been associated with Takotsubo Cardiomyopathy. Pathological findings suggesting that this cardiomyopathy is a kind of inflammatory disease, but not a coronary disease. There is also a report describing histological myocardial damage without coronary heart disease.

Signs and symptoms

The most common signs and symptoms of broken heart syndrome are chest pain and shortness of breath. In this syndrome, these symptoms usually occur suddenly in people who had no history of heart disease .

Arrhythmias or cardiogenic shock may also occur . Cardiogenic shock is a situation in which the weakened heart cannot pump enough blood to meet the body’s needs.

Some of the signs and symptoms of broken heart syndrome are different from those of heart attack . For example, in people with broken heart syndrome, the following happens:

  • Symptoms occur suddenly after suffering extreme emotional or physical stress.
  • The results of the electrocardiogramdo not look like those of a person who has a heart attack.
  • Blood tests show no signs or slight signs of heartinjury .
  • Tests show no signs of blockage of the coronary arteries.
  • Tests show unusual swelling and movement of the left lower chamber of the heart (the left ventricle).
  • Recovery time is fast, usually between days and weeks, compared to a heart attack, which is a month or more.

Clinical manifestations

The clinical and laboratory manifestations are extremely similar to those of a patient with an ongoing AMI, even with regard to the elevation of the so-called cardiac enzymes. So much so, that it has been postulated that between 1% and 2% of cases currently treated as acute coronary events have gone unnoticed, in part because of the benign and reversible nature of the condition.


There is no unified definition of its basic diagnostic criteria, which is why its actual prevalence is unknown. A series of diagnostic criteria were initially proposed by Abe and Kondo in 2003 , who took as major criteria the presence of a reversible abnormality in the movements of the apical wall of the left ventricle, and the evidence of electrocardiographic alterations that simulated an AMI. The same authors also demarcated three minor criteria, which consisted of the presence of a previous stressful event that could have triggered the crisis, a limited elevation of cardiac enzymes, and the presence of precordialgia.


Optimal treatment remains fully empirical, in part because of still limited knowledge of its pathophysiology . It is clear that, since there is no type of obstructive pathology at the level of the coronary arteries , the application of fibrinolytic agents would not be indicated; however, Tarkin et al. suggests that in all patients with precordial pain compatible with AMI, the picture should be managed as such, regardless of how large the diagnostic suspicion is. This is useful from a practical point of view, since differentiating between the two pathologies from a clinical point of view can be extremely difficult and, as already mentioned, urgent coronary angiography is not available in all care centers.


The prognosis is benign, both when compared with ST-elevation infarctions and non-ST-segment elevation infarcts. No patient died during admission and during follow-up (mean of 596 months) two of them required readmission for cardiovascular causes and two other patients died (one with dyspnea and sudden death and the other with sepsis ). Recurrences are rare; in the bibliography they are estimated at around 3%.


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