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| {{Stress cardiomyopathy}} | | {{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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| ==Risk Factors== | | == [[Stress cardiomyopathy pathophysiology|Pathophysiology]] == |
| 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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| Although 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 <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>. Thus, it cannot be assumed that all stress cardiomyopathy patients experience a common trigger, and a stress cardiomyopathy diagnosis cannot be discounted if a trigger is not present.
| | == [[Stress cardiomyopathy causes|Causes]] == |
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| ==Natural History, Complications and Prognosis== | | == [[Stress cardiomyopathy differential diagnosis|Differentiating Stress Cardiomyopathy from other Diseases]] == |
| 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>== | | == [[Stress cardiomyopathy epidemiology and demographics|Epidemiology and Demographics]] == |
| *[[Heart failure]]
| | ==[[Stress cardiomyopathy risk factors | Risk Factors]]== |
| *[[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== | | == [[Stress cardiomyopathy natural history, complications and prognosis|Natural History, Complications and Prognosis]] == |
| 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== | | == Diagnosis == |
| ===History===
| | [[Stress cardiomyopathy criteria| Diagnostic Criteria]] | |
| 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.
| | [[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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| ===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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| ===Physical examination=== | | == Treatment == |
| * Bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted.
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| ===Electrocardiogram===
| | [[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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| 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.
| | == Case Studies == |
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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.]]
| | : [[Stress cardiomyopathy case study one|Case #1]] |
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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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| The use of [[Magnetic resonance imaging|MRIs]] as a valuable diagnostic tool in differentiating cardiomyopathy from acute [[myocardial infarction]] and [[myocarditis]] cases. Cardiac magnetic resonance imaging is helpful in excluding a [[myocardial infarction]] due to the absence of delayed gadolinium hyperenhancement.
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| The Eitel study is the largest (n=256), (multi-center) cardiovascular MRI imaging series of stress cardiomyopathy <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>. 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. 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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| ====MRI Examples====
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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.
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| </gallery>
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| </div>
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| 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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| ===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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| ==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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