Stress cardiomyopathy

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Classification according to ICD-10
I42 Cardiomyopathy
I42.88 Other cardiomyopathies
ICD-10 online (WHO version 2019)
Normal human heart and heart with a different shape of the left ventricle at the end of the systole in Broken Heart Syndrome

The stress cardiomyopathy (also Broken Heart Syndrome , Tako-Tsubo cardiomyopathy , Tako-Tsubo syndrome , transient left ventricular apical ballooning or Broken-Heart Syndrome ) is a rare, acute onset and often fatal disorder of the heart muscle , which mainly occurs in older women. The symptoms are similar to those of a heart attack and usually occur immediately after an extraordinary emotional or physical stress. The cause of the disorder, which was only described as an independent disease in the 1990s, is unclear; the mostly significantly increased blood levels of stress hormones , especially the body's own catecholamines such as adrenaline and noradrenaline , seem to be of decisive importance. The prognosis is favorable for most of the patients, and after a few weeks the heart function is normal in the majority of them. In the acute stage, however, serious and life-threatening complications are common.

history

Japanese squid traps, the shape of which the disease is named after

The clinical picture was first described in 1991, named after a Japanese squid trap in the form of a jug with a short neck ( Tako-Tsubo , see illustration). The peculiar shape of the left ventricle (left ventricle) at the end of the systole , which is reminiscent of this, was viewed by the first authors as the result of a circulatory disorder of the heart muscle , caused by the spasmodic narrowing of several coronary arteries (coronary spasms ).

In the definition and classification of cardiomyopathies of the American Heart Association (AHA), which was updated in March 2006, "stress ('Tako-Tsubo") cardiomyopathy is classified as an acquired primary cardiomyopathy alongside myocarditis .

Epidemiology

There is a lack of reliable epidemiological data, knowledge about stress cardiomyopathy is based on descriptions of individual cases and the description of “very small series” with a few patients. By mid-2006, only about 700 patients with Tako-Tsubo cardiomyopathy had been described worldwide, about 400 of them in Japan and about 150 each in Europe and North America. Since 2004 there have also been reports on patients in Australia and South America, so that a worldwide and so far underestimated spread is assumed.

Based on the small number of patients in each case, it has so far been established that in Japan 1.2 to 2.2%, in the USA around 2.2% and in Germany 2.3 to 2.6% of all patients with an acute coronary syndrome suffer from stress Cardiomyopathy suffered; this proportion was around 7.5% of the female patients. More than 90% of the patients described were women; the mean age was 62–75 years.

Extremely spicy foods can also trigger Tako Tsubo cardiomyopathy.

Pathophysiology

The origin and development of the disease ( pathogenesis ) are not fully understood. In many patients with stress cardiomyopathy, significantly increased blood levels of the body's own catecholamines have been found. Adrenaline , noradrenaline , metanephrine (metanephrine and normetanephrine) and vanillin-mandelic acid have been found in higher concentrations than in severe heart attacks. The high concentration of these substances, also known as stress hormones , is discussed as the cause of stress cardiomyopathy, which is supported by several individual observations of Tako-Tsubo -like events in patients with pheochromocytoma , a catecholamine-producing tumor of the adrenal gland . In 2004, two sisters with apical ballooning were reported for the first time , which suggests a genetic predisposition. On the occasion of the detection of an infection with the cytomegalovirus in a patient with Tako-Tsubo syndrome, a possible cause by viruses was also discussed in 2006 .

With regard to the pathophysiology , it is assumed that the greatly increased catecholamine concentration changes the activity of the heart muscle in such a way that the walls of the coronary arteries cramp or become overloaded with calcium . According to previous knowledge, the cause of the increased catecholamine levels could be an overactivity of the autonomic nervous system , which produces too many stress hormones due to the sudden stressful situation. A relative lack of estrogens after menopause may contribute to increased activation of the sympathetic nervous system . The unusual affliction for other circulatory disorders of the heart, especially in the muscle regions near the tip, could be due to a different density of beta-adrenoceptors , which has been proven at least in dogs.

Clinical picture

Acute phase

The symptoms of stress cardiomyopathy are similar to those of a heart attack . Characteristic are sudden and severe chest pain ( angina pectoris ) and shortness of breath ( dyspnoea ). In the acute stage, it is not possible to differentiate it from a heart attack without a cardiac catheter examination, so the event is initially referred to and treated as an acute coronary syndrome .

Almost all patients have in common that the symptoms shortly after an emotionally stressful event such as the death of a loved one, separation from a partner, an accident, a robbery, a natural disaster, a violent argument, the loss of material existence or the diagnosis of a serious illness, but certainly also after pleasant surprises such as the news of a bigger lottery win. Contrary to initial assumptions, which are still widely expressed today, Tako Tsubo cardiomyopathy is not without risk. The risk of serious complications is particularly high in the first few hours. Information about their frequency varies between 18.9% and up to 46%. A cardiogenic shock occurs in about 15%, a serious cardiac arrhythmia ( ventricular tachycardia or ventricular fibrillation in the patient) at about 9%.

Course and prognosis

The changes in the heart muscle usually regress completely within weeks, and the ECG usually normalizes as well. In an overview published in 2005 of all cases published to date, a mortality of 3.2% is given. After surviving the acute phase, the risk of a recurrence ( relapse ) of the syndrome appears to be low.

ECG (leads V1-V6) with normal T waves (green arrows) about one hour after the onset of pain and negative T waves (red arrows) about four hours later

Diagnosis

The diagnostic criteria for stress cardiomyopathy are:

  • a temporary movement disorder of the left ventricle that does not correspond to the supply area of ​​a coronary artery ,
  • the exclusion of severe constrictions of the coronary arteries,
  • newly occurred EKG changes similar to those of a heart attack and
  • the temporal connection with a previous stressful situation.

The physical exam may reveal normal findings or reveal signs of heart failure, such as a third heartbeat or rattle in the lungs.

In terms of differential diagnosis , it is important to distinguish stress cardiomyopathy on the one hand from an acute coronary syndrome based on coronary heart disease and on the other hand from a pheochromocytoma or, thirdly, from hypertrophic obstructive cardiomyopathy .

EKG

In the acute phase, the ECG shows elevations in the ST segment (see ECG nomenclature ) or diffuse changes in the T wave, and within the first 48 hours often an increase in the QT time. The EKG changes are similar to those in a heart attack and often appear in multiple EKG leads.

Imaging procedures

Ventriculography of the left ventricle in Tako Tsubo cardiomyopathy
Contours of the left ventricle in diastole (black) and systole (gray). Schematic representation.
A stress cardiomyopathy
B normal person

The X-ray of the thoracic organs is normal or shows what is known as pulmonary congestion ("water in the lungs") as a result of heart failure. With echocardiography , the movement disorder ( contraction disorder ) of the left ventricle, which is typical for Tako-Tsubo syndrome, is often detectable, apical ballooning . This contraction disorder of the left ventricle, which can also be detected in the course of a cardiac catheter examination , is often noticeable as an impressive immobility ( akinesia ) or even as a paradoxical mobility ( dyskinesia ) of the apex of the heart, which can be similar to an aneurysm .

In contrast to myocardial infarction, however, coronary angiography does not reveal any blockage of the coronary arteries. Only this finding of the cardiac catheter examination allows a reliable differentiation from myocardial infarction.

Magnetic resonance imaging (MRI) also provides meaningful results , which shows both the movement disorder of the heart muscle in good quality and, after gadolinium administration, the absence of scarring.

Laboratory tests

The so-called cardiac markers troponin and creatine kinase (CK), determined in the blood serum when a heart attack is suspected, are usually increased in stress cardiomyopathy as in a heart attack, but to a lesser extent than the ECG changes and the movement disorder of the heart muscle suggest. In 80–90% of patients, a slight increase in troponin can be demonstrated in the acute stage, although this rarely exceeds two to three times the upper limit of normal. A likewise usually small increase in CK is observed in 50–70% of patients. The Brain Natriuretic Peptide (BNP) is significantly increased in many patients.

The blood concentrations of stress hormones from the group of catecholamines ( adrenaline , noradrenaline , dopamine and derivatives ) are increased in most patients, on average two to four times higher than in patients with a heart attack. This corresponds to an increase of 7 to 34 times the concentrations usual for symptom-free people. The excessive hormone level can usually be detected in the blood a few days after the triggering event. Since Tako-Tsubo -like events and increased catecholamine concentrations also occur in patients with a pheochromocytoma , this tumor should be excluded, especially in patients without a triggering stress event.

therapy

In the absence of appropriate therapy studies, there is no standard therapy for stress cardiomyopathy that is backed up by objective data. Due to the high rate of complications in the acute stage, monitor monitoring is carried out in the intensive care unit. Since the high catecholamine levels are seen as the cause, it is advisable to be as reluctant as possible when taking additional catecholamines . Careful volume administration is recommended for patients in shock , including early use of the intra-aortic balloon pump (IABP) if necessary . Analogous to the therapy of the pheochromocytoma crisis, alpha blockers and, in hemodynamically stable patients, beta blockers can be useful.

literature

  • Grawe H et al .: Stress cardiomyopathy mimicking acute coronary syndrome: case presentation and review of the literature . Clin Res Cardiol (2006) 96: 179-185. PMID 16598532
  • Pilgrim ™, Wyss TR. Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: A systematic review. Int J Cardiol . 2008 Mar 14; 124 (3): 283-92. PMID 17651841
  • Hugo A. Katus and Benjamin Meder, Ioana Barb: Broken Heart. When women's hearts break. In: Ruperto Carola Research Magazine, Heidelberg, No. 10 (2017): Frau & Mann , pp. 67–73. Digitized

swell

  1. ↑ Dote K et al .: Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases . J Cardiol (1991) 21: 203-214. PMID 1841907 .
  2. ^ Maron BJ et al .: Contemporary Definitions and Classification of the Cardiomyopathies. An American Heart Association Scientific Statement From the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation (2006) 113: 1807-1816. PMID 16567565 .
  3. ↑ a b c d e f Schneider B: Tako Tsubo cardiomyopathy - what is behind it? . Cardiology up2date (2006) 2: 131-136.
  4. ↑ Wedekind H et al .: Tako-Tsubo cardiomyopathy. Incidence in patients with acute coronary syndrome . Heart (2006) 31: 339-346. PMID 16810474 .
  5. ↑ a b c Donohue D, Movahed MR: Clinical characteristics, demographics and prognosis of transient left ventricular apical ballooning syndrome . Heart Fail Rev (2005) 10: 311-316. PMID 16583180 .
  6. ↑ Weil J et al .: Transient left ventricular apical ballooning, differential diagnosis of acute coronary syndrome . Intensivmed (2006) 43: 213-218.
  7. ↑ Irene Berres: Woman confuses wasabi with avocado - and suffers broken heart syndrome. In: Spiegel Online . September 25, 2019, accessed May 15, 2020 .
  8. ↑ a b Spes C, Knape A, Mudra H: Recurrent tako-tsubo-like left ventricular dysfunction (apical ballooning) in a patient with pheochromocytoma - a case report . In: Clinical Research in Cardiology (2006) 95: 307-311
  9. ↑ Pison L: Apical ballooning in relative . Heart (2004) 90: e67. PMID 15547001
  10. ↑ Göttingen researchers decipher important functional aspects of the broken heart syndrome University of Göttingen Human Genetics, September 4, 2017
  11. ↑ Greco C et al .: Tako-tsubo syndrome: a potential role for cytomegalovirus infection . J Cardiovasc Med (2006) 7: 623-627. PMID 16858242 .
  12. ↑ Mori H et al .: Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli . Cardiovasc Res (1993) 27: 192-198. PMID 8386061 .
  13. ↑ Sato, M. et al .: Increased incidence of transient left ventricular apical ballooning (so-called; takotsubo 'cardiomyopathy) after the mid-niigata prefecture earthquake. Circ J. 2006 70: 947-953. PMID 16864923 .
  14. ↑ Bybee KA et al .: Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction . Ann Intern Med (2004) 141: 858-865. PMID 15583228 .
  15. ↑ Takotsubo syndrome. In: Medical Tribune. Retrieved July 17, 2019 .
  16. ^ Wittstein IS et al .: Neurohumoral features of myocardial stunning due to sudden emotional stress . N Engl J Med (2005) 352: 539-548. PMID 15703419 .
This version was added to the list of articles worth reading on August 13, 2006 .