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| {{Infobox_Disease | | {{Infobox_Disease |
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| {{SI}} | | {{Stress cardiomyopathy}} |
| {{CMG}} | | {{CMG}}; {{AE}}{{DN}} {{AKK}} |
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| {{SK}} Takotsubo cardiomyopathy; Tako-tsubo syndrome; Left Ventricular Apical Ballooning Syndrome; Ampulla-Shaped Cardiomyopathy; Broken Heart Syndrome; transient apical dysfunction | | {{SK}} Takotsubo cardiomyopathy; Tako-tsubo syndrome; left ventricular apical ballooning syndrome; LVABS; ampulla-shaped cardiomyopathy; broken heart syndrome; transient apical dysfunction; stress-induced cardiomyopathy; SIC |
| | == [[Stress cardiomyopathy overview|Overview]] == |
| | ==[[ Stress cardiomyopathy historical perspective| Historical Perspective]]== |
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| == Overview == | | == [[Stress cardiomyopathy classification|Classification]] == |
| Stress cardiomyopathy is a cardiac syndrome characterized by a reversible transient apical ventricular dysfunction.
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| ==Historical Perspective== | | == [[Stress cardiomyopathy pathophysiology|Pathophysiology]] == |
| 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. <ref name="pmid16567565">{{cite journal |author=Maron BJ, Towbin JA, Thiene G, ''et al'' |title=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 |journal=Circulation |volume=113 |issue=14 |pages=1807–16 |year=2006 |pmid=16567565 |doi=10.1161/CIRCULATIONAHA.106.174287}}</ref>
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| ==Pathophysiology== | | == [[Stress cardiomyopathy causes|Causes]] == |
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| 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]]. <ref name="pmid15703419">{{cite journal |author=Wittstein IS, Thiemann DR, Lima JA, ''et al'' |title=Neurohumoral features of myocardial stunning due to sudden emotional stress |journal=N. Engl. J. Med.|volume=352 |issue=6 |pages=539–48 |year=2005 |pmid=15703419 |doi=10.1056/NEJMoa043046}}</ref>
| | == [[Stress cardiomyopathy differential diagnosis|Differentiating Stress Cardiomyopathy from other Diseases]] == |
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| Several other pathophysiologic mechanisms have been proposed. Lyon et al have hypothesized that the syndrome is a form of [[myocardial stunning]] that is mediated by [[epinephrine]]. <ref name="pmid18094670">{{cite journal |author=Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE |title=Stress (Takotsubo) cardiomyopathy--a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning |journal=Nat Clin Pract Cardiovasc Med |volume=5 |issue=1 |pages=22–9 |year=2008 |pmid=18094670 |doi=10.1038/ncpcardio1066}}</ref> These authors hypothesize that high levels of circulating [[epinephrine]] observed in the syndrome trigger a switch in intracellular signal trafficking.
| | == [[Stress cardiomyopathy epidemiology and demographics|Epidemiology and Demographics]] == |
| | ==[[Stress cardiomyopathy risk factors | Risk Factors]]== |
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| In particular, they hypothesize that ventricular [[cardiomyocytes]] (particularly those at the apex), switch from [[G(s) protein]] to [[G(i) protein]] signaling via the [[beta(2)-adrenoceptor]]. One potential benefit of this switch to beta(2)-adrenoceptor-G(i) protein signaling is that this may afford protection against the proapoptotic effects of intense activation of [[beta(1)-adrenoceptor]]s. On the other hand, this switch is also negatively [[inotropic]]. Because beta-adrenoceptor density is greatest at the apex of the left ventricle (455 vs 341 fmol/mg),<ref name="pmid8386061">{{cite journal |author=Mori H, Ishikawa S, Kojima S, ''et al'' |title=Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli |journal=Cardiovasc. Res. |volume=27 |issue=2 |pages=192–8 |year=1993 |pmid=8386061 |doi=}}</ref> the mechanical impact of the switch is also greatest at the apical myocardium. <ref name="pmid18094670">{{cite journal |author=Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE |title=Stress (Takotsubo) cardiomyopathy--a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning |journal=Nat Clin Pract Cardiovasc Med |volume=5 |issue=1 |pages=22–9 |year=2008 |pmid=18094670 |doi=10.1038/ncpcardio1066}}</ref>
| | == [[Stress cardiomyopathy natural history, complications and prognosis|Natural History, Complications and Prognosis]] == |
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| Patients who develop stress cardiomyopathy appear to have a higher prevalence of anxiety disorders preceding the event which suggests that psychosocial stress may be a predisposing factor <ref>Summers et al. JACC 2010</ref>.
| | == Diagnosis == |
| | [[Stress cardiomyopathy criteria| Diagnostic Criteria]] | |
| | [[Stress cardiomyopathy history and symptoms|History and Symptoms]] | [[Stress cardiomyopathy physical examination|Physical Examination]] | [[Stress cardiomyopathy laboratory findings|Laboratory Findings]] | [[Stress cardiomyopathy electrocardiogram|Electrocardiogram]] | [[Stress cardiomyopathy chest x ray | Chest X Ray]] | [[Stress cardiomyopathy CT| CT]] | [[Stress cardiomyopathy MRI|MRI]] | [[Stress cardiomyopathy echocardiography or ultrasound|Echocardiography]] | [[Stress cardiomyopathy other imaging findings| Other Imaging Findings]] | [[Stress cardiomyopathy other diagnostic studies|Other Diagnostic Studies]] |
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| While some of the original researchers of apical ballooning suggested that [[coronary spasm|spasm]] in multiple coronary arteries could reduce [[epicardial blood flow]] to cause transient stunning of the myocardium (Kurisu et al. American Heart Journal 2002), other researchers have shown that vasospasm is much less common than initially thought (Tsuchuhashi K et al. JACC 2001, Kawai et al. JPJ 2000, Desmet et al. Heart 2003). It has also been noted that when there is epicardial artery vasospasm, even in multiple arteries, that they do not correlate with the areas of myocardium that are hypokinetic (Abe et al. JACC 2003).
| | == Treatment == |
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| One final hypothesis is that the syndrome is due to microvascular dysfunction.
| | [[Stress cardiomyopathy medical therapy|Medical Therapy]] | [[Stress cardiomyopathy surgery|Surgery]] | [[Stress cardiomyopathy primary prevention|Primary Prevention]] | [[Stress cardiomyopathy secondary prevention|Secondary Prevention]] | [[Stress cardiomyopathy cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Stress cardiomyopathy future or investigational therapies|Future or Investigational Therapies]] |
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| It may be that the pathophysiology is multifactorial.
| | == Case Studies == |
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| == Differentiating Stress Cardiomyopathy from other Conditions ==
| | : [[Stress cardiomyopathy case study one|Case #1]] |
| Other conditions that stress cardiomyopathy should be distinguished from include:
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| #[[Acute Coronary Syndrome]] (common)
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| #[[Myocarditis]] (uncommon) | |
| #[[Pheochromocytoma]] induced cardiomyopathy (rare)
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| == Epidemiology and Demographics ==
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| The exact incidence is unknown, but it is estimated that apical ballooning syndrome may account for 1-2% of patients who present with an [[acute myocardial infarction]]. The cardiomyopathy appears to occur almost exclusively in post-menopausal women, although a few cases have been reported in younger women and males.<ref name=Azzarelli-2006>{{cite journal | author=Azzarelli S, Galassi AR, Amico F, Giacoppo M, Argentino V, Tomasello SD, Tamburino C, Fiscella A. | title=Clinical features of transient left ventricular apical ballooning | journal=Am J Cardiol. | year=2006 | volume=98 | issue=9 | pages=1273-6 | id=PMID 17056345}}</ref>
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| ==Risk Factors==
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| Often there is a history of a recent severe emotional or physical stress.<ref name=Azzarelli-2006 /> Case series looking at large groups of patients report that some patients develop apical balloon syndrome 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 <ref>{{cite journal |last=Elesber |first=AA |year=2007 |month=July |title=Four-Year Recurrence Rate and Prognosis of the Apical Ballooning Syndrome |journal=J Amer Coll Card |volume=50 |issue=5 |pages=448-52}}</ref>. The syndrome has been reported to occur after earthquakes, <ref name="pmid8615397">{{cite journal |author=Yamabe H, Hanaoka J, Funakoshi T, ''et al'' |title=Deep negative T waves and abnormal cardiac sympathetic image (123I-MIBG) after the Great Hanshin Earthquake of 1995 |journal=Am. J. Med. Sci. |volume=311 |issue=5 |pages=221–4 |year=1996 |pmid=8615397 |doi=}}</ref> after non-cardiac surgery, <ref name="pmid17184686">{{cite journal |author=Berman M, Saute M, Porat E, ''et al'' |title=Takotsubo cardiomyopathy: expanding the differential diagnosis in cardiothoracic surgery |journal=Ann. Thorac. Surg. |volume=83 |issue=1 |pages=295–8 |year=2007 |pmid=17184686 |doi=10.1016/j.athoracsur.2006.05.115}}</ref> and in patients with noncardiac medical emergencies. <ref name="pmid11796564">{{cite journal |author=Akashi YJ, Sakakibara M, Miyake F |title=Reversible left ventricular dysfunction "takotsubo" cardiomyopathy associated with pneumothorax |journal=Heart |volume=87 |issue=2 |pages=E1 |year=2002 |pmid=11796564 |doi=}}</ref>
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| ==Natural History, Complications and Prognosis==
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| Provided that the individual survives their initial presentation, the left ventricular function improves within days to weeks.<ref name="pmid17483198">{{cite journal |author=Akashi YJ, Barbaro G, Sakurai T, Nakazawa K, Miyake F |title=Cardiac autonomic imbalance in patients with reversible ventricular dysfunction takotsubo cardiomyopathy |journal=QJM |volume=100 |issue=6 |pages=335–43 |year=2007 |pmid=17483198 |doi=10.1093/qjmed/hcm028}}</ref>
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| ==Complications<ref name="pmid17692942">{{cite journal |author=Brunetti ND, Ieva R, Rossi G, Barone N, De Gennaro L, Pellegrino PL, Mavilio G, Cuculo A, Di Biase M |title=Ventricular outflow tract obstruction, systolic anterior motion and acute mitral regurgitation in Tako-Tsubo syndrome |journal=[[International Journal of Cardiology]] |volume=127 |issue=3 |pages=e152–7 |year=2008 |month=July |pmid=17692942 |doi=10.1016/j.ijcard.2007.04.149 |url=http://linkinghub.elsevier.com/retrieve/pii/S0167-5273(07)01161-8 |accessdate=2011-04-16}}</ref>==
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| *[[Heart failure]]
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| *[[Cardiogenic shock]]
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| *[[Left ventricular outflow tract obstruction]]
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| *[[Mitral regurgitation]]<ref name="pmid19774331">{{cite journal |author=Haghi D, Röhm S, Suselbeck T, Borggrefe M, Papavassiliu T |title=Incidence and clinical significance of mitral regurgitation in Takotsubo cardiomyopathy |journal=[[Clinical Research in Cardiology : Official Journal of the German Cardiac Society]] |volume=99 |issue=2 |pages=93–8 |year=2010 |month=February |pmid=19774331 |doi=10.1007/s00392-009-0078-1 |url=http://dx.doi.org/10.1007/s00392-009-0078-1 |accessdate=2011-04-16}}</ref><ref>http://circimaging.ahajournals.org/content/early/2011/04/15/CIRCIMAGING.110.962845.abstract</ref>
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| *[[Ventricular arrhythmias]]
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| ==Prognosis==
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| The recurrence rate is about 3%<ref name="pmid1765184">{{cite journal |author=Barkhattov TP |title=[The pathological preliminary period] |language=Russian |journal=[[Felʹdsher I Akusherka]] |volume=56 |issue=8 |pages=51–4 |year=1991 |month=August |pmid=1765184 |doi= |url= |accessdate=2011-04-16}}</ref><ref name="pmid18294473">{{cite journal |author=Prasad A, Lerman A, Rihal CS |title=Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction |journal=[[American Heart Journal]] |volume=155 |issue=3 |pages=408–17 |year=2008 |month=March |pmid=18294473 |doi=10.1016/j.ahj.2007.11.008 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-8703(07)00914-3 |accessdate=2011-04-16}}</ref>. The in-hospital mortality is very low (1-2%), typically related to the underlying disease in those with physical stressors. Long term survival is good.
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| ==Diagnosis==
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| ===History===
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| A directed history should be obtained to evaluate if the patient has a history of emotional stress such as the death of a loved one or loss of job.
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| ===Symptoms===
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| *The typical presentation of patients with stress cardiomyopathy includes acute onset of [[chest pain]] or [[shortness of breath]], and is similar to an [[acute coronary syndrome]]
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| * Sudden onset of [[congestive heart failure]]
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| ===Physical examination===
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| * Bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted.
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| ===Coronary Angiography and Left Ventriculography===
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| Evaluation of individuals with takotsubo cardiomyopathy typically include a [[coronary angiogram]], which does not reveal any significant blockages that would cause the [[left ventricle|left ventricular]] dysfunction.
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| ===Mayo Criteria===
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| Mayo Clinic Criteria for Apical Ballooning Syndrome. All 4 must be present <ref name="pmid17283269">{{cite journal |author=Prasad A |title=Apical ballooning syndrome: an important differential diagnosis of acute myocardial infarction |journal=Circulation |volume=115 |issue=5 |pages=e56–9 |year=2007 |pmid=17283269 |doi=10.1161/CIRCULATIONAHA.106.669341}}</ref>:
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| #Transient hypokinesis, akinesis or dyskinesis of the left ventricular mid-segments with or without apical involvement. The regional wall motion abnormalities extend beyond a single epicardial vascular distribution. A stressful trigger is often, but not always present
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| #Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
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| #New electrocardiographic abnormalities (either ST-segment elevation and/or T- wave inversion) or modest elevation in cardiac [[troponin]].
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| #Absence of [[pheochromocytoma]] and [[myocarditis]]
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| ===Electrocardiogram===
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| The [[electrocardiogram|EKG]] findings are often confused with those of an acute anterior wall [[myocardial infarction]].<ref name=Azzarelli-2006 /><ref name=Bybee-2006>{{cite journal | author=Bybee KA, Motiei A, Syed IS, Kara T, Prasad A, Lennon RJ, Murphy JG, Hammill SC, Rihal CS, Wright RS | title=Electrocardiography cannot reliably differentiate transient left ventricular apical ballooning syndrome from anterior ST-segment elevation myocardial infarction | journal=J Electrocardiol | year=2006 | id=PMID 17067626}}</ref> While the ECG may reveal ST-segment elevation, it may also reveal non-specific ST/T wave abnormality, usually in the precordial leads. The 12-lead ECG alone is not helpful in differentiating apical ballooning syndrome from a traditional thrombotic [[ST-elevation myocardial infarction]]. Evolutionary changes occur over 2 to 3 days that are characteristic and include resolution of the ST-segment elevation and development of diffuse and frequently deep T-wave inversion.
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| [[Image:Takotsubo ECG.JPEG|thumb|center|ECG showing [[sinus tachycardia]] and non-specific [[ST segment|ST]] and [[T wave]] changes from a patient with confirmed Takotsubo cardiomyopathy.]]
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| The diagnosis of takotsubo cardiomyopathy may be difficult upon presentation. The [[electrocardiogram|EKG]] findings are often confused with those found during an acute anterior wall [[myocardial infarction]].<ref name=Azzarelli-2006 /><ref name=Bybee-2006>{{cite journal | author=Bybee KA, Motiei A, Syed IS, Kara T, Prasad A, Lennon RJ, Murphy JG, Hammill SC, Rihal CS, Wright RS | title=Electrocardiography cannot reliably differentiate transient left ventricular apical ballooning syndrome from anterior ST-segment elevation myocardial infarction | journal=J Electrocardiol | year=2006 | pmid=17067626}}</ref>
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| ==== Biomarker Studies ====
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| Cardiac biomarkers of myonecrosis, especially [[troponin]], are invariably elevated.
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| ====Echocardiography====
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| [[Image:Takotsubo ultrasound.gif|center|thumb|(A) [[Echocardiograph]] showing dilatation of the left ventricle in the acute phase. (B) Resolution of left ventricular function on repeat echocardiograph 6 days later.]]
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| ====Cardiac Catheterization====
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| Coronary angiography usually demonstrates normal coronary arteries or mild coronary atherosclerosis. The left ventriculogram usually reveals characteristic regional wall motion abnormalities which involve the mid and usually the apical segments. There is sparing of the basal systolic function, and the wall motion abnormality extends beyond the distribution of any one single coronary artery.
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| [[Image:Takotsubo left ventriculogram.jpg|center|thumb|Left ventriculogram during [[systole]] displaying the characteristic apical ballooning with apical motionlessness in a patient with Takotsubo cardiomyopathy.]]
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| 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.
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| ====Magnetic Resonance Imaging====
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| Cardiac magnetic resonance imaging is helpful in excluding a [[myocardial infarction]] due to the absence of delayed gadolinium hyperenhancement.
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| The MRIs below show a patients heart with apical ballooning and then later after resolution of the apical ballooning.
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| MRI during apical balllooning:
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| <youtube v=23w6f71zTXI/>
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| ____
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| MRI following resolution of apical ballooning:
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| <youtube v=qE0YrlQ5d1o/>
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| ====The Various Patterns of Wall Motion Abnormalities====
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| It should be that the wall motion abnormalities are not always anteroapical.
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| <div align="center">
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| <gallery heights="175" widths="175">
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| Image:Takotsubo Diagram.jpg|Different end-systolic left ventricular (LV) silhouettes. A, <ref>Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol. 2003;41:737-742.</ref>; B, <ref>San Roman Sanchez D, Medina O, Jimenez F, Rodriguez JC, Nieto V. Dynamic intraventricular obstruction in acute myocardial infarction. Echocardiography. 2001;18:515-518.</ref>; C, <ref>Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med. 2005;352:539-548.</ref>; D, <ref>Rivera JM, Locketz AJ, Fritz KD, et al. “Broken heart syndrome” after separation (from OxyContin). Mayo Clin Proc. 2006;81:825-828.</ref>; E, <ref>Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart. 2003;89:1027-1031.</ref>; and F, <ref>Reyburn AM, Vaglio JC Jr. Transient left ventricular apical ballooning syndrome. Mayo Clin Proc. 2006;81:824.</ref>. There is wide heterogeneity among the different patterns, varying from a relatively small akinetic apical area in C to a wide global akinesia in D and E. <ref>Ibanez B. Takotsubo Syndrome: A Bayesian Approach to Interpreting Its Pathogenesis Mayo Clin Proc. 2006; 81: 732-735</ref>
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| </gallery>
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| </div>
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| ===The Eitel Study===
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| Recent research has acknowledged the shortcoming of existing data <ref>Eitel I, von Knobelsdorff-Brekenhoff F, Bernhardt P, et al. Clinical characteristics and CV magnetic resonance findings in stress (Takotsubo) cardiomyopathy. JAMA 2011; 306:277-286.</ref>. An attempt has been made to prospectively evaluate the influence of stress cardiomyopathy. The Eitel study, conducted by Dr. Ingo Eitel of the University of Leipzig Heart Center, Germany, evaluated a population of 256 European and North American patients who presented with stress cardiomyopathy at tertiary care centers. Patients were prospectively followed up with between the first and sixth month after the acute event. The primary outcome of this study was the complete recovery of the left ventricular [[Left ventricle|(LV)]] [[LV dysfunction|dysfunction]]. Study demographics revealed that those patients presenting with stress cardiomyopathy included members of the populations not previously thought to be afflicted with the syndrome. [[menopause|Post-menopausal]]women made up 81% of enrolled patients, while 8% were younger women, and 11% were men. The data suggests that stress cardiomyopathy has a much broader range of influence than originally conceived.
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| Similarly, though it had been previously reported that an identifiable stressful event occurred in most patients (90%) prior to onset of stress cardiomyopathy, only 71% of patients in Eitel et al.’s study experienced a clearly identifiable emotional or physical trigger. Thus, it cannot be assumed that all stress cardiomyopathy patients experience a common trigger, and a stress cardiomyopathy diagnosis cannot be discounted.
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| To date, the Eitel study is the largest, (multi-center) cardiovascular MRI imaging series of stress cardiomyopathy. Though more research is needed to examine this rare disease, Eitel et al have found that stress cardiomyopathy can be accurately diagnosed by identifying a typical pattern of LV dysfunction, myocardial edema, absence of significant necrosis/fibrosis, and markers of myocardial inflammation.
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| Of the 256 study patients, 239 patients (93%) had cardiovascular MRI data available. This data shows that there are four distinct patterns of regional ventricular ballooning: apical (82%), biventricular (34%), midventricular (17%), and basal (1%). Because patients with [[Right ventricle|RV]] involvement tended to be older, hospitalized for longer, and have markers of heart failure, biventricular ballooning on MRI “may portend a longer and more severe course of disease compared with patients with isolated [[Left ventricle|(LV)]] involvement.” Dysfunctions in the right ventricle are important to identify due to its effects on morbidity, treatment, and outcome. During follow up MRIs, patients exhibited normalization of [[Ejection fraction|LVEF]] (66%) and inflammatory markers in the absence of significant fibrosis in all patients.
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| ==Treatment==
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| The treatment of stress cardiomyopathy is supportive as the condition is reversible. Initial treatment should be similar to that of an acute coronary syndrome with therapy directed at relieving myocardial ischemia with administration of aspirin, intravenous heparin and [[beta blockers]]. Once a diagnosis of stress cardiomyopathy has been confirmed and an acute coronary syndrome excluded, consideration should be given to continuing beta-blocker therapy empirically since catecholamines are suspected of contributing to the syndrome. Diuretics are effective for the treatment of congestive heart failure. [[Angiotensin converting enzyme inhibitors]] may be used if the diagnosis is uncertain, until there is complete recovery of systolic function. Insofar as the left ventricular function and apical wall motion return to normal within days or weeks, long-term anti-coagulation does not appear to be necessary.
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| ==References==
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| {{Reflist|2}}
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| [[de:Stress-Kardiomyopathie]]
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