Tako-tsubo cmI42.88

In 1990, H. Sato et al. described in Japan for the first time the ballooning of the apex of the heart combined with a left ventricular motion pattern as a so-called Tako-Tsubo cardiomyopathy. (Takotsubo refers to the Japanese octopus trap) (Merchant 2008). It was not until 2005 that the hitherto benign picture of a TC of Donohue and Movahed was eliminated. (Donohue 2005).

Schneider tried to quantify the disease in Germany in 2006 (Solf 2017).

Tako- Tsubo- Cardiomyopathy (TC) is a reversible endsystolic (Stierle 2017) left ventricular dysfunction with predominantly apically localized movement disorders.

TC is a rare disease, accounting for 2% of all acute coronary syndromes. It occurs predominantly (90%) in women.
The risk of TC is increased in patients with pheochromocytoma. A genetic disposition and / or an infectious etiology are also suspected due to a family history of TC (Solf 2017 / (Reeder 2019). Up to 47 % of patients have a history of neurological or psychiatric disease (Pinger 2019).

It is a dysfunction of the autonomic nervous system (Stierle 2017), caused by emotional and/or psychological stress (Herold 2020), post-operatively after major surgery or by a craniocerebral trauma, and probably triggers coronary vasospasms (Solf 2017).

Pathophysiologically, it is a special form of regionally limited cardiomyopathy (Stierle 2017), whose pathophysiology is largely insufficiently understood. A catecholamine-mediated cardiotoxicity seems to be certain (Pinger 2019).

The average age of the disease is over 60 years. It affects postmenopausal women in 81% (Pinger 2019). Studies have also found a higher incidence of oestrogen deficiency (Komamura 2014).

In TC the picture of an acute coronary syndrome occurs in up to 88% (Pinger 2019) with:

• thoracic pain
• Dyspnea (10 % to 50 % [Pinger 2019])
• Syncopes (3 % to 4 % [Pinger 2019])
• Asystole (1%)(Pinger 2019)
• Tachyarrhythmias up to ventricular fibrillation
• Bradyarrhythmias (shipowner 2019)

Diagnostics

Auscultation

• sometimes 3rd heart sound auscultable (Herold 2020)

ECG

• temporary ST-segment elevation (lasting minutes to days)
• lack of change in Q-waves
• T-wave inversion (in up to 38% [Pinger 2019])
• prolongation of QT time (Reeder 2019)

Lab

• typical - but not mandatory - is a marked increase in catecholamines (Reeder 2019)
• Increase in troponin (usually between 0.8 - 14.8 ng / ml [Pinger 2019])
• CK- MB shows at most a slight increase (Herold 2020).

Echocardiography:

• in the apical region of the posterior wall reversible disturbances of the wall motion of the left ventricle (Stierle 2017).
• Consecutive formation of a SAM- phenomenon = systolic anterior motion in M- mode possible (the anterior mitral leaflet moves forward in systole [Piper 2013]).
• subaortic obstruction
• reduced ejection fraction (Herold 2020)

Cardio- MRI:

Cardio- MRI can be helpful in diagnosis, especially when a definitive diagnosis cannot be made by echocardiography or in the presence of coexisting coronary artery disease. Typical findings are:

• No late enhancement (important for differential diagnosis of myocardial infarctionor myocarditis [Reeder 2019]).
• edema in up to 81 % in the areas of wall motion disturbance (Pinger 2019)
• In up to 26 %, wall motion abnormalities of the right ventricle with further changes are also found:
• Pleural effusion (67% vs 8% with only left ventricular dysfunction; sensitivity 67% and specificity 92% [Haghi 2006])
• Left ventricular ejection fraction is significantly lower (Reeder 2019).

Cardiac catheterization

If coronary artery disease is suspected, coronary angiography should be performed. Here, the coronaries present completely unremarkable by TC (Herold 2020). However, additional signs of coronary artery disease are found in approximately 15.3% of patients (Reeder 2019).

• Myocarditis (patterns of wall movement usually differ; cardiovascular MRT helpful)
• Acute coronary syndrome:
  • coronary heart disease
  • critical coronary stenosis
• hypertrophic cardiomyopathy (HOCM)
  • cocaine-induced (e.g. medical history, toxicological tests)
• Pheochromocytoma (hyperhidrosis, tachycardia, headache, hypertension etc.)(Reeder 2019)
• Esophageal spasm
• gastroesophageal reflux disease
• Aortic dissection
• acute pericarditis
• Pneumothorax
• cardiogenic pulmonary oedema
• Pulmonary embolism
• Boerhaave syndrome (spontaneous esophageal rupture)
• Cardiac tamponade
• cardiogenic shock
• dilated cardiomyopathy

(Komamura 2014)

An evidence-based therapy of TC does not exist so far. However, it has been shown that the blockade of the renin- angiotensin- aldosterone system (RAAS blockade) by ACE inhibitors is associated with a higher probability of survival. Treatment with beta blockers has no effect on mortality (Pinger 2019)

The therapy should be similar to that of a STEMI or NSTEMI - with the exception of the re-perfusion, which is not necessary (Stierle 2017). Heart failure should be treated with the usual medication (avoiding catecholamines, as these are already elevated by the clinical picture) (Herold 2020).

The clinical picture usually recedes rapidly and the course of the disease is in most cases favourable. After only 1 week there is usually a significant improvement in systolic function. It usually takes between 3 - 4 weeks until complete recovery. If the systolic function has not normalized even after 12 weeks, the diagnosis TC should be doubted (Komamura 2014).

Serious complications are found in 18.9% of patients, such as:

• cardiogenic shock (10 %)
• Ventricular fibrillation (1.8 %)
• ventricular tachycardia (3.4%) (Pinger 2019)
• Recurrences occur in 1.8 % / year
• after 4 years the recurrence rate is 11
• after > 4 years there is a normal life expectancy (Pinger 2019)
• in 3.2 % a lethal outcome occurs in the acute phase (Solf 2017)
• the long-term mortality (observation period 3.8 years) is, according to a study by Stiermaier (2016), at 24.7% significantly higher than that of a patient with STEMI (15.1%)

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