COVID-19-associated stress cardiomyopathy: Difference between revisions

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{{SI}}
{{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==
==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]] 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 or [[physical]] stress such as [[surgery]], [[infection]], [[hypoxia]]. The latter  may have worse prognosis in terms of [[mortality]] compared with [[emotional]] [[trigger]].
[[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==
==Historical Perspective==
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===Gender===
===Gender===
*[[Male]] are more commonly affected with [[stress cardiomyopathy]] secondary to [[covid-19]].
*[[Male]] are more commonly affected with [[stress cardiomyopathy]] secondary to [[covid-19]].
* Primary [[stress cardiomyopathy]] is much more common in [[women]]..


===Race===
===Race===
*There is no racial predilection for [[stress cardiomyopathy]] in [[covid-19]] [[patients]].
*There is no racial predilection for [[stress cardiomyopathy]] in [[covid-19]] [[patients]].
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*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]].   
*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" />
* [[Patients]] with [[stress cardiomyopathy]] associated with [[covid-19]] had a longer hospital days admission compared with the pre-pandemic period.<ref name="pmid32644140" />
*In the presence of [[cardiogenic shock]], [[stress cardiomyopathy]] in critically ill [[covid-19]] [[patients]] may progress to develop [[pulmonary edema]], [[hemodynamic collapse]], and [[death]].
* [[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]].   
* [[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]].   
* In general population most of the [[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>
* 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]] during [[covid-19]] pandemic is approximately 5%  (similar to pre-pandemic [[covid-19]] period).<ref name="pmid32644140" />
* 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>
* 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>
**Severe [[Heart failure]]
**Severe [[Heart failure]]
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**[[Cardiogenic shock]]
**[[Cardiogenic shock]]
**Dynamic [[left ventricular outflow tract obstruction]] (peak gradients >25 mmhg in [[echo]] or [[cath]])
**Dynamic [[left ventricular outflow tract obstruction]] (peak gradients >25 mmhg in [[echo]] or [[cath]])
**[[Hypotesion]]
**[[Hypotension]]
** Moderete to severe acute functional [[mitral regurgitation]]
** Moderete to severe acute functional [[mitral regurgitation]]
**[[Bradycardia]]
**[[Bradycardia]]
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==Diagnosis==
==Diagnosis==


*In the development of new [[hypotension]] and [[tachycardia]] in hospitalized [[covid-19]] [[patients]] with risk factors mentioned above, investigation with [[taking ]] [[ECG]] and check of [[cardiac biomarkers]] ( [[troponin]], NT-Pro [[BNP]]) should be done.
*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
* In the presence of any [[ECG]] changes or [[cardiac biomarkers]] abnormality, [[transthoracic echocardiography]] should be done


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===Diagnostic Study of Choice===
===Diagnostic Study of Choice===
* [[Echocardiography]] is the gold standard of diagnosis of [[takotsubo cardiomyopathy]].
* [[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:
* 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.
**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.
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====Myocardial Biopsy ====
====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" />
*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]]
**[[Inflammatory]] infiltrates, consisting of [[mononuclear lymphocytes]], [[leukocytes]] and [[macrophages]]
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===Medical Therapy===
===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===
===Surgery===
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===Primary Prevention===
===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.
* Preventive measures should be taken to avoid [[COVID-19]] infection.



Latest revision as of 16:53, 10 March 2022

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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

Classification




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



 
 
 
 
 
 
 
 
 
 
 
 
 
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:

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

Age

Gender

Race

Risk Factors




Screening

Natural History, Complications, and Prognosis

Diagnosis


Diagnostic Study of Choice

History and Symptoms

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

Physical Examination

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

Laboratory Findings

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]

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]

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

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

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

Other Diagnostic Studies

Cardiac Catheterization

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

Myocardial Biopsy

Treatment

Medical Therapy

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

References

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