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Stress cardiomyopathy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Arzu Kalayci, M.D. [3]

Synonyms and keywords: Takotsubo cardiomyopathy; Tako-tsubo syndrome; left ventricular apical ballooning syndrome; LVABS; ampulla-shaped cardiomyopathy; broken heart syndrome; transient apical dysfunction; stress-induced cardiomyopathy; SIC

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Arzu Kalayci, M.D. [3]

Overview

Stress cardiomyopathy is a relatively new disease, with the first case documented in literature under the name of Takotsobu Cardiomyopathy in Japan in 1991. It is not very well understood, but the disease is thought to arise following intense emotional or physical stress. Stress cardiomyopathy mostly affects post-menopausal women. The clinical presentation, laboratory findings and imaging studies largely mimic that of anterior MI. However, the absence of significant coronary artery stenosis supports the diagnosis of stress cardiomyopathy. It is generally a self-limiting disease and the majority of patients have a restored cardiac function within a matter of weeks. Complications and death are relatively rare, but they are mostly related to the development of heart failure and pulmonary edema.

Historical Perspective

Stress cardiomyopathy is a relatively new disease, with the first case documented in literature in Japan in 1991. However, cases of death upon going through severe emotional or psychological stress have been described as early as the biblical times.[1][2]

Classification

Stress cardiomyopathy can be divided into several types, depending on the location of regional wall motion abnormality. The area of motion abnormality (whether hypokinesia, dyskinesia or akinesia) can be detected on echocardiography or left ventriculography. The most common type is the apical type, resulting in apical ballooning.[3][4][5][6]

Pathophysiology

The pathogenesis of stress cardiomyopathy is not completely understood. However, the most accepted theory behind it is thought to be due to catecholamine surge, which are thought to contribute to myocardial necrosis and stunning seen in stress cardiomyopathy.[2][7][8] On biopsy, findings include an inflammatory infiltrate, fibrosis and formation of contraction bands, which may or may not be associated with myocardial necrosis.[9][10] Stress cardiomyopathy is associated with various neurological and psychological conditions.

Causes

The cause of stress cardiomyopathy is largely unknown. However, it is usually triggered by emotional and/or physical stress and may be related to certain medical conditions.

Differentiating Stress Cardiomyopathy from Other Diseases

The clinical presentation, laboratory findings and imaging studies of stress cardiomyopathy resembles that of anterior MI and must be differentiated from it. Also, stress cardiomyopathy must be differentiated from other medical conditions, such as pheochromocytoma, dilated cardiomyopathy and hypertrophic cardiomyopathy.[11][12]

Epidemiology and Demographics

The true incidence and prevalence of stress cardiomyopathy is unknown. However, this disease most commonly affects post-menopausal women, with the mean age of diagnosis ranging between 58-75 years.[2][3][1][13][14]

Risk Factors

Stress cardiomyopathy seems to be triggered by intense emotional or physical stress, mostly the unexpected death of a loved one.[2]

Screening

There are no screening recommendations for stress cardiomyopathy.[15]

Natural History, Complications and Prognosis

The prognosis of stress cardiomyopathy is generally excellent, with most patients making a complete recovery within a matter of weeks. However, death from complications of heart failure and heart rupture may occur.[2][13][16]

Diagnostic Criteria

In 2004, researchers at the Mayo Clinic proposed a criteria for the diagnosis of stress cardiomyopathy. All 4 points of the criteria must be fulfilled, which include ruling out other medical conditions, such as obstructive coronary disease, myocarditis and pheochromocytoma.[13][2]

History and Symptoms

The most common presenting symptoms of stress cardiomyopathy are shortness of breath and chest pain.[2][10][13][14][3][17]

Physical Examination

Physical examination findings in patients with stress cardiomyopathy are non-specific and non-diagnostic. The diagnosis of stress cardiomyopathy is largely based on ECG, echocardiographic findings, as well as cardiac catheterization.[18]

Laboratory Findings

Elevated levels of catecholamines, cardiac enzymes and BNP may be seen in patients with stress cardiomyopathy. However, none of these laboratory findings are specific to stress cardiomyopathy.[2][10][14][17]

ECG

ECG findings in stress cardiomyopathy are similar to those seen in anterior MI. The most common findings include ST elevation in the precordial leads, T wave inversion and the formation of a Q wave.[19][2] Findings on ECG include:[2][10][13][16][14][3][17]

Chest X-Ray

 Typical findings on chest x-ray include apical ballooning and narrowing of the neck.

CT Scan

A CT scan may be done in patients with stress cardiomyopathy to asses coronary anatomy, as well as detect the presence of regional wall motion abnormalities.[17]

MRI

Cardiac magnetic resonance (CMR) is a useful imaging modality in distinguishing between stress cardiomyopathy and myocarditis or MI. The most common findings on CMR in patients with stress cardiomyopathy include absence of gadolinium hyper-enhancement, as well as myocardial edema.[13][20][21][22][23][24][25][26][27][5][28]

Echocardiography

Echocardiography is done in patients with stress cardiomyopathy to document apical ballooning, dyskinesia/akinesia and reduced ejection fraction.[10][13][16][17]

Other Imaging Findings

In patients with stress cardiomyopathy, coronary angiography usually shows normal anatomy of the coronary arteries no evidence of coronary artery stenosis.[2][14][17]

Other Diagnostic Studies

Coronary angiography and cardiac catheterization are the diagnostic modalities of choice to distinguish between stress cardiomyopathy and acute anterior MI. Normal anatomy of the coronary arteries, along with a reduced ejection fraction supports the diagnosis of stress cardiomyopathy.[10][16][14]

Medical Therapy

Medical therapy in stress cardiomyopathy is indicated to treat the complications that may arise. The most common complications related to stress cardiomyopathy include heart failure and pulmonary edema. Diuretics and anti-heart failure medications are the treatment of choice in these conditions.[1][10]

Surgery

Treatment of stress cardiomyopathy is mostly supportive and medications are used to treat complications.[1][10] There is no role for surgery in the treatment of stress cardiomyopathy.

Primary Prevention

There are no means of prevention of stress cardiomyopathy.

Secondary Prevention

Stress cardiomyopathy is a self-limiting disease, which usually resolves within a few weeks. However, medical therapy may be necessary during the acute phase of the illness or when complications arise.[1][10]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Omerovic E (2011). “How to think about stress-induced cardiomyopathy?–Think “out of the box”!”. Scand. Cardiovasc. J. 45 (2): 67–71. doi:10.3109/14017431.2011.565794. PMID 21401402.
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  3. ↑ 3.0 3.1 3.2 3.3 Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF (2015). “Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy”. N. Engl. J. Med. 373 (10): 929–38. doi:10.1056/NEJMoa1406761. PMID 26332547.
  4. ↑ Kurowski V, Kaiser A, von Hof K, Killermann DP, Mayer B, Hartmann F, Schunkert H, Radke PW (2007). “Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis”. Chest. 132 (3): 809–16. doi:10.1378/chest.07-0608. PMID 17573507.
  5. ↑ 5.0 5.1 Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, Carbone I, Muellerleile K, Aldrovandi A, Francone M, Desch S, Gutberlet M, Strohm O, Schuler G, Schulz-Menger J, Thiele H, Friedrich MG (2011). “Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy”. JAMA. 306 (3): 277–86. doi:10.1001/jama.2011.992. PMID 21771988.
  6. ↑ Win CM, Pathak A, Guglin M (2011). “Not takotsubo: a different form of stress-induced cardiomyopathy–a case series”. Congest Heart Fail. 17 (1): 38–41. doi:10.1111/j.1751-7133.2010.00195.x. PMID 21272226.
  7. ↑ Goico A, Chandrasekaran M, Herrera CJ (2016). “Novel developments in stress cardiomyopathy: From pathophysiology to prognosis”. Int. J. Cardiol. 223: 1053–1058. doi:10.1016/j.ijcard.2016.08.241. PMID 27611570.
  8. ↑ Testa M, Feola M (2014). “Usefulness of myocardial positron emission tomography/nuclear imaging in Takotsubo cardiomyopathy”. World J Radiol. 6 (7): 502–6. doi:10.4329/wjr.v6.i7.502. PMC 4109102. PMID 25071891.
  9. ↑ Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  10. ↑ 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 Brenner ZR, Powers J (2008). “Takotsubo cardiomyopathy”. Heart Lung. 37 (1): 1–7. doi:10.1016/j.hrtlng.2006.12.003. PMID 18206521.
  11. ↑ Parodi G, Del Pace S, Carrabba N, Salvadori C, Memisha G, Simonetti I, Antoniucci D, Gensini GF (2007). “Incidence, clinical findings, and outcome of women with left ventricular apical ballooning syndrome”. Am. J. Cardiol. 99 (2): 182–5. doi:10.1016/j.amjcard.2006.07.080. PMID 17223415.
  12. ↑ Mikail N, Hess S, Jesel L, El Ghannudi S, El Husseini Z, Trinh A, Ohlmann P, Morel O, Imperiale A (2013). “Takotsubo and Takotsubo-like syndrome: a common neurogenic myocardial stunning pathway?”. Int. J. Cardiol. 166 (1): 248–50. doi:10.1016/j.ijcard.2012.09.116. PMID 23058349.
  13. ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 Prasad A, Lerman A, Rihal CS (2008). “Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction”. Am. Heart J. 155 (3): 408–17. doi:10.1016/j.ahj.2007.11.008. PMID 18294473.
  14. ↑ 14.0 14.1 14.2 14.3 14.4 14.5 Bybee KA, Prasad A, Barsness GW, Lerman A, Jaffe AS, Murphy JG, Wright RS, Rihal CS (2004). “Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome”. Am. J. Cardiol. 94 (3): 343–6. doi:10.1016/j.amjcard.2004.04.030. PMID 15276100.
  15. ↑ U.S. Preventive Services Task Force https://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=stress+cardiomyopathy. Accessed on Jan 9, 2017.
  16. ↑ 16.0 16.1 16.2 16.3 Tsai TT, Nallamothu BK, Prasad A, Saint S, Bates ER (2009). “Clinical problem-solving. A change of heart”. N. Engl. J. Med. 361 (10): 1010–6. doi:10.1056/NEJMcps0903023. PMID 19726776.
  17. ↑ 17.0 17.1 17.2 17.3 17.4 17.5 Efferth T, Banerjee M, Paul NW (2016). “Broken heart, tako-tsubo or stress cardiomyopathy? Metaphors, meanings and their medical impact”. Int. J. Cardiol. doi:10.1016/j.ijcard.2016.12.129. PMID 28041712.
  18. ↑ Y-Hassan S, Yamasaki K (2013). “History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies”. Int. J. Cardiol. 166 (3): 736–7. doi:10.1016/j.ijcard.2012.09.183. PMID 23073280.
  19. ↑ Bybee KA, Motiei A, Syed IS, Kara T, Prasad A, Lennon RJ, Murphy JG, Hammill SC, Rihal CS, Wright RS (2006). “Electrocardiography cannot reliably differentiate transient left ventricular apical ballooning syndrome from anterior ST-segment elevation myocardial infarction”. J Electrocardiol. PMID 17067626.
  20. ↑ Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ (2005). “Acute and reversible cardiomyopathy provoked by stress in women from the United States”. Circulation. 111 (4): 472–9. doi:10.1161/01.CIR.0000153801.51470.EB. PMID 15687136.
  21. ↑ Haghi D, Fluechter S, Suselbeck T, Kaden JJ, Borggrefe M, Papavassiliu T (2007). “Cardiovascular magnetic resonance findings in typical versus atypical forms of the acute apical ballooning syndrome (Takotsubo cardiomyopathy)”. Int. J. Cardiol. 120 (2): 205–11. doi:10.1016/j.ijcard.2006.09.019. PMID 17175045.
  22. ↑ Mitchell JH, Hadden TB, Wilson JM, Achari A, Muthupillai R, Flamm SD (2007). “Clinical features and usefulness of cardiac magnetic resonance imaging in assessing myocardial viability and prognosis in Takotsubo cardiomyopathy (transient left ventricular apical ballooning syndrome)”. Am. J. Cardiol. 100 (2): 296–301. doi:10.1016/j.amjcard.2007.02.091. PMID 17631086.
  23. ↑ Deetjen AG, Conradi G, Mollmann S, Rad A, Hamm CW, Dill T (2006). “Value of gadolinium-enhanced magnetic resonance imaging in patients with Tako-Tsubo-like left ventricular dysfunction”. J Cardiovasc Magn Reson. 8 (2): 367–72. PMID 16669180.
  24. ↑ Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H (2003). “Assessment of clinical features in transient left ventricular apical ballooning”. J. Am. Coll. Cardiol. 41 (5): 737–42. PMID 12628715.
  25. ↑ Dec GW (2005). “Recognition of the apical ballooning syndrome in the United States”. Circulation. 111 (4): 388–90. doi:10.1161/01.CIR.0000155234.69439.E4. PMID 15687123.
  26. ↑ Handy AD, Prasad A, Olson TM (2009). “Investigating genetic variation of adrenergic receptors in familial stress cardiomyopathy (apical ballooning syndrome)”. J Cardiol. 54 (3): 516–7. doi:10.1016/j.jjcc.2009.08.008. PMID 19944334.
  27. ↑ Sharkey SW, Maron BJ, Nelson P, Parpart M, Maron MS, Bristow MR (2009). “Adrenergic receptor polymorphisms in patients with stress (tako-tsubo) cardiomyopathy”. J Cardiol. 53 (1): 53–7. doi:10.1016/j.jjcc.2008.08.006. PMID 19167638.
  28. ↑ Eitel I, Behrendt F, Schindler K, Kivelitz D, Gutberlet M, Schuler G, Thiele H (2008). “Differential diagnosis of suspected apical ballooning syndrome using contrast-enhanced magnetic resonance imaging”. Eur. Heart J. 29 (21): 2651–9. doi:10.1093/eurheartj/ehn433. PMID 18820322.

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Overview

Stress cardiomyopathy is a relatively new disease, with the first case documented in literature in Japan in 1991. However, cases of death upon going through severe emotional or psychological stress have been described as early as the biblical times.

Historical Perspective

  • Stress cardiomyopathy is a fairly new disease, which was first reported in Japan in 1991 and the term Takotsubo Cardiomyopathy came to use.[1][2]
  • The term “takotsubo” was taken from the Japanese name for an octopus trap which resembles the shape of systolic apical ballooning of the left ventricle.
  • However, the term “Broken Heart” was used in literature before 1990. While it was not labeled as a disease entity, death from psychological or emotional stress has been described even in biblical times.[3]
  • After 2000, there were many reported cases of chest pain and associated reversible left ventricular dysfunction, which were linked to preceding emotional stress. Such cases had normal coronary angiography findings, as well as minimal rise in serum cardiac enzymes.[2]
  • Since the cardiomyopathy is often triggered by emotional stress, such as the death of a loved one, the condition is sometimes also referred to as the Broken Heart Syndrome. In 2006, the syndrome was renamed Stress Cardiomyopathy, and was classified as an acquired cardiomyopathy.[4]

References

  1. ↑ Omerovic E (2011). “How to think about stress-induced cardiomyopathy?–Think “out of the box”!”. Scand. Cardiovasc. J. 45 (2): 67–71. doi:10.3109/14017431.2011.565794. PMID 21401402.
  2. ↑ 2.0 2.1 Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  3. ↑ Y-Hassan S, Yamasaki K (2013). “History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies”. Int. J. Cardiol. 166 (3): 736–7. doi:10.1016/j.ijcard.2012.09.183. PMID 23073280.
  4. ↑ Maron BJ, Towbin JA, Thiene G; et al. (2006). “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. 113 (14): 1807–16. doi:10.1161/CIRCULATIONAHA.106.174287. PMID 16567565.

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Classification

Classification


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Arzu Kalayci, M.D. [3]

Overview

Stress cardiomyopathy can be divided into several types, depending on the location of regional wall motion abnormality. The area of motion abnormality (whether hypokinesia, dyskinesia or akinesia) can be detected on echocardiography or left ventriculography. The most common type is the apical type, resulting in apical ballooning. In a minority of patients reverse takotsubo have been described in which unlike apical ballooning the basal and mid ventricular segments of the left ventricle become akinetic.

Classification

Stress cardiomyopathy can affect different segments of the heart. The region of wall motion abnormality can be detected on echocardiography or left ventriculography. The most common type of stress cardiomyopathy is the apical type, which results in hypokinesia of the apical and mid-ventricular segments. Stress cardiomyopathy can be divided according to location of wall motion abnormality into:[1][2][3][4]

Type of Stress Cardiomyopathy Location of Wall Motion Abnormality Incidence (%) Properties
Typical Type(s) Apical Type 81.7
Atypical Type(s) Mid-ventricular Type 14.6
Basal Type

(Reverse Takotsubo)

2.2
Focal Type 1.5
Global Type Very rare

References

  1. ↑ Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF (2015). “Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy”. N. Engl. J. Med. 373 (10): 929–38. doi:10.1056/NEJMoa1406761. PMID 26332547.
  2. ↑ Kurowski V, Kaiser A, von Hof K, Killermann DP, Mayer B, Hartmann F, Schunkert H, Radke PW (2007). “Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis”. Chest. 132 (3): 809–16. doi:10.1378/chest.07-0608. PMID 17573507.
  3. ↑ Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, Carbone I, Muellerleile K, Aldrovandi A, Francone M, Desch S, Gutberlet M, Strohm O, Schuler G, Schulz-Menger J, Thiele H, Friedrich MG (2011). “Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy”. JAMA. 306 (3): 277–86. doi:10.1001/jama.2011.992. PMID 21771988.
  4. ↑ Win CM, Pathak A, Guglin M (2011). “Not takotsubo: a different form of stress-induced cardiomyopathy–a case series”. Congest Heart Fail. 17 (1): 38–41. doi:10.1111/j.1751-7133.2010.00195.x. PMID 21272226.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Arzu Kalayci, M.D. [3]

Overview

The pathogenesis of stress cardiomyopathy is not completely understood. However, the most accepted theory behind it is thought to be due to catecholamine surge, which are thought to contribute to myocardial necrosis and stunning seen in stress cardiomyopathy. On biopsy, findings include an inflammatory infiltrate, fibrosis and formation of contraction bands, which may or may not be associated with myocardial necrosis. Stress cardiomyopathy is associated with various neurological and psychological conditions.

Pathophysiology

The cause of stress cardiomyopathy is unknown. Several theories have been postulated to explain the pathophysiology behind it:[1][2][3][4]

Catecholamine Cardiotoxicity:

The etiology of stress cardiomyopathy appears to involve the response of the myocardium to a hyperadrenergic state. The syndrome is often preceded by significant emotional and physical stress. Serum catecholamines may be markedly elevated in patients with stress cardiomyopathy with levels greater than seen in patients with thrombotic ST elevation myocardial infarction or congestive heart failure, though this is not always present. Thus, it has been postulated that catecholamine excess contributes at least in part to the pathophysiology, and that catecholamines may cause direct myonecrosis.[5] It is thought that myocardial stunning seen in stress cardiomyopathy is largely mediated by the effects of epinephrine.[6]

Multi-vessel Epicardial Coronary Artery Spasms:

This theory is not well accepted, as it has been noted that multi-vessel epicardial coronary artery vasospasm does not correlate with the areas of myocardium that are hypokinetic.

Coronary Microvascular Impairment

Myocardial stunning can occur because of microvascular spasm or direct myocardial toxicity of catecholamines. [7] [8]

Mid-cavity or Left Ventricular Outflow Tract Obstruction

Dynamic mid-cavity or left ventricular outflow tract obstruction may induce the apical dysfunction.

Microscopic Pathology

The histological findings on myocardial biopsy in patients with stress cardiomyopathy include:[9][10]

Genetics

There are no identified genes linked to the development of stress cardiomyopathy. However, there are cases of stress cardiomyopathy occurring among first degree relatives (among 2 sisters and among a patient and her mother), which point out to a possible genetic link to this condition.[11][12][13] In addition, genetic variation in adrenergic receptors and signaling pathways may be associated with stress cardiomyopathy.[14][15][16][17]

Associated Conditions

  • Many neurological and psychiatric conditions are associated with the development of stress cardiomyopathy. These include:[18]
  • It can also be associated with malignancies.[25]

References

  1. ↑ Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  2. ↑ Goico A, Chandrasekaran M, Herrera CJ (2016). “Novel developments in stress cardiomyopathy: From pathophysiology to prognosis”. Int. J. Cardiol. 223: 1053–1058. doi:10.1016/j.ijcard.2016.08.241. PMID 27611570.
  3. ↑ Testa M, Feola M (2014). “Usefulness of myocardial positron emission tomography/nuclear imaging in Takotsubo cardiomyopathy”. World J Radiol. 6 (7): 502–6. doi:10.4329/wjr.v6.i7.502. PMC 4109102. PMID 25071891.
  4. ↑ Ramaraj R (2007). “Stress cardiomyopathy: aetiology and management”. Postgrad Med J. 83 (982): 543–6. doi:10.1136/pgmj.2007.058776. PMC 2600114. PMID 17675548.
  5. ↑ Wittstein IS, Thiemann DR, Lima JA; et al. (2005). “Neurohumoral features of myocardial stunning due to sudden emotional stress”. N. Engl. J. Med. 352 (6): 539–48. doi:10.1056/NEJMoa043046. PMID 15703419.
  6. ↑ Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE (2008). “Stress (Takotsubo) cardiomyopathy–a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning”. Nat Clin Pract Cardiovasc Med. 5 (1): 22–9. doi:10.1038/ncpcardio1066. PMID 18094670.
  7. ↑ Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E (2006). dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16720686 “Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review” Check |url= value (help). Eur Heart J. 27 (13): 1523–9. doi:10.1093/eurheartj/ehl032. PMID 16720686.
  8. ↑ Nef HM, Möllmann H, Kostin S, Troidl C, Voss S, Weber M; et al. (2007). “Tako-Tsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery”. Eur Heart J. 28 (20): 2456–64. doi:10.1093/eurheartj/ehl570. PMID 17395683.
  9. ↑ Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  10. ↑ Brenner ZR, Powers J (2008). “Takotsubo cardiomyopathy”. Heart Lung. 37 (1): 1–7. doi:10.1016/j.hrtlng.2006.12.003. PMID 18206521.
  11. ↑ Pison L, De Vusser P, Mullens W (2004). “Apical ballooning in relatives”. Heart. 90 (12): e67. doi:10.1136/hrt.2004.046813. PMC 1768596. PMID 15547001.
  12. ↑ Kumar G, Holmes DR, Prasad A (2010). ““Familial” apical ballooning syndrome (Takotsubo cardiomyopathy)”. Int. J. Cardiol. 144 (3): 444–5. doi:10.1016/j.ijcard.2009.03.078. PMID 19375184.
  13. ↑ Ikutomi M, Yamasaki M, Matsusita M, Watari Y, Arashi H, Endo G, Yamaguchi J, Ohnishi S (2014). “Takotsubo cardiomyopathy in siblings”. Heart Vessels. 29 (1): 119–22. doi:10.1007/s00380-013-0345-y. PMID 23563753.
  14. ↑ Handy AD, Prasad A, Olson TM (2009). “Investigating genetic variation of adrenergic receptors in familial stress cardiomyopathy (apical ballooning syndrome)”. J Cardiol. 54 (3): 516–7. doi:10.1016/j.jjcc.2009.08.008. PMID 19944334.
  15. ↑ Sharkey SW, Maron BJ, Nelson P, Parpart M, Maron MS, Bristow MR (2009). “Adrenergic receptor polymorphisms in patients with stress (tako-tsubo) cardiomyopathy”. J Cardiol. 53 (1): 53–7. doi:10.1016/j.jjcc.2008.08.006. PMID 19167638.
  16. ↑ Novo G, Giambanco S, Guglielmo M, Arvigo L, Sutera MR, Giambanco F, Evola S, Vaccarino L, Bova M, Lio D, Assennato P, Novo S (2015). “G-protein-coupled receptor kinase 5 polymorphism and Takotsubo cardiomyopathy”. J Cardiovasc Med (Hagerstown). 16 (9): 639–43. doi:10.2459/JCM.0000000000000120. PMID 25010510.
  17. ↑ Goodloe AH, Evans JM, Middha S, Prasad A, Olson TM (2014). “Characterizing genetic variation of adrenergic signalling pathways in Takotsubo (stress) cardiomyopathy exomes”. Eur. J. Heart Fail. 16 (9): 942–9. doi:10.1002/ejhf.145. PMID 25132214.
  18. ↑ Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF (2015). “Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy”. N. Engl. J. Med. 373 (10): 929–38. doi:10.1056/NEJMoa1406761. PMID 26332547.
  19. ↑ Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown RD, Wijdicks EF (2006). “Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: an underappreciated ventricular dysfunction”. J. Neurosurg. 105 (2): 264–70. doi:10.3171/jns.2006.105.2.264. PMID 17219832.
  20. ↑ Le Ven F, Pennec PY, Timsit S, Blanc JJ (2011). “Takotsubo syndrome associated with seizures: an underestimated cause of sudden death in epilepsy?”. Int. J. Cardiol. 146 (3): 475–9. doi:10.1016/j.ijcard.2010.12.028. PMID 21194774.
  21. ↑ Sharp RP, Welch EB (2011). “Takotsubo cardiomyopathy as a complication of electroconvulsive therapy”. Ann Pharmacother. 45 (12): 1559–65. doi:10.1345/aph.1Q393. PMID 22116995.
  22. ↑ Riera M, Llompart-Pou JA, Carrillo A, Blanco C (2010). “Head injury and inverted Takotsubo cardiomyopathy”. J Trauma. 68 (1): E13–5. doi:10.1097/TA.0b013e3181469d5b. PMID 19065115.
  23. ↑ Yoshimura S, Toyoda K, Ohara T, Nagasawa H, Ohtani N, Kuwashiro T, Naritomi H, Minematsu K (2008). “Takotsubo cardiomyopathy in acute ischemic stroke”. Ann. Neurol. 64 (5): 547–54. doi:10.1002/ana.21459. PMID 18688801.
  24. ↑ Summers MR, Lennon RJ, Prasad A (2010). “Pre-morbid psychiatric and cardiovascular diseases in apical ballooning syndrome (tako-tsubo/stress-induced cardiomyopathy): potential pre-disposing factors?”. J. Am. Coll. Cardiol. 55 (7): 700–1. doi:10.1016/j.jacc.2009.10.031. PMID 20170799.
  25. ↑ https://doi.org/10.1161/JAHA.118.010881

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Causes

Causes


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Arzu Kalayci, M.D. [3]

Overview

The cause of stress cardiomyopathy is largely unknown. However, it is usually triggered by emotional and/or physical stress and may be related to certain medical conditions. According to a study in the literature, plasma catecholamine levels were higher in patients with stress cardiomyopathy compared to the patients with myocardial infarction. However, other studies showed that catecholamine levels were similar in both groups. [1] In addition stress cardiomyopathy can be induced by high doses of catecholamines and even standard doses of dobutamine in daily clinical practise. [2] [3] It is not understood why the disease mostly affects postmenopausal women and why the apex and mid-ventricular part of left ventricle are specifically affected.

Causes

The cause of stress cardiomyopathy is unknown. However, stress cardiomyopathy can result from various medical conditions including:[4][5][6]


References

  1. ↑ Madhavan M, Borlaug BA, Lerman A, Rihal CS, Prasad A (2009). “Stress hormone and circulating biomarker profile of apical ballooning syndrome (Takotsubo cardiomyopathy): insights into the clinical significance of B-type natriuretic peptide and troponin levels”. Heart. 95 (17): 1436–41. doi:10.1136/hrt.2009.170399. PMID 19468013.
  2. ↑ Sharkey SW, Windenburg DC, Lesser JR, Maron MS, Hauser RG, Lesser JN; et al. (2010). “Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy”. J Am Coll Cardiol. 55 (4): 333–41. doi:10.1016/j.jacc.2009.08.057. PMID 20117439.
  3. ↑ Abraham J, Mudd JO, Kapur NK, Kapur N, Klein K, Champion HC; et al. (2009). “Stress cardiomyopathy after intravenous administration of catecholamines and beta-receptor agonists”. J Am Coll Cardiol. 53 (15): 1320–5. doi:10.1016/j.jacc.2009.02.020. PMID 19358948.
  4. ↑ Kotsiou OS, Douras A, Makris D, Mpaka N, Gourgoulianis KI (2017). “Takotsubo cardiomyopathy: a known unknown foe of asthma”. J Asthma: 0. doi:10.1080/02770903.2016.1276586. PMID 28055270.
  5. ↑ Gill D, Liu K (2016). “Takotsubo cardiomyopathy associated with Miller-Fisher syndrome”. Am J Emerg Med. doi:10.1016/j.ajem.2016.12.050. PMID 28040387.
  6. ↑ Murdoch D, O’Callaghan W, Reda E, Niranjan S (2016). “Takotsubo Cardiomyopathy Associated with Primary Hyperthyroidism Secondary to Toxic Multinodular Goiter”. Int J Angiol. 25 (5): e121–e122. doi:10.1055/s-0035-1548548. PMC 5186230. PMID 28031674.

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Differentiating Stress Cardiomyopathy from other Diseases

Differentiating Stress Cardiomyopathy from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Arzu Kalayci, M.D. [3]

Overview

The clinical presentation, laboratory findings and imaging studies of stress cardiomyopathy resembles that of anterior MI and must be differentiated from it. Also, stress cardiomyopathy must be differentiated from Takotsubo-like cardiomyopathy, such as that due to pheochromocytoma.

Differentiating Stress Cardiomyopathy from other Diseases

The presentation of stress cardiomyopathy mimics that of anterior wall MI and must be differentiated from it. There are some studies in the literature comparing left ventricular functions between acute myocardial infarction and stress cardiomyopathy. Although, systolic functions of the left ventricle were more impaired in stress cardiomyopathy group compared with acute myocardial infarction group, diastolic functions were better in these patients. [1] [2]

Disease Can Present With Cardiac Enzymes Catecholamine Levels ECG Findings Echocardiography Findings
Stress Cardiomyopathy Chest pain, dyspnea ↑ Transiently elevated ST elevation in precordial leads LV regional dysfunction
Pheochromocytoma Chest pain, dyspnea Can be positive Persistently elevated ST elevation in precordial leads LV regional dysfunction
Anterior MI Chest pain, dyspnea ↑↑↑ – ST elevation in precordial leads Dysfunction at area of infarction
Myocarditis Chest pain, dyspnea, fever May be acutely elevated – May show atrial fibrillation, LBBB or AV block Diffuse hypokinesia
Dilated Cardiomyopathy Dyspnea, dyspnea on exertion, cough, edema, fatigue Usually negative – May show atrial fibrillation, LBBB or AV block LV enlargement
Hypertrophic Cardiomyopathy Chest pain, dyspnea, syncope, sudden cardiac death Usually negative – Common findings include: LV hypertrophy, systolic anterior motion of the mitral valve, asymmetric septal hypertrophy

References

  1. ↑ Medeiros K, O’Connor MJ, Baicu CF, Fitzgibbons TP, Shaw P, Tighe DA; et al. (2014). “Systolic and diastolic mechanics in stress cardiomyopathy”. Circulation. 129 (16): 1659–67. doi:10.1161/CIRCULATIONAHA.113.002781. PMID 24503950.
  2. ↑ Park SM, Prasad A, Rihal C, Bell MR, Oh JK (2009). “Left ventricular systolic and diastolic function in patients with apical ballooning syndrome compared with patients with acute anterior ST-segment elevation myocardial infarction: a functional paradox”. Mayo Clin Proc. 84 (6): 514–21. doi:10.1016/S0025-6196(11)60583-1. PMC 2688625. PMID 19483168.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Overview

The true incidence and prevalence of stress cardiomyopathy is unknown. However, this disease most commonly affects post-menopausal women, with the mean age of diagnosis ranging between 58-75 years.

Epidemiology

Incidence

  • The true incidence of stress cardiomyopathy is unknown and is thought to be underestimated, because there is a number of sub-clinical and milder forms of the disease, which do not come to clinical attention.[1] However, approximately 1-2% of patients thought to have acute coronary syndrome or myocardial infarction at initial presentation eventually receive the diagnosis of stress cardiomyopathy instead.[2][3][4][5]
  • In the United States, the overall incidence of stress cardiomyopathy is estimated at 5.2 per 100,000 cases in women and 0.6 per 100,000 cases in men.[6]

Prevalence

  • The prevalence of stress cardiomyopathy is unknown.

Demographics

Age

  • Stress cardiomyopathy occurs mostly in older people, mostly in post-menopausal women.[2][7][8]
  • The mean age of diagnosis ranges between 58 to 75 years old, with less than 3% of patients being younger than 50 years old at presentation.[2]

Gender

Stress cardiomyopathy is much more common in women, with female patients accounting for 80-100% of patients.[7][9][1][2][8]

References

  1. ↑ 1.0 1.1 Omerovic E (2011). “How to think about stress-induced cardiomyopathy?–Think “out of the box”!”. Scand. Cardiovasc. J. 45 (2): 67–71. doi:10.3109/14017431.2011.565794. PMID 21401402.
  2. ↑ 2.0 2.1 2.2 2.3 Prasad A, Lerman A, Rihal CS (2008). “Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction”. Am. Heart J. 155 (3): 408–17. doi:10.1016/j.ahj.2007.11.008. PMID 18294473.
  3. ↑ Elian D, Osherov A, Matetzky S, Hod H, Guetta V, Feinberg MS, Di Segni E (2006). “Left ventricular apical ballooning: not an uncommon variant of acute myocardial infarction in women”. Clin Cardiol. 29 (1): 9–12. PMID 16477771.
  4. ↑ Pillière R, Mansencal N, Digne F, Lacombe P, Joseph T, Dubourg O (2006). “Prevalence of tako-tsubo syndrome in a large urban agglomeration”. Am. J. Cardiol. 98 (5): 662–5. doi:10.1016/j.amjcard.2006.03.048. PMID 16923457.
  5. ↑ Parodi G, Del Pace S, Carrabba N, Salvadori C, Memisha G, Simonetti I, Antoniucci D, Gensini GF (2007). “Incidence, clinical findings, and outcome of women with left ventricular apical ballooning syndrome”. Am. J. Cardiol. 99 (2): 182–5. doi:10.1016/j.amjcard.2006.07.080. PMID 17223415.
  6. ↑ Chou AY, Saw J (2014). “Basis for sex-specific expression of Takotsubo cardiomyopathy, cardiac syndrome X, and spontaneous coronary artery dissection”. Can J Cardiol. 30 (7): 738–46. doi:10.1016/j.cjca.2013.12.008. PMID 24656530.
  7. ↑ 7.0 7.1 Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  8. ↑ 8.0 8.1 Bybee KA, Prasad A, Barsness GW, Lerman A, Jaffe AS, Murphy JG, Wright RS, Rihal CS (2004). “Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome”. Am. J. Cardiol. 94 (3): 343–6. doi:10.1016/j.amjcard.2004.04.030. PMID 15276100.
  9. ↑ Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF (2015). “Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy”. N. Engl. J. Med. 373 (10): 929–38. doi:10.1056/NEJMoa1406761. PMID 26332547.

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Overview

Stress cardiomyopathy seems to be triggered by intense emotional or physical stress, mostly the unexpected death of a loved one.

Risk Factors

Risk factors associated with the development of stress cardiomyopathy include:[1]

References

  1. ↑ Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Overview

The prognosis of stress cardiomyopathy is generally excellent, with most patients making a complete recovery within weeks. However, death from complications of heart failure and heart rupture may occur.

Natural History

Provided that patients survive the initial insult without any complications, most patients recover and have a normalized cardiac function within a few weeks.[1][2][3]

Complications

Complications of stress cardiomyopathy include:[1][4][5][3][6][7][8][9][10][11]

Prognosis

The prognosis of stress cardiomyopathy is generally good, even without medical therapy.[5][3] Most patients have a restored cardiac function within a few weeks.[2][3] However, fatal complications such as LV free wall rupture and heart rupture may occur and mortality rate in patients with stress cardiomyopathy ranges from 0-8%.[1][5]

References

  1. ↑ 1.0 1.1 1.2 Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). “Takotsubo cardiomyopathy: a new form of acute, reversible heart failure”. Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
  2. ↑ 2.0 2.1 Prasad A, Lerman A, Rihal CS (2008). “Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction”. Am. Heart J. 155 (3): 408–17. doi:10.1016/j.ahj.2007.11.008. PMID 18294473.
  3. ↑ 3.0 3.1 3.2 3.3 Tsai TT, Nallamothu BK, Prasad A, Saint S, Bates ER (2009). “Clinical problem-solving. A change of heart”. N. Engl. J. Med. 361 (10): 1010–6. doi:10.1056/NEJMcps0903023. PMID 19726776.
  4. ↑ Omerovic E (2011). “How to think about stress-induced cardiomyopathy?–Think “out of the box”!”. Scand. Cardiovasc. J. 45 (2): 67–71. doi:10.3109/14017431.2011.565794. PMID 21401402.
  5. ↑ 5.0 5.1 5.2 Brenner ZR, Powers J (2008). “Takotsubo cardiomyopathy”. Heart Lung. 37 (1): 1–7. doi:10.1016/j.hrtlng.2006.12.003. PMID 18206521.
  6. ↑ Efferth T, Banerjee M, Paul NW (2016). “Broken heart, tako-tsubo or stress cardiomyopathy? Metaphors, meanings and their medical impact”. Int. J. Cardiol. doi:10.1016/j.ijcard.2016.12.129. PMID 28041712.
  7. ↑ Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS (2004). “Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction”. Ann. Intern. Med. 141 (11): 858–65. PMID 15583228.
  8. ↑ Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I (2001). “Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan”. J. Am. Coll. Cardiol. 38 (1): 11–8. PMID 11451258.
  9. ↑ Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ (2005). “Acute and reversible cardiomyopathy provoked by stress in women from the United States”. Circulation. 111 (4): 472–9. doi:10.1161/01.CIR.0000153801.51470.EB. PMID 15687136.
  10. ↑ Desmet WJ, Adriaenssens BF, Dens JA (2003). “Apical ballooning of the left ventricle: first series in white patients”. Heart. 89 (9): 1027–31. PMC 1767823. PMID 12923018.
  11. ↑ Krishnamoorthy P, Garg J, Sharma A, Palaniswamy C, Shah N, Lanier G, Patel NC, Lavie CJ, Ahmad H (2015). “Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database”. Cardiology. 132 (2): 131–136. doi:10.1159/000430782. PMID 26159108.

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Diagnosis

Diagnosis

Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1


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