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Latest revision as of 16:53, 10 March 2022

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2] Sara Zand, M.D.[3]

Synonyms and keywords: Takotsubo syndrome, TTS, Takotsubo cardiomyopathy, broken heart syndrome, Stress cardiomyopathy, left ventricular outflow obstruction ( LVOTO)

Overview

COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020. This disorder is the result of extreme sympathetic stimulation due to the abnormal release of catecholamines and cortisol leading to rapid, severe, reversible cardiac dysfunction, as well as, wall motion abnormality of the left ventricle subtending more than one coronary artery territory, without evidence of significant obstructive coronary artery disease. Few cases of stress cardiomyopathy reported in literature due to direct consequences of covid-19 on the myocardium. However, due to increased psychological, social, economical distress during covid-19 pandemic, the incidence of stress cardiomyopathy in non-covid-19 patients increased significantly compared with prepandemic periods. In general, stress cardiomyopathy may develope in the setting of emotional stress or secondary to infections such as covid-19. The latter may have worse prognosis in terms of mortality compared with emotional trigger.

Historical Perspective

COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020.^[1]

Classification

Takotsubo cardiomyopathy is classified as follows:^[2]

Primary takotsubo cardiomyopathy: acute cardiac symptoms resulting from emotional or physical stress, main cause of seeking medical attention
Secondary takotsubo cardiomyopathy: developing in hospitalized patients for other reasons

Apical type	Midventricular type	Basal type	Focal type
Common type (>80%), hypokinesia or dyskinesia of midventricular and apical parts of anterior, septal, inferior and lateral walls of left ventricle associated with hyperkinesia of basal segments	Hypokinesia or dyskinesia of midventricular segments, like a cuff in most cases, with normokinesia or hyperkinesia of basal and apical segments	Inverse takotsubo cardiomyopathy, wall motion abnormality is reciprocal to apical type, hypokinesia or dyskinesia of basal segments, normokinesia or hyperkinesia of midventricular, anterior, antroseptal, and antroapikal segments of left ventricle	Focal hypkinesia or dyskinesia of any segments of the left ventricle , commonly antroseptal wall

Pathophysiology

Inflammation and cytokine storm are the underlying mechanisms of cathecolamines release in patients with covid-19.
It is thought that COVID-19-associated stress cardiomyopathy is the result of extreme sympathetic stimulation due to abnormal release of catecholamines such as epinephrine, norepinephrine, dopamine and also high level of cortisol.
Increase level of cathecolamines and cortisol in patients with covid-19 may cause direct toxic effect on cardiomyocytes and stress cardiomyopathy.
Direct effect of cathecolamine on cardiomyocytes may lead to myocardial stunning, hyperdynamic contractility, multiple vessles spasm, and/or microvascular dysfunction.
Increased cortisol level observed in patients with covid-19 may cause isometric tension, reduced relaxasion of papillary muscles, reduced total relaxation time, without any effect on contraction time.^[3]
The mechanisms occurring in COVID-19 patients may lead to myocardial injury and left ventricular dysfunction are:.^[4]
Stress-induced adrenergic discharge as consequence of fever and inflammatory response to infection

The direct SARS-CoV-2 injury causing endothelial dysfunction, which may cause microvascular vasoconstriction that can manifest in a transient left ventricular apical dysfunction, (apical ballooning).^[5]
Proposed mechanisms that have the potential to cause myocardial injury in acute coronavirus disease 2019 cardiovascular syndrome:^[6]

Stress Induced Cardiomyopathy

Microvascular/Thrombotic Injury

Cytokine Storm

Pre-existing cardiovascular Disease

Acute Myocardial Injury Characterized by Abnormal Troponin

Viral Myocarditis

Hypoxemia

Hypotension +/- Shock

Ventricular or atrial arrhythmias

Causes

Common causes of stress cardiomyopathy include:

Physical stressors
Emotional stressors (anger, argument, surgery, natural disasters, grief, happiness)
Several medications
General anesthesia
Infectious disease
Novel coronavirus disease 2019^[5]

Differentiating COVID-19-associated stress cardiomyopathy from other Diseases

For further information about the differential diagnosis, click here.
To view the differential diagnosis of COVID-19, click here.

Differentiating diagnosis	Takotsubo cardiomyopathy	STEMI
Stressful trigger	Prominent stressful event (79%)	8%
Elevated troponin on admission	91%	37%
LVEF<40%	Higher incidence of decreased LVEF at presentation (80%)	31%
Symptoms	Chest pain (73%)	Higher rate of chest pain (100%)
Sex	Female	Male
Age	Older age (66 years old)	Mean age 60 years old
Risk factors	Lower incidence of HLP, smoking, diabetes mellitus	HLP, smoking, diabetes mellitus
Coronary angiography	Lower incidence of stenosis> 50% (15%)	Stenosis> 50% in 100%
In-hospital mortality	1.3%	3.6%

Epidemiology and Demographics

The incidence of stress cardiomyopathyassociated covid-19 is approximately 7.8% of all patients presenting acute coronary syndrome which is higher than pre-pandemic period.^[5]
In critically ill covid-19 patients, the incidence of stress cardiomyopathy is approximitely 2-4%, compared to 1-2% among general population.^[7]

Age

Stress cardiomyopathy is more commonly observed among elderly patients with a mean age of 64.6 years.

Gender

Male are more commonly affected with stress cardiomyopathy secondary to covid-19.
Primary stress cardiomyopathy is much more common in women..

Race

There is no racial predilection for stress cardiomyopathy in covid-19 patients.

Risk Factors

There are no established risk factors for COVID-19-associated stress cardiomyopathy.
In general population, secondary stress cardiomyopathy is much more commen in older men , as well as with higher incidence of conventional risk factors including HTN, diabetes mellitus, dyslipidemia, cerebrovascular disease, cardiac arrhythmia.
Common risk factors in reported takotsubo cardiomyopathy secondary to covid-19 include:
Older age

HTN

DM

Dyslipidemia

Prior stroke

Atrial fibrillation
Psychiatric illness
Hypoxia
Severe covid-19 pneumonia requiring mechanical ventilation support

Common triggers associated with development of secondary takotsubo cardiomyopathy in severe covid-19 pneumonia include:^[8]^[2]
Respiratory condition

Intubation

Medication use

Epinephrine use

Anxiety

Betablocker withdraw

Screening

There is insufficient evidence to recommend routine screening for COVID-19-associated stress cardiomyopathy.

Natural History, Complications, and Prognosis

There are varied degree of the recovery of patients with stress cardiomyopathy associated covid-19 reported in literature within two months.^[9] ^[10]^[11]

Early clinical features include acute coronary syndrome with chest pain and ECG changes and rise of troponin, acute pulmonary edema, decreased oxygen saturation without response to O2 therapy, hemodynamic instability.
Patients with stress cardiomyopathy associated with covid-19 had a longer hospital days admission compared with the pre-pandemic period.^[5]
Stress cardiomyopathy in critically ill covid-19 patients may progress to develop cardiogenic shock, pulmonary edema, hemodynamic collapse, and death.
Patients with secondary takotsubo cardiomyopathy may experience cardiogenic shock, respiratory failure requiring mechanical ventilation support and coagulation disorder. However, in reported patients with takotsubo cardiomyopathy exacerbation of respiratory status may be due to covid-19 complicating takotsubo cardiomyopathy.
Some patients may recover and have a normalized cardiac function within a few weeks. .^[12]^[13]^[14]
Prognosis of stress cardiomyopathy associated covid-19 is not clearly described yet, and mortality rate of patients with stress cardiomyopathy without covid-19 infection is approximately 5% during pandemic (similar to pre-pandemic covid-19 period). However, the mortality rate of takotsubo cardiomyopathy secondary to covid-19 pneumonia is 10 times higher than non-covid-19 patients.^[5]
Complications of stress cardiomyopathy include:^[12]^[15]^[16]^[14]^[17]^[18]^[19]^[20]^[21]^[22]
- Severe Heart failure
- Acute pulmonary edema
- Cardiogenic shock
- Dynamic left ventricular outflow tract obstruction (peak gradients >25 mmhg in echo or cath)
- Hypotension
- Moderete to severe acute functional mitral regurgitation
- Bradycardia
- QT prolongation and ventricular arrhythmias
- Torsade de pointes
- Left ventricular mural thrombus
- Mitral valve dysfunction
- Pulmonary embolism
- Systemic embolism, stroke
- LV free wall rupture
- Acute renal failure
- In-hospital death

Diagnosis

In the development of new hypotension and tachycardia in intubated covid-19 patients with comorbidities ( HTN, dyslipidemia, atrial fibrillation, previous stroke) or the need for vasopressor and presence of hypoxia, investigation about stress cardiomyopathy should be done by taking ECG and check of cardiac biomarkers ( troponin, NT-Pro BNP.
In the presence of any ECG changes or cardiac biomarkers abnormality, transthoracic echocardiography should be done

Diagnostic Study of Choice

Echocardiography is the gold standard of diagnosis of takotsubo cardiomyopathy.
High risk feature of takotsubo cardiomyopathy on echocardiography include: LVEF<45%, Moderate to severe mitral regurgitation, right ventricular involvement.
The diagnosis of stress cardiomyopathy is made when all 4 of the following diagnostic criteria are met:
- 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.
- Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
- New electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin.
- Absence of pheochromocytoma and myocarditis.^[13]^[12]
The diagnosis of COVID-19-associated stress cardiomyopathy is largely the same, but happening in the context of a SARS-CoV2 infection.

History and Symptoms

Symptoms of stress cardiomyopathy can mimic acute coronary syndrome. The most common presenting symptoms are:^[12]^[16]^[13]^[18]^[23]^[17]

Chest pain or chest tightness
Shortness of breath
Vomiting
Loss of consciousness due to syncope or cardiac arrest in rare cases

Considering emotional factors such as fear of severity of covid-19, contact with a hospitalized family member, worry about socioeconomic costs, intrusive thoughts about morbidity of covid-19 that may lead to stress cardiomyopathy. ^[11]

Physical Examination

The following physical examination findings may be seen in patients with stress cardiomyopathy:^[24]^[12]^[15]^[16]^[14]^[17]^[18]^[19]^[25]^[21]^[26]

Organ System	Findings	Suggestive Of
General appearance	Patient may be anxious, ill-appearing or diaphoretic
Vital signs	Tachypnea Tachycardia or bradycardia Hypotension	Cardiogenic shock
Cardiac	Murmurs, S3, gallop rhythm, Displaced point of maximal impulse (PMI)	Heart failure
Respiratory	Rales, crackles	Pulmonary edema

Laboratory Findings

Laboratory findings consistent with the diagnosis of stress cardiomyopathy in covid-19 patients include elevated troponin and Pro-BNP.^[5]
Elevated levels of serum catecholamines may also be found in patients with stress cardiomyopathy.^[12]^[16]^[18]^[17]
Evidence of ongoing COVID-19 disease is required to establish the diagnosis.

Electrocardiogram

The ECG findings are largely the same of the regular stress cardiomyopathy, and are often confused with those of an acute anterior wall myocardial infarction.^[12]^[18] Findings on ECG include:^[12]^[16]^[13]^[14]^[18]^[23]^[17]

ST elevation in the precordial leads
T wave inversion
Q wave formation
QT prolongation
New-onset bundle branch block (BBB)
Rarely, malignant ventricular arrhythmias may be seen

X-ray

Takotsubo refers to a ceramic pot used to trap octopuses in the Japanese language. The typical chest x-ray findings in patients with stress cardiomyopathy include a takotsubo-shaped heart, in which there is apical ballooning and narrowing of the proximal portion near the great vessels.

Echocardiography or Ultrasound

The following echocardiographic findings may be seen in patients with stress cardiomyopathy:^[16]^[13]^[14]^[17]

Apical ballooning
Apical or mid-segment dyskinesia or akinesia
Left ventricular systolic dysfunction
Reduced ejection fraction

CT scan

A cardiac CT scan can also help differentiate between stress cardiomyopathy and acute MI. Regional abnormalities in the wall motion of the heart, along with absence of coronary atherosclerosis support the diagnosis of stress cardiomyopathy over an acute MI.^[17]

Chest CT scan may also show findings associated with COVID-19 and they can include:

Unilateral or bilateral pneumonia^[27]^[28]^[29]
Mottling and ground-glass opacity
Focal or multifocal opacities
Consolidation
Septal thickening
Subpleural and lower lobe involvement more likely

MRI

Cardiac magnetic resonance (CMR) is a useful imaging modality in distinguishing between stress cardiomyopathy and myocarditis or MI. In the case of myocarditis or MI, there is delayed hyper-enhancement of gadolinium. However, absence of gadolinium hyper-enhancement supports the diagnosis of stress cardiomyopathy. Also, stress cardiomyopathy results in regional wall abnormality and its extent can best be documented using cardiac magnetic resonance.^[13]^[20]^[30]^[31]^[32]^[33]^[34]^[35]^[20]^[36]^[37]
CMR in stress cardiomyopathy shows absence of irreversible damage and segmental LV dysfunction.^[31]

Other findings on CMR include:^[17]^[20]

Hypokinetic or dyskinetic areas in the wall of the heart
Myocardial edema
Apical thrombi

Other Imaging Findings

Positron Emission Tomography (PET) Scan

In patients with stress cardiomyopathy, a PET scan may be done. Areas of hypokinesia or dyskinesia have reduced glucose utilization compared to normal regions.^[38]

Coronary Angiography

Stress cardiomyopathy can mimic an acute MI, mainly anterior MI, since the clinical presentation, ECG and laboratory findings are similar. Hence, coronary angiography is considered a great diagnostic modality to differentiate between the two diagnoses.
A normal angiography or absence of substantial coronary stenosis supports the diagnosis of stress cardiomyopathy.^[18]^[12]^[17]

Other Diagnostic Studies

Cardiac Catheterization

When patients with stress cardiomyopathy undergo cardiac catheterization, the following findings are usually reported:^[16]^[18]^[14]

Normal anatomy of the coronary arteries, without evidence of acute plaque rupture
Low ejection fraction (EF)
Minimal or no evidence of coronary vasospasm
Minimal disturbance of microcirculation

Myocardial Biopsy

The histological findings on myocardial biopsy in patients with stress cardiomyopathy include:^[12]^[16]
- Inflammatory infiltrates, consisting of mononuclear lymphocytes, leukocytes and macrophages
- Myocardial fibrosis
- Contraction bands, which may or may not be associated with necrosis

The combination of inflammatory changes and contraction bands distinguish stress cardiomyopathy from coagulative necrosis seen in MI.^[12]

Treatment

Medical Therapy

The mainstay of therapy of stress cardiomyopathy associated with covid-19 is supportive care.
In mild TTS without signs of heart failure, beta-blocker and ACEI or ARB are recommended and inotrope agents such as epinephrine, norepinephrine, dobutamine, milrinone, isoproterenol should be avoided.
In the presence of pulmonary edema without evidence of left ventricular outflow obstruction, administration of ACEI, betablockers, diuretic and nitroglycerin are recommended.
In the presence of cardiogenic shock and left ventricular outflow obstruction (no heart failure symptoms), short acting betablocker, IV fluide, and placing impella are recommended.
Diuretic, nitroglycerin, intraaortic ballon pump should be avoided in the evidence of cardiogenic shock and left ventricular outflow obstruction.
If there is evidence of pump failure in the context of cardiogenic shock, levosimentan, ECMO, impella are considered.
Arrhythmia such as VT, VF, torsades de pointes, bradycardia, long QT interval should be managed.
Temporary RV pacing is recommended in the presence of AV block and placement of permanent device is not recommended.
In the presence of bradycardia and long QTc >500 ms, betablocker should be avoided.
In the presence of left ventricular clot or large portion of akinesia of left ventricle involving apex, anticougulation therapy is recommende.
Classic treatment of heart failure including ACEI and betablocker should be kept at least three months or untill recovery of regional wall motion abnormality.
Treatment of underlying disorders such as coronary artery disease is reasonable by continuing aspirin and statin.

Surgery

Surgical intervention is not recommended for the management of COVID-19-associated stress cardiomyopathy.

Primary Prevention

There are no established measures for the primary prevention of COVID-19-associated stress cardiomyopathy.
Preventive measures should be taken to avoid COVID-19 infection.

Secondary Prevention

There are no established measures for the secondary prevention of COVID-19-associated stress cardiomyopathy.

References

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↑ 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.
↑ ^23.0 ^23.1 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.
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↑ 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.
↑ 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.
↑ Paul NS, Roberts H, Butany J, Chung T, Gold W, Mehta S, Konen E, Rao A, Provost Y, Hong HH, Zelovitsky L, Weisbrod GL (2004). "Radiologic pattern of disease in patients with severe acute respiratory syndrome: the Toronto experience". Radiographics. 24 (2): 553–63. doi:10.1148/rg.242035193. PMID 15026600.
↑ Ajlan AM, Ahyad RA, Jamjoom LG, Alharthy A, Madani TA (October 2014). "Middle East respiratory syndrome coronavirus (MERS-CoV) infection: chest CT findings". AJR Am J Roentgenol. 203 (4): 782–7. doi:10.2214/AJR.14.13021. PMID 24918624.
↑ Chen, Nanshan; Zhou, Min; Dong, Xuan; Qu, Jieming; Gong, Fengyun; Han, Yang; Qiu, Yang; Wang, Jingli; Liu, Ying; Wei, Yuan; Xia, Jia'an; Yu, Ting; Zhang, Xinxin; Zhang, Li (2020). "Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study". The Lancet. doi:10.1016/S0140-6736(20)30211-7. ISSN 0140-6736.
↑ 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.
↑ ^31.0 ^31.1 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.
↑ 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.

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[pmid28041712-17] 17.0 ^17.1 ^17.2 ^17.3 ^17.4 ^17.5 ^17.6 ^17.7 ^17.8 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.

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[pmid15687136-20] 20.0 ^20.1 ^20.2 ^20.3 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.

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[pmid26159108-22] 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.

[pmid263325472-23] 23.0 ^23.1 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.

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[pmid156871362-25] 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.

[pmid261591082-26] 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.

[pmid15026600-27] Paul NS, Roberts H, Butany J, Chung T, Gold W, Mehta S, Konen E, Rao A, Provost Y, Hong HH, Zelovitsky L, Weisbrod GL (2004). "Radiologic pattern of disease in patients with severe acute respiratory syndrome: the Toronto experience". Radiographics. 24 (2): 553–63. doi:10.1148/rg.242035193. PMID 15026600.

[pmid24918624-28] Ajlan AM, Ahyad RA, Jamjoom LG, Alharthy A, Madani TA (October 2014). "Middle East respiratory syndrome coronavirus (MERS-CoV) infection: chest CT findings". AJR Am J Roentgenol. 203 (4): 782–7. doi:10.2214/AJR.14.13021. PMID 24918624.

[ChenZhou2020-29] Chen, Nanshan; Zhou, Min; Dong, Xuan; Qu, Jieming; Gong, Fengyun; Han, Yang; Qiu, Yang; Wang, Jingli; Liu, Ying; Wei, Yuan; Xia, Jia'an; Yu, Ting; Zhang, Xinxin; Zhang, Li (2020). "Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study". The Lancet. doi:10.1016/S0140-6736(20)30211-7. ISSN 0140-6736.

[pmid17175045-30] 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.

[pmid17631086-31] 31.0 ^31.1 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.

[pmid16669180-32] 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.

[pmid12628715-33] 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.

[pmid15687123-34] 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.

[pmid19944334-35] 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.

[pmid21771988-36] 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.

[pmid18820322-37] 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.

[pmid25071891-38] 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.

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@@ Line 2: / Line 2: @@
 {{SI}}
-{{CMG}}; {{AE}} {{Jose}}
+{{CMG}}; {{AE}} {{Jose}} {{Sara.Zand}}
-{{SK}} Takotsubo syndrome, Takotsubo cardiomyopathy, broken heart syndrome, Stress cardiomyopathy
+{{SK}} Takotsubo syndrome, TTS, Takotsubo cardiomyopathy, broken heart syndrome, Stress cardiomyopathy, left ventricular outflow obstruction ( LVOTO)
 ==Overview==
-COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020. This disorder is the result of extreme [[Sympathetic nervous system|sympathetic]] stimulation due to the abnormal release of [[catecholamines]] causing [[epicardial]] [[coronary vasospasm]]. The [[incidence]] of COVID-19-associated [[stress cardiomyopathy]] is approximately 7.8% of all patients presenting [[acute coronary syndrome]].
+[[COVID-19]]-associated [[stress cardiomyopathy]] was first described by Elena Roca, an Italian physician, in April 2020. This disorder is the result of extreme [[Sympathetic nervous system|sympathetic]] stimulation due to the abnormal release of [[catecholamines]] and [[cortisol]] leading to rapid, severe, reversible  [[cardiac dysfunction]], as well as, [[wall motion abnormality]] of the [[left ventricle]] subtending more than one [[coronary artery]] territory, without evidence of significant [[obstructive]] [[coronary artery disease]]. Few cases of  [[stress cardiomyopathy]] reported in literature due to direct consequences of [[covid-19]] on the [[myocardium]]. However, due to increased [[psychological]], [[social]], [[economical]] distress during [[covid-19]] pandemic, the incidence of [[stress cardiomyopathy]] in non-[[covid-19]] [[patients]] increased significantly compared with prepandemic periods. In general,  [[stress cardiomyopathy]] may develope in the setting of [[emotional stress]] or secondary to infections such as [[covid-19]]. The latter  may have worse prognosis in terms of [[mortality]] compared with [[emotional]] [[trigger]].
 ==Historical Perspective==
@@ Line 14: / Line 15: @@
 ==Classification==
-* [[Takotsubo cardiomyopathy]] is classified into two groups:<ref name="pmid26332547">{{cite journal |vauthors=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 |title=Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy |journal=N Engl J Med |volume=373 |issue=10 |pages=929–38 |date=September 2015 |pmid=26332547 |doi=10.1056/NEJMoa1406761 |url=}}</ref>
+* [[Takotsubo cardiomyopathy]] is classified as follows:<ref name="pmid26332547">{{cite journal |vauthors=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 |title=Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy |journal=N Engl J Med |volume=373 |issue=10 |pages=929–38 |date=September 2015 |pmid=26332547 |doi=10.1056/NEJMoa1406761 |url=}}</ref>
-:* Apical [[takotsubo cardiomyopathy]] which is the most common form (80%)
-:* Midventricular form (20%)
+* Primary [[takotsubo cardiomyopathy]]: acute [[cardiac]] [[symptoms]] resulting from [[emotional]] or [[physical stress]], main cause of seeking [[medical attention]]
+* Secondary [[takotsubo cardiomyopathy]]: developing in [[hospitalized]] [[patients]] for other reasons
-==Pathophysiology==
-* It is thought that COVID-19-associated [[stress cardiomyopathy]] is the result of extreme [[Sympathetic nervous system|sympathetic]] stimulation due to abnormal release of [[catecholamines]] such as [[epinephrine]], [[norepinephrine]], [[dopamine]] causing [[epicardial]] [[coronary vasospasm]].
+{| style="border: 2px solid #4479BA; align="left"
+! style="width: 200px; background: #4479BA;" | {{fontcolor|#FFF|Apical type}}
+! style="width: 300px; background: #4479BA;" | {{fontcolor|#FFF|Midventricular type}}
+! style="width: 400px; background: #4479BA;" | {{fontcolor|#FFF|Basal type}}
+! style="width: 400px; background: #4479BA;" | {{fontcolor|#FFF|Focal type}}
+|-
+| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | Common type (>80%), [[hypokinesia]] or [[dyskinesia]] of [[midventricular]] and [[apical]] parts of [[anterior]], septal, inferior and lateral walls of [[left ventricle]] associated with [[hyperkinesia]] of basal segments
+| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[Hypokinesia]] or [[dyskinesia]] of [[midventricular segments]], like a '''[[cuff]]''' in most cases, with normokinesia or hyperkinesia  of basal and apical segments
+| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | '''Inverse takotsubo cardiomyopathy''', [[wall motion abnormality]] is reciprocal to apical type, [[hypokinesia]] or [[dyskinesia]] of basal segments, normokinesia or [[hyperkinesia]] of [[midventricular]], anterior, [[antroseptal]], and [[antroapikal]] segments of [[left ventricle]]
+| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | Focal [[hypkinesia]] or [[dyskinesia]] of any segments of the [[left ventricle]] , commonly [[antroseptal wall]]
+|-
+|}
-* Many mechanisms occurring in [[COVID-19]] patients may lead to [[myocardial injury]] and [[left ventricular dysfunction]].<ref name="pmid32523926">{{cite journal| author=Pasqualetto MC, Secco E, Nizzetto M, Scevola M, Altafini L, Cester A | display-authors=etal| title=Stress Cardiomyopathy in COVID-19 Disease. | journal=Eur J Case Rep Intern Med | year= 2020 | volume= 7 | issue= 6 | pages= 001718 | pmid=32523926 | doi=10.12890/2020_001718 | pmc=7279910 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32523926  }}</ref>
+==Pathophysiology==
-*One of the proposed theory is that patients may experience [[Stress (medicine)|stress-induced]] [[adrenergic]] discharge as consequence of [[fever]] and [[inflammatory]] response to [[infection]]. One other factor to consider is the direct [[SARS-CoV-2]] injury causing [[endothelial dysfunction]], which may cause [[Microvascular angina|microvascular]] [[vasoconstriction]] that can manifest in a transient [[Left ventricular dysfunction|left ventricular apical dysfunction]], (apical ballooning).<ref name="pmid32644140" />
+* [[Inflammation]] and [[cytokine storm]] are the underlying mechanisms of  [[cathecolamines release]] in [[patients]] with [[covid-19]].
+* It is thought that [[COVID-19]]-associated [[stress cardiomyopathy]] is the result of extreme [[Sympathetic nervous system|sympathetic]] stimulation due to abnormal release of [[catecholamines]] such as [[epinephrine]], [[norepinephrine]], [[dopamine]] and also high level of [[cortisol]].
+* Increase level of [[cathecolamines]] and [[cortisol]] in [[patients]] with [[covid-19]] may cause direct [[toxic effect]] on [[cardiomyocytes]] and [[stress cardiomyopathy]].
+* Direct effect of [[cathecolamine]] on [[cardiomyocytes]] may lead to [[myocardial stunning]], [[hyperdynamic contractility]], [[multiple vessles spasm]], and/or [[microvascular dysfunction]].
+*
+* Increased  [[ cortisol]] level  observed in [[patients]] with [[covid-19]] may cause [[isometric tension]], reduced relaxasion of [[papillary muscles]], reduced total relaxation time, without any effect on contraction time.<ref name="pmid32563278">{{cite journal |vauthors=Tan T, Khoo B, Mills EG, Phylactou M, Patel B, Eng PC, Thurston L, Muzi B, Meeran K, Prevost AT, Comninos AN, Abbara A, Dhillo WS |title=Association between high serum total cortisol concentrations and mortality from COVID-19 |journal=Lancet Diabetes Endocrinol |volume=8 |issue=8 |pages=659–660 |date=August 2020 |pmid=32563278 |pmc=7302794 |doi=10.1016/S2213-8587(20)30216-3 |url=}}</ref>
+* The mechanisms occurring in [[COVID-19]] [[patients]] may lead to [[myocardial injury]] and [[left ventricular dysfunction]] are:.<ref name="pmid32523926">{{cite journal| author=Pasqualetto MC, Secco E, Nizzetto M, Scevola M, Altafini L, Cester A | display-authors=etal| title=Stress Cardiomyopathy in COVID-19 Disease. | journal=Eur J Case Rep Intern Med | year= 2020 | volume= 7 | issue= 6 | pages= 001718 | pmid=32523926 | doi=10.12890/2020_001718 | pmc=7279910 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32523926  }}</ref>
+*:: [[Stress (medicine)|Stress-induced]] [[adrenergic]] discharge as consequence of [[fever]] and [[inflammatory]] response to [[infection]]
+*:: The direct [[SARS-CoV-2]] injury causing [[endothelial dysfunction]], which may cause [[Microvascular angina|microvascular]] [[vasoconstriction]] that can manifest in a transient [[Left ventricular dysfunction|left ventricular apical dysfunction]], (apical ballooning).<ref name="pmid32644140" />
 * Proposed mechanisms that have the potential to cause [[myocardial injury]] in acute [[coronavirus]] disease 2019 cardiovascular syndrome:<ref name="pmid32297796">{{cite journal| author=Hendren NS, Drazner MH, Bozkurt B, Cooper LT| title=Description and Proposed Management of the Acute COVID-19 Cardiovascular Syndrome. | journal=Circulation | year= 2020 | volume= 141 | issue= 23 | pages= 1903-1914 | pmid=32297796 | doi=10.1161/CIRCULATIONAHA.120.047349 | pmc=7314493 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32297796  }} </ref><br />
 <br>
@@ Line 29: / Line 54: @@
 {{familytree/start}}
 {{familytree | | | | | | | | | | | | | | A01 | | |A01=Stress Induced Cardiomyopathy}}
-{{familytree | | | | | | | | | | B01 |-|.|!|,|-| B02 | | | | | | | |B01=Microvascular/Thrombotic Injury|B02=Cytokine Storm}}
+{{familytree | | | | | | | | | | B01 |-|.|!|,|-| B02 | | | | | | | |B01=Microvascular/[[Thrombotic]] Injury|B02=[[Cytokine Storm]]}}
-{{familytree | | | | | | C01 |-|-|-|-|-| C02 |-|-|-|-|-| C03 | | | |C01=Pre-existing [[cardiovascular Disease]]|C02=Acute Myocardial Injury Characterized by Abnormal [[Troponin]]|C03=Viral [[Myocarditis]]}}
+{{familytree | | | | | | C01 |-|-|-|-|-| C02 |-|-|-|-|-| C03 | | | |C01=Pre-existing [[cardiovascular Disease]]|C02=Acute [[Myocardial Injury]] Characterized by Abnormal [[Troponin]]|C03=Viral [[Myocarditis]]}}
 {{familytree | | | | | | | | | | D01 |-|'|!|`|-| D02 | | | | | | | |D01=[[Hypoxemia]]|D02=[[Hypotension]] +/- [[Shock]] }}
-{{familytree | | | | | | | | | | | | | | E01 | | | | | | | | | | | |E01=[[Ventricular arrhythmias|Ventricular]] or [[Atrial Arrhythmias]]}}
+{{familytree | | | | | | | | | | | | | | E01 | | | | | | | | | | | |E01=[[Ventricular]] or [[atrial]] arrhythmias}}
 {{familytree | | | | | | | | | | | | | | | | | | | | | | | | | | | |}}
 {{familytree | | | | | | | | | | | | | | | | | | | | | | | | | | | |}}
@@ Line 38: / Line 63: @@
 ==Causes==
+Common causes of [[stress cardiomyopathy]] include:
-* COVID-19-associated [[stress cardiomyopathy]] may be caused by a very intense [[Sympathetic nervous system|sympathetic]] stimulation which is theorized to be caused either due to direct viral action or the ongoing [[psychological]], economical and social effects (physical distancing rules, lack of social interaction) of the [[Pandemics|pandemic]] due to the imposed [[quarantine]].<ref name="pmid32644140">{{cite journal| author=Jabri A, Kalra A, Kumar A, Alameh A, Adroja S, Bashir H | display-authors=etal| title=Incidence of Stress Cardiomyopathy During the Coronavirus Disease 2019 Pandemic. | journal=JAMA Netw Open | year= 2020 | volume= 3 | issue= 7 | pages= e2014780 | pmid=32644140 | doi=10.1001/jamanetworkopen.2020.14780 | pmc=7348683 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32644140  }}</ref>
+* [[Physical stressors]]
+* [[Emotional]] stressors ([[anger]], [[argument]], [[surgery]], [[natural disasters]], [[ grief]], [[happiness]])
+* Several [[medications]]
+* General [[anesthesia]]
+*[[Infectious disease]]
+* [[Novel coronavirus disease 2019]]<ref name="pmid32644140">{{cite journal| author=Jabri A, Kalra A, Kumar A, Alameh A, Adroja S, Bashir H | display-authors=etal| title=Incidence of Stress Cardiomyopathy During the Coronavirus Disease 2019 Pandemic. | journal=JAMA Netw Open | year= 2020 | volume= 3 | issue= 7 | pages= e2014780 | pmid=32644140 | doi=10.1001/jamanetworkopen.2020.14780 | pmc=7348683 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32644140  }}</ref>
 ==Differentiating COVID-19-associated stress cardiomyopathy from other Diseases==
 * For further information about the differential diagnosis, click [[COVID-19-associated stress cardiomyopathy differential diagnosis|here]].
 *To view the differential diagnosis of COVID-19, [[COVID-19 differential diagnosis|click here]].<br />
+{| class="wikitable"
+|-
+!  Differentiating diagnosis
+!  [[Takotsubo cardiomyopathy]]
+!  [[STEMI]]
+|-
+| [[Stressful trigger]]
+| [[Prominent stressful event]] (79%)
+| 8%
+|-
+|  Elevated [[troponin]] on admission
+| 91%
+| 37%
+|-
+| [[LVEF]]<40%
+|  Higher incidence of decreased [[LVEF]] at presentation (80%)
+| 31%
+|-
+| [[Symptoms]]
+| [[Chest pain]] (73%)
+| Higher rate of [[chest pain]] (100%)
+|-
+| [[Sex]]
+| [[Female]]
+| [[Male]]
+|-
+| [[Age]]
+| [[Older age ]] (66 years old)
+| [[Mean]] age 60 years old
+|-
+| [[Risk factors]]
+| Lower incidence of [[HLP]], [[smoking]], [[diabetes mellitus]]
+| [[HLP]], [[smoking]], [[diabetes mellitus]]
+|-
+| [[Coronary angiography]]
+|  Lower incidence of [[stenosis]]> 50% (15%)
+| [[Stenosis]]> 50% in 100%
+|-
+| [[In-hospital mortality]]
+| 1.3%
+| 3.6%
+|}
 ==Epidemiology and Demographics==
-* The [[incidence]] of COVID-19-associated [[stress cardiomyopathy]] is approximately 7.8% of all patients presenting [[acute coronary syndrome]].<ref name="pmid32644140" />
+* The [[incidence]] of [[stress cardiomyopathy]]associated [[covid-19]] is approximately 7.8% of all [[patients]] presenting [[acute coronary syndrome]] which is higher than pre-pandemic period.<ref name="pmid32644140" />
-* In comparison, the [[stress cardiomyopathy]] [[Incidence (epidemiology)|incidence]] in the pre-[[COVID-19]] period was varying between 1.5-1.8%.<ref name="pmid32644140" />
+* In critically ill [[covid-19]] [[patients]], the incidence of [[stress cardiomyopathy]] is approximitely 2-4%, compared  to 1-2% among general population.<ref name="pmid2589">{{cite journal |vauthors=Beppu M, Terao T, Osawa T, Jentsch F |title=Photoaffinity labeling of concanavalin A. Preparation of a concanavalin A derivative with reduced valence |journal=J Biochem |volume=78 |issue=5 |pages=1013–9 |date=November 1975 |pmid=2589 |doi=10.1093/oxfordjournals.jbchem.a130978 |url=}}</ref>
+===Age===
+*[[Stress cardiomyopathy]] is more commonly observed among [[elderly]] [[patients]] with a mean age of 64.6 years.
+===Gender===
+*[[Male]] are more commonly affected with [[stress cardiomyopathy]] secondary to [[covid-19]].
+* Primary [[stress cardiomyopathy]] is much more common in [[women]]..
+===Race===
+*There is no racial predilection for [[stress cardiomyopathy]] in [[covid-19]] [[patients]].
 ==Risk Factors==
-* There are no established risk factors for COVID-19-associated [[stress cardiomyopathy]].
+* There are no established risk factors for [[COVID-19]]-associated [[stress cardiomyopathy]].
-*[[Hypertension, systemic|Hypertension]] was, however, the most frequently [[comorbidity]] found across the groups in the [[COVID-19]] period patients, as was [[hyperlipidemia]].<ref name="pmid32644140" />
+* In general population,  secondary [[stress cardiomyopathy]] is much more commen in older [[men]] , as well as with higher incidence of conventional risk factors including [[HTN]], [[diabetes mellitus]], [[dyslipidemia]], [[cerebrovascular disease]], [[cardiac arrhythmia]].
+*  Common risk factors in reported [[takotsubo cardiomyopathy]] secondary to [[covid-19]] include:
+*:[[Older]] [[age]]
+*: [[HTN]]
+*:[[DM]]
+*:[[ Dyslipidemia]]
+*:Prior [[stroke]]
+:* [[Atrial fibrillation]]
+:* [[Psychiatric illness]]
+:* [[Hypoxia]]
+:*Severe [[covid-19]] [[pneumonia]] requiring [[mechanical ventilation]] support
+*Common triggers associated with development of secondary [[takotsubo cardiomyopathy]] in severe [[covid-19]] [[pneumonia]] include:<ref name="pmid24685327">{{cite journal |vauthors=Singh K, Carson K, Shah R, Sawhney G, Singh B, Parsaik A, Gilutz H, Usmani Z, Horowitz J |title=Meta-analysis of clinical correlates of acute mortality in takotsubo cardiomyopathy |journal=Am J Cardiol |volume=113 |issue=8 |pages=1420–8 |date=April 2014 |pmid=24685327 |doi=10.1016/j.amjcard.2014.01.419 |url=}}</ref><ref name="pmid26332547">{{cite journal |vauthors=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 |title=Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy |journal=N Engl J Med |volume=373 |issue=10 |pages=929–38 |date=September 2015 |pmid=26332547 |doi=10.1056/NEJMoa1406761 |url=}}</ref>
+*: [[Respiratory condition]]
+*: [[Intubation]]
+*: [[Medication]] use
+*: [[Epinephrine]] use
+*: [[Anxiety]]
+*: [[Betablocker]] withdraw
 ==Screening==
@@ Line 61: / Line 166: @@
 ==Natural History, Complications, and Prognosis==
-*[[COVID-19]]-associated [[stress cardiomyopathy]] outcomes were similar to the [[stress cardiomyopathy]] not related to [[COVID-19]] with regard to mortality and 30-day rehospitalization.<ref name="pmid32644140" />
-* The same study showed that COVID-19-associated [[stress cardiomyopathy]] patients had a significantly longer hospital length of stay. in comparison to the ones not related to [[COVID-19]].<ref name="pmid32644140" />
-* Provided that patients survive the initial insult without any complications, most patients recover and have a normalized cardiac function within a few weeks.<ref name="pmid19106400">{{cite journal |vauthors=Akashi YJ, Goldstein DS, Barbaro G, Ueyama T |title=Takotsubo cardiomyopathy: a new form of acute, reversible heart failure |journal=Circulation |volume=118 |issue=25 |pages=2754–62 |year=2008 |pmid=19106400 |pmc=4893309 |doi=10.1161/CIRCULATIONAHA.108.767012 |url=}}</ref><ref name="pmid18294473">{{cite journal |vauthors=Prasad A, Lerman A, Rihal CS |title=Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction |journal=Am. Heart J. |volume=155 |issue=3 |pages=408–17 |year=2008 |pmid=18294473 |doi=10.1016/j.ahj.2007.11.008 |url=}}</ref><ref name="pmid19726776">{{cite journal |vauthors=Tsai TT, Nallamothu BK, Prasad A, Saint S, Bates ER |title=Clinical problem-solving. A change of heart |journal=N. Engl. J. Med. |volume=361 |issue=10 |pages=1010–6 |year=2009 |pmid=19726776 |doi=10.1056/NEJMcps0903023 |url=}}</ref>
+*  There are varied degree of the recovery of [[patients]] with [[stress cardiomyopathy]] associated [[covid-19]] reported  in literature within two months.<ref name="pmid32267502">{{cite journal |vauthors=Sala S, Peretto G, Gramegna M, Palmisano A, Villatore A, Vignale D, De Cobelli F, Tresoldi M, Cappelletti AM, Basso C, Godino C, Esposito A |title=Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection |journal=Eur Heart J |volume=41 |issue=19 |pages=1861–1862 |date=May 2020 |pmid=32267502 |pmc=7184339 |doi=10.1093/eurheartj/ehaa286 |url=}}</ref> <ref name="pmid32328588">{{cite journal |vauthors=Dabbagh MF, Aurora L, D'Souza P, Weinmann AJ, Bhargava P, Basir MB |title=Cardiac Tamponade Secondary to COVID-19 |journal=JACC Case Rep |volume=2 |issue=9 |pages=1326–1330 |date=July 2020 |pmid=32328588 |pmc=7177077 |doi=10.1016/j.jaccas.2020.04.009 |url=}}</ref><ref name="pmid33458567">{{cite journal |vauthors=Sharma K, Desai HD, Patoliya JV, Jadeja DM, Gadhiya D |title=Takotsubo Syndrome a Rare Entity in COVID-19: a Systemic Review-Focus on Biomarkers, Imaging, Treatment, and Outcome |journal=SN Compr Clin Med |volume= |issue= |pages=1–11 |date=January 2021 |pmid=33458567 |pmc=7799869 |doi=10.1007/s42399-021-00743-4 |url=}}</ref>
+*Early clinical features include  [[acute coronary syndrome]] with [[chest pain]] and [[ECG]] changes and rise of [[troponin]], [[acute pulmonary edema]], decreased [[oxygen]] saturation without response to O2 therapy, [[hemodynamic instability]].
+* [[Patients]] with [[stress cardiomyopathy]] associated with [[covid-19]] had a longer hospital days admission compared with the pre-pandemic period.<ref name="pmid32644140" />
+* [[Stress cardiomyopathy]] in critically ill [[covid-19]] [[patients]] may progress to develop [[cardiogenic shock]], [[pulmonary edema]], [[hemodynamic collapse]], and [[death]].
+* [[Patients]] with secondary [[takotsubo cardiomyopathy]] may experience [[cardiogenic shock]], [[respiratory failure]] requiring [[mechanical ventilation]] support and [[coagulation]] disorder. However, in  reported [[patients]] with [[takotsubo cardiomyopathy]] exacerbation of [[respiratory]] status may be due to [[covid-19]] complicating [[takotsubo cardiomyopathy]].
+* Some [[patients]] may recover and have a normalized [[cardiac]] function within a few weeks. .<ref name="pmid19106400">{{cite journal |vauthors=Akashi YJ, Goldstein DS, Barbaro G, Ueyama T |title=Takotsubo cardiomyopathy: a new form of acute, reversible heart failure |journal=Circulation |volume=118 |issue=25 |pages=2754–62 |year=2008 |pmid=19106400 |pmc=4893309 |doi=10.1161/CIRCULATIONAHA.108.767012 |url=}}</ref><ref name="pmid18294473">{{cite journal |vauthors=Prasad A, Lerman A, Rihal CS |title=Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction |journal=Am. Heart J. |volume=155 |issue=3 |pages=408–17 |year=2008 |pmid=18294473 |doi=10.1016/j.ahj.2007.11.008 |url=}}</ref><ref name="pmid19726776">{{cite journal |vauthors=Tsai TT, Nallamothu BK, Prasad A, Saint S, Bates ER |title=Clinical problem-solving. A change of heart |journal=N. Engl. J. Med. |volume=361 |issue=10 |pages=1010–6 |year=2009 |pmid=19726776 |doi=10.1056/NEJMcps0903023 |url=}}</ref>
+* Prognosis of [[stress cardiomyopathy]] associated [[covid-19]] is not clearly described yet, and [[mortality rate]] of [[patients]]  with [[stress cardiomyopathy]] without [[covid-19]] [[infection]]  is approximately 5% during  pandemic  (similar to pre-pandemic [[covid-19]] period). However, the [[mortality rate]] of [[takotsubo cardiomyopathy]] secondary to [[covid-19]] [[pneumonia]] is 10 times higher than non-[[covid-19]] [[patients]].<ref name="pmid32644140" />
 * Complications of [[stress cardiomyopathy]] include:<ref name="pmid19106400" /><ref name="pmid21401402">{{cite journal |vauthors=Omerovic E |title=How to think about stress-induced cardiomyopathy?--Think "out of the box"! |journal=Scand. Cardiovasc. J. |volume=45 |issue=2 |pages=67–71 |year=2011 |pmid=21401402 |doi=10.3109/14017431.2011.565794 |url=}}</ref><ref name="pmid18206521">{{cite journal |vauthors=Brenner ZR, Powers J |title=Takotsubo cardiomyopathy |journal=Heart Lung |volume=37 |issue=1 |pages=1–7 |year=2008 |pmid=18206521 |doi=10.1016/j.hrtlng.2006.12.003 |url=}}</ref><ref name="pmid19726776" /><ref name="pmid28041712">{{cite journal |vauthors=Efferth T, Banerjee M, Paul NW |title=Broken heart, tako-tsubo or stress cardiomyopathy? Metaphors, meanings and their medical impact |journal=Int. J. Cardiol. |volume= |issue= |pages= |year=2016 |pmid=28041712 |doi=10.1016/j.ijcard.2016.12.129 |url=}}</ref><ref name="pmid15583228">{{cite journal |vauthors=Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS |title=Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction |journal=Ann. Intern. Med. |volume=141 |issue=11 |pages=858–65 |year=2004 |pmid=15583228 |doi= |url=}}</ref><ref name="pmid11451258">{{cite journal |vauthors=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 |title=Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan |journal=J. Am. Coll. Cardiol. |volume=38 |issue=1 |pages=11–8 |year=2001 |pmid=11451258 |doi= |url=}}</ref><ref name="pmid15687136">{{cite journal |vauthors=Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ |title=Acute and reversible cardiomyopathy provoked by stress in women from the United States |journal=Circulation |volume=111 |issue=4 |pages=472–9 |year=2005 |pmid=15687136 |doi=10.1161/01.CIR.0000153801.51470.EB |url=}}</ref><ref name="pmid12923018">{{cite journal |vauthors=Desmet WJ, Adriaenssens BF, Dens JA |title=Apical ballooning of the left ventricle: first series in white patients |journal=Heart |volume=89 |issue=9 |pages=1027–31 |year=2003 |pmid=12923018 |pmc=1767823 |doi= |url=}}</ref><ref name="pmid26159108">{{cite journal |vauthors=Krishnamoorthy P, Garg J, Sharma A, Palaniswamy C, Shah N, Lanier G, Patel NC, Lavie CJ, Ahmad H |title=Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database |journal=Cardiology |volume=132 |issue=2 |pages=131–136 |year=2015 |pmid=26159108 |doi=10.1159/000430782 |url=}}</ref>
-**[[Heart failure]]
+**Severe [[Heart failure]]
-**[[Pulmonary edema]]
+**Acute [[pulmonary edema]]
 **[[Cardiogenic shock]]
+**Dynamic [[left ventricular outflow tract obstruction]] (peak gradients >25 mmhg in [[echo]] or [[cath]])
+**[[Hypotension]]
+** Moderete to severe acute functional [[mitral regurgitation]]
 **[[Bradycardia]]
-**[[Arrythmias]], mainly [[QT prolongation]] and [[ventricular arrhythmias]]
+**[[QT prolongation]] and [[ventricular arrhythmias]]
+** [[Torsade de pointes]]
 **[[Left ventricular]] [[mural thrombus]]
 **[[Mitral valve]] dysfunction
 **[[Pulmonary embolism]]
-**[[Mitral regurgitation]]
+** Systemic [[embolism]], [[stroke]]
 **[[LV]] [[free wall rupture]]
-**[[Myocardial rupture|Heart rupture]]
+** [[Acute renal failure]]
-**Death
+** In-hospital death
 ==Diagnosis==
-* Diagnostic findings are largely the same in comparison to [[stress cardiomyopathy]], and these are listed below. There is however a need to show evidence of ongoing [[COVID-19]] infection.
+*In the development of new [[hypotension]] and [[tachycardia]] in intubated [[covid-19]] [[patients]] with comorbidities ( [[HTN]], [[dyslipidemia]], [[atrial fibrillation]], previous [[stroke]]) or the need for [[vasopressor]] and presence of [[hypoxia]], investigation  about [[stress cardiomyopathy]] should be done by [[taking ]] [[ECG]] and check of [[cardiac biomarkers]] ( [[troponin]], NT-Pro [[BNP]].
+* In the presence of any [[ECG]] changes or [[cardiac biomarkers]] abnormality, [[transthoracic echocardiography]] should be done
 ===Diagnostic Study of Choice===
+* [[Echocardiography]] is the gold standard of diagnosis of [[takotsubo cardiomyopathy]].
+* High risk feature of [[takotsubo cardiomyopathy]] on [[echocardiography]] include: [[LVEF]]<45%, Moderate to severe [[mitral regurgitation]], [[right ventricular]] involvement.
 * The diagnosis of [[stress cardiomyopathy]] is made when all 4 of the following diagnostic criteria are met:
 **Transient [[Hypokinesia|hypokinesis]], [[Akinesia|akinesis]], or [[Dyskinesia|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.
@@ Line 101: / Line 217: @@
 *[[Loss of consciousness]] due to [[syncope]] or [[cardiac arrest]] in rare cases
-When taking the history from a patient with suspected [[stress cardiomyopathy]], it is important to ask about:<ref name="pmid18206521" /><ref name="pmid15583228" />
+* Considering [[emotional factors]] such as  fear of severity of [[covid-19]], contact with a hospitalized family member, worry about [[socioeconomic costs]], [[intrusive]] thoughts about [[morbidity]] of [[covid-19]] that may lead to [[stress cardiomyopathy]]. <ref name="pmid33458567">{{cite journal |vauthors=Sharma K, Desai HD, Patoliya JV, Jadeja DM, Gadhiya D |title=Takotsubo Syndrome a Rare Entity in COVID-19: a Systemic Review-Focus on Biomarkers, Imaging, Treatment, and Outcome |journal=SN Compr Clin Med |volume= |issue= |pages=1–11 |date=January 2021 |pmid=33458567 |pmc=7799869 |doi=10.1007/s42399-021-00743-4 |url=}}</ref>
-*Personal history of [[hypertension]], [[hyperlipidemia]], [[paroxysmal atrial fibrillation]], [[syncope]], [[hypoglycemia]] or [[stroke]]
-*Triggering event(s) to symptoms such as an unexpected death, being a victim of domestic violence or engaging in an argument or performing strenuous [[Physical exercise|physical activity]]
 ===Physical Examination===
@@ Line 127: / Line 240: @@
 |-
 !Cardiac
-|[[Murmurs]], [[S3]], [[gallop rhythm]], [[Displaced point of maximal impulse|displaced PMI]]
+|[[Murmurs]], [[S3]], [[gallop rhythm]], [[Displaced point of maximal impulse]] ([[PMI]])
 |[[Heart failure]]
 |-
@@ Line 137: / Line 250: @@
 ===Laboratory Findings===
-* Laboratory findings consistent with the diagnosis of COVID-19-associated [[stress cardiomyopathy]] include elevated [[troponin]] and Pro-[[BNP]].<ref name="pmid32644140" />
+* Laboratory findings consistent with the diagnosis of  [[stress cardiomyopathy]] in [[covid-19]] [[patients]] include elevated [[troponin]] and Pro-[[BNP]].<ref name="pmid32644140" />
 *Elevated levels of [[serum]] [[catecholamines]] may also be found in patients with [[stress cardiomyopathy]].<ref name="pmid19106400" /><ref name="pmid18206521" /><ref name="pmid15583228" /><ref name="pmid28041712" />
 *Evidence of ongoing [[COVID-19]] disease is required to establish the diagnosis.
@@ Line 147: / Line 260: @@
 *[[T wave inversion]]
 *[[Q wave]] formation
-*[[QT prolongation]]
+*[[QTc|QT prolongation]]
 *New-onset [[Bundle branch block|bundle branch block (BBB)]]
 *Rarely, malignant [[ventricular arrhythmias]] may be seen
 ===X-ray===
-[[Takotsubo cardiomyopathy|Takotsubo]] in Japanese language refer to a ceramic pot, which is used to trap octopus. The typical [[Chest X-ray|chest x-ray]] findings in patients with stress cardiomyopathy include a takotsubo-shaped [[heart]], in which there is [[apical ballooning]] and narrowing of the [[Anatomical terms of location|proximal]] portion near the [[great vessels]].
+[[Takotsubo cardiomyopathy|Takotsubo]] refers to a ceramic pot used to trap octopuses in the Japanese language. The typical [[Chest X-ray|chest x-ray]] findings in patients with stress cardiomyopathy include a [[takotsubo]]-shaped [[heart]], in which there is [[apical ballooning]] and narrowing of the [[Anatomical terms of location|proximal]] portion near the [[great vessels]].
 ===Echocardiography or Ultrasound===
@@ Line 203: / Line 316: @@
 ====Myocardial Biopsy ====
-*[[Myocardial biopsy]], although not necessary for diagnosis, can distinguish between [[stress cardiomyopathy]] and [[MI]].
 *The histological findings on [[myocardial biopsy]] in patients with [[stress cardiomyopathy]] include:<ref name="pmid19106400" /><ref name="pmid18206521" />
 **[[Inflammatory]] infiltrates, consisting of [[mononuclear lymphocytes]], [[leukocytes]] and [[macrophages]]
@@ Line 215: / Line 326: @@
 ===Medical Therapy===
-* There is no treatment for specific treatment for [[stress cardiomyopathy]] when associated with [[COVID-19]]. The mainstay of therapy is supportive care, which is the same for the [[stress cardiomyopathy]] not related to [[COVID-19]].
+* The mainstay of therapy of [[stress cardiomyopathy]] associated with [[covid-19]] is supportive care.
+*In mild [[TTS]] without signs of [[heart failure]], [[beta-blocker]] and [[ACEI]] or [[ARB]] are recommended and [[inotrope]] agents such as [[epinephrine]], [[norepinephrine]], [[dobutamine]], [[milrinone]], [[isoproterenol]] should be avoided.
-* Medical therapy in patients with [[stress cardiomyopathy]] is mostly targeted towards the treatment of complications. For [[stress cardiomyopathy]] per se, the use of [[heparin]] and [[aspirin]] are controversial. It must be noted that the use of [[beta blockers]] alone is not advised, as this will result unopposed activity of [[catecholamines]] at the [[alpha receptors]] and can cause further prolongation of the [[QT interval]]. The combined use of [[Alpha blockers|alpha-]] and [[beta blockers]] is reasonable.<ref name="pmid21401402" />
+*In the presence of [[pulmonary edema]] without evidence of [[left ventricular outflow obstruction]], administration of [[ACEI]], [[betablocker]]s, [[diuretic]] and [[nitroglycerin]] are recommended.
+*In the presence of [[cardiogenic shock]] and [[left ventricular outflow obstruction]] (no [[heart failure]] [[symptoms]]), short acting [[betablocker]], IV [[fluide]], and placing  [[impella]] are recommended.
-====Treatment of Complications ====
+* [[Diuretic]], [[nitroglycerin]], [[intraaortic ballon pump]] should be avoided in the evidence of [[cardiogenic shock]] and [[left ventricular outflow obstruction]].
-The following interventions are performed if their associated complications arise:<ref name="pmid21401402" /><ref name="pmid18206521" /><ref name="pmid15583228" />
+*If there is evidence of [[pump failure]] in the context of [[cardiogenic shock]], [[levosimentan]], [[ECMO]], [[impella ]] are considered.
+*[[Arrhythmia]] such as [[VT]], [[VF]], [[torsades de pointes]], [[ bradycardia]], [[long QT interval]] should be managed.
-*[[Cardiogenic shock]] is treated with [[intraaortic balloon pump]]
+* Temporary [[RV pacing]] is recommended in the presence of [[AV block]] and placement of [[permanent device]] is not recommended.
-*[[Pulmonary edema]] is treated by advising the patient to adopt an upright position, supplementation of [[oxygen]], and administration of [[diuretics]], [[morphine]] and [[sedatives]]
+* In the presence of [[bradycardia]] and [[long QTc]] >500 ms, [[betablocker]] should be avoided.
-*[[Heart failure]] is managed [[ACE inhibitor|ACE inhibitors]], [[Angiotensin II receptor antagonist|ARBs]], [[diuretics]] and [[nitrates]]
+*In the presence of [[left ventricular]] clot or large portion of [[akinesia]] of [[left ventricle]] involving [[apex]], [[anticougulation]] therapy  is recommende.
+* Classic treatment of [[heart failure]] including [[ACEI]] and [[betablocker]] should be kept at least three months or untill recovery of [[regional wall motion abnormality]].
+* Treatment of underlying disorders such as [[coronary artery disease]] is reasonable by continuing  [[aspirin]] and [[statin]].
 ===Surgery===
@@ Line 232: / Line 345: @@
 ===Primary Prevention===
-* There are no established measures for the primary prevention of COVID-19-associated [[stress cardiomyopathy]] if a patient has acquired [[COVID-19]] infection.
+* There are no established measures for the primary prevention of COVID-19-associated [[stress cardiomyopathy]].
 * Preventive measures should be taken to avoid [[COVID-19]] infection.