COVID-19-associated stress cardiomyopathy: Difference between revisions
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* 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> | * 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> | ||
* Complications of stress cardiomyopathy include:<ref name=" | * 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]] | **[[Heart failure]] | ||
**[[Pulmonary edema]] | **[[Pulmonary edema]] | ||
| Line 82: | Line 82: | ||
**Absence of obstructive [[Coronary heart disease|coronary disease]] or [[angiographic]] evidence of [[acute]] [[plaque rupture]]. | **Absence of obstructive [[Coronary heart disease|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]]. | ** New [[electrocardiographic]] abnormalities (either [[ST-segment elevation]] and/or [[T-wave inversion]]) or modest elevation in [[cardiac troponin]]. | ||
** Absence of [[pheochromocytoma]] and [[myocarditis]].<ref name=" | ** Absence of [[pheochromocytoma]] and [[myocarditis]].<ref name="pmid18294473" /><ref name="pmid19106400" /> | ||
* The diagnosis of COVID-19-associated stress cardiomyopathy is largely the same, but happening in the context of a SARS-CoV2 infection. | * 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=== | ===History and Symptoms=== | ||
Symptoms of stress cardiomyopathy can mimic [[acute coronary syndrome]]. The most common presenting symptoms are:<ref name=" | Symptoms of stress cardiomyopathy can mimic [[acute coronary syndrome]]. The most common presenting symptoms are:<ref name="pmid19106400" /><ref name="pmid18206521" /><ref name="pmid18294473" /><ref name="pmid15583228" /><ref name="pmid263325472">{{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 |year=2015 |pmid=26332547 |doi=10.1056/NEJMoa1406761 |url=}}</ref><ref name="pmid28041712" /> | ||
*[[Chest pain]] or [[chest tightness]] | *[[Chest pain]] or [[chest tightness]] | ||
| Line 93: | Line 93: | ||
*[[Loss of consciousness]] due to [[syncope]] or [[cardiac arrest]] in rare cases | *[[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=" | When taking the history from a patient with suspected stress cardiomyopathy, it is important to ask about:<ref name="pmid18206521" /><ref name="pmid15583228" /> | ||
*Personal history of [[hypertension]], [[hyperlipidemia]], [[paroxysmal atrial fibrillation]], [[syncope]], [[hypoglycemia]] or [[stroke]] | *Personal history of [[hypertension]], [[hyperlipidemia]], [[paroxysmal atrial fibrillation]], [[syncope]], [[hypoglycemia]] or [[stroke]] | ||
| Line 100: | Line 100: | ||
===Physical Examination=== | ===Physical Examination=== | ||
* The following physical examination findings may be seen in patients with stress cardiomyopathy:<ref name="pmid23073280">{{cite journal |vauthors=Y-Hassan S, Yamasaki K |title=History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies |journal=Int. J. Cardiol. |volume=166 |issue=3 |pages=736–7 |year=2013 |pmid=23073280 |doi=10.1016/j.ijcard.2012.09.183 |url=}}</ref><ref name=" | * The following physical examination findings may be seen in patients with stress cardiomyopathy:<ref name="pmid23073280">{{cite journal |vauthors=Y-Hassan S, Yamasaki K |title=History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies |journal=Int. J. Cardiol. |volume=166 |issue=3 |pages=736–7 |year=2013 |pmid=23073280 |doi=10.1016/j.ijcard.2012.09.183 |url=}}</ref><ref name="pmid19106400" /><ref name="pmid21401402" /><ref name="pmid18206521" /><ref name="pmid19726776" /><ref name="pmid28041712" /><ref name="pmid15583228" /><ref name="pmid11451258" /><ref name="pmid156871362">{{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" /><ref name="pmid261591082">{{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> | ||
{| class="wikitable" | {| class="wikitable" | ||
| Line 129: | Line 129: | ||
* 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 COVID-19-associated stress cardiomyopathy 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=" | *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" /> | ||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
The [[ECG]] findings are largely the same of the regular stress cardiomyopathy, and are often confused with those of an [[Anterior myocardial infarction|acute anterior wall myocardial infarction]].<ref name=" | The [[ECG]] findings are largely the same of the regular stress cardiomyopathy, and are often confused with those of an [[Anterior myocardial infarction|acute anterior wall myocardial infarction]].<ref name="pmid19106400" /><ref name="pmid15583228" /> Findings on [[ECG]] include:<ref name="pmid19106400" /><ref name="pmid18206521" /><ref name="pmid18294473" /><ref name="pmid19726776" /><ref name="pmid15583228" /><ref name="pmid263325472" /><ref name="pmid28041712" /> | ||
*[[ST elevation]] in the [[precordial leads]] | *[[ST elevation]] in the [[precordial leads]] | ||
| Line 145: | Line 145: | ||
===Echocardiography or Ultrasound=== | ===Echocardiography or Ultrasound=== | ||
The following [[echocardiographic]] findings may be seen in patients with stress cardiomyopathy:<ref name=" | The following [[echocardiographic]] findings may be seen in patients with stress cardiomyopathy:<ref name="pmid18206521" /><ref name="pmid18294473" /><ref name="pmid19726776" /><ref name="pmid28041712" /> | ||
*[[Apical ballooning]] | *[[Apical ballooning]] | ||
| Line 157: | Line 157: | ||
===MRI=== | ===MRI=== | ||
*[[Cardiovascular magnetic resonance imaging (CMR)|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 [[Cardiovascular magnetic resonance imaging (CMR)|cardiac magnetic resonance]].<ref name=" | *[[Cardiovascular magnetic resonance imaging (CMR)|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 [[Cardiovascular magnetic resonance imaging (CMR)|cardiac magnetic resonance]].<ref name="pmid18294473" /><ref name="pmid15687136" /><ref name="pmid17175045">{{cite journal |vauthors=Haghi D, Fluechter S, Suselbeck T, Kaden JJ, Borggrefe M, Papavassiliu T |title=Cardiovascular magnetic resonance findings in typical versus atypical forms of the acute apical ballooning syndrome (Takotsubo cardiomyopathy) |journal=Int. J. Cardiol. |volume=120 |issue=2 |pages=205–11 |year=2007 |pmid=17175045 |doi=10.1016/j.ijcard.2006.09.019 |url=}}</ref><ref name="pmid17631086">{{cite journal |vauthors=Mitchell JH, Hadden TB, Wilson JM, Achari A, Muthupillai R, Flamm SD |title=Clinical features and usefulness of cardiac magnetic resonance imaging in assessing myocardial viability and prognosis in Takotsubo cardiomyopathy (transient left ventricular apical ballooning syndrome) |journal=Am. J. Cardiol. |volume=100 |issue=2 |pages=296–301 |year=2007 |pmid=17631086 |doi=10.1016/j.amjcard.2007.02.091 |url=}}</ref><ref name="pmid16669180">{{cite journal |vauthors=Deetjen AG, Conradi G, Mollmann S, Rad A, Hamm CW, Dill T |title=Value of gadolinium-enhanced magnetic resonance imaging in patients with Tako-Tsubo-like left ventricular dysfunction |journal=J Cardiovasc Magn Reson |volume=8 |issue=2 |pages=367–72 |year=2006 |pmid=16669180 |doi= |url=}}</ref><ref name="pmid12628715">{{cite journal |vauthors=Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H |title=Assessment of clinical features in transient left ventricular apical ballooning |journal=J. Am. Coll. Cardiol. |volume=41 |issue=5 |pages=737–42 |year=2003 |pmid=12628715 |doi= |url=}}</ref><ref name="pmid15687123">{{cite journal |vauthors=Dec GW |title=Recognition of the apical ballooning syndrome in the United States |journal=Circulation |volume=111 |issue=4 |pages=388–90 |year=2005 |pmid=15687123 |doi=10.1161/01.CIR.0000155234.69439.E4 |url=}}</ref><ref name="pmid19944334">{{cite journal |vauthors=Handy AD, Prasad A, Olson TM |title=Investigating genetic variation of adrenergic receptors in familial stress cardiomyopathy (apical ballooning syndrome) |journal=J Cardiol |volume=54 |issue=3 |pages=516–7 |year=2009 |pmid=19944334 |doi=10.1016/j.jjcc.2009.08.008 |url=}}</ref><ref name="pmid15687136" /><ref name="pmid21771988">{{cite journal |vauthors=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 |title=Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy |journal=JAMA |volume=306 |issue=3 |pages=277–86 |year=2011 |pmid=21771988 |doi=10.1001/jama.2011.992 |url=}}</ref><ref name="pmid18820322">{{cite journal |vauthors=Eitel I, Behrendt F, Schindler K, Kivelitz D, Gutberlet M, Schuler G, Thiele H |title=Differential diagnosis of suspected apical ballooning syndrome using contrast-enhanced magnetic resonance imaging |journal=Eur. Heart J. |volume=29 |issue=21 |pages=2651–9 |year=2008 |pmid=18820322 |doi=10.1093/eurheartj/ehn433 |url=}}</ref> | ||
*[[Cardiovascular magnetic resonance imaging (CMR)|CMR]] in stress cardiomyopathy shows absence of irreversible damage and segmental [[LV dysfunction]].<ref name="pmid17631086" /> | *[[Cardiovascular magnetic resonance imaging (CMR)|CMR]] in stress cardiomyopathy shows absence of irreversible damage and segmental [[LV dysfunction]].<ref name="pmid17631086" /> | ||
Other findings on [[CMR]] include:<ref name=" | Other findings on [[CMR]] include:<ref name="pmid28041712" /><ref name="pmid15687136" /> | ||
*[[Hypokinesia|Hypokinetic]] or [[dyskinetic]] areas in the wall of the [[heart]] | *[[Hypokinesia|Hypokinetic]] or [[dyskinetic]] areas in the wall of the [[heart]] | ||
| Line 172: | Line 172: | ||
* 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. | * 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.<ref name=" | *A normal [[angiography]] or absence of substantial [[coronary]] [[stenosis]] supports the diagnosis of stress cardiomyopathy.<ref name="pmid15583228" /><ref name="pmid19106400" /><ref name="pmid28041712" /> | ||
===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
====Cardiac Catheterization ==== | ====Cardiac Catheterization ==== | ||
When patients with stress cardiomyopathy undergo [[cardiac catheterization]], the following findings are usually reported:<ref name=" | When patients with stress cardiomyopathy undergo [[cardiac catheterization]], the following findings are usually reported:<ref name="pmid18206521" /><ref name="pmid15583228" /><ref name="pmid19726776" /> | ||
*Normal [[anatomy]] of the [[coronary arteries]], without evidence of [[acute]] [[plaque rupture]] | *Normal [[anatomy]] of the [[coronary arteries]], without evidence of [[acute]] [[plaque rupture]] | ||
| Line 186: | Line 186: | ||
*Myocardial biopsy, although not necessary for diagnosis, can distinguish between stress cardiomyopathy and [[MI]]. | *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=" | *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]] | ||
**[[Myocardial]] [[fibrosis]] | **[[Myocardial]] [[fibrosis]] | ||
**Contraction bands, which may or may not be associated with [[necrosis]] | **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]].<ref name=" | *The combination of inflammatory changes and contraction bands distinguish stress cardiomyopathy from [[coagulative necrosis]] seen in [[MI]].<ref name="pmid19106400" /> | ||
==Treatment== | ==Treatment== | ||
| Line 198: | Line 198: | ||
* 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.. | * 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.. | ||
* 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=" | * 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" /> | ||
====Treatment of Complications ==== | ====Treatment of Complications ==== | ||
The following interventions are performed if their associated complications arise:<ref name=" | The following interventions are performed if their associated complications arise:<ref name="pmid21401402" /><ref name="pmid18206521" /><ref name="pmid15583228" /> | ||
*[[Cardiogenic shock]] is treated with [[intraaortic balloon pump]] | *[[Cardiogenic shock]] is treated with [[intraaortic balloon pump]] | ||
Revision as of 22:59, 17 July 2020
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2]
Synonyms and keywords:
Overview
Historical Perspective
- COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020.[1]
Classification
- There is no established system for the classification of COVID-19-associated stress cardiomyopathy.
Pathophysiology
- It is thought that COVID-19-associated stress cardiomyopathy is the result of extreme sympathetic stimulation due to abnormal release of catecholamines causing epicardial coronary vasospasm.
- Many mechanisms occurring in COVID-19 patients may lead to myocardial injury and left ventricular dysfunction.[2]
- One of the proposed theory is that patients may experience 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 vasoconstriction that can manifest in a transient left ventricular apical dysfunction, (apical ballooning).[3]
- Proposed mechanisms that have the potential to cause myocardial injury in acute coronavirus disease 2019 cardiovascular syndrome:[4]
| 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
- COVID-19-associated stress cardiomyopathy may be caused by a very intense 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 pandemic due to the imposed quarantine.[3]
Differentiating COVID-19-associated stress cardiomyopathy from other Diseases
- COVID-19-associated stress cardiomyopathy must be differentiated from other diseases that cause left ventricular dysfunction such as acute myocardial infarction (STEMI and NSTEMI) and viral myocarditis.
Epidemiology and Demographics
- The incidence of COVID-19-associated stress cardiomyopathy is approximately 7.8% of all patients presenting acute coronary syndrome.[3]
- In comparison, the stress cardiomyopathy incidence in the pre-COVID-19 period was varying between 1.5-1.8%.[3]
Risk Factors
- There are no established risk factors for COVID-19-associated stress cardiomyopathy.
- Hypertension was, however, the most frequently comorbidity found across the groups in the COVID-19 period patients, as was hyperlipidemia.[3]
Screening
- There is insufficient evidence to recommend routine screening for COVID-19-associated stress cardiomyopathy.
Natural History, Complications, and Prognosis
- A study evaluated the outcomes for patients with stress cardiomyopathy. 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.[3]
- 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.[3]
- Provided that patients survive the initial insult without any complications, most patients recover and have a normalized cardiac function within a few weeks.[5][6][7]
Diagnosis
Diagnostic Study of Choice
- 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.[6][5]
- 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:[5][9][6][11][16][10]
- Chest pain or chest tightness
- Shortness of breath
- Vomiting
- 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:[9][11]
- 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 activity
Physical Examination
- The following physical examination findings may be seen in patients with stress cardiomyopathy:[17][5][8][9][7][10][11][12][18][14][19]
| 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 PMI | Heart failure |
| Respiratory | Rales, crackles | Pulmonary edema |
Laboratory Findings
- Laboratory findings consistent with the diagnosis of COVID-19-associated stress cardiomyopathy include elevated troponin and Pro-BNP.[3]
- Elevated levels of serum catecholamines may also be found in patients with stress cardiomyopathy.[5][9][11][10]
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.[5][11] Findings on ECG include:[5][9][6][7][11][16][10]
- 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 in Japanese language refer to a ceramic pot, which is used to trap octopus. 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:[9][6][7][10]
- 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.[10]
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.[6][13][20][21][22][23][24][25][13][26][27]
- CMR in stress cardiomyopathy shows absence of irreversible damage and segmental LV dysfunction.[21]
Other findings on CMR include:[10][13]
- 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.[28]
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.[11][5][10]
Other Diagnostic Studies
Cardiac Catheterization
When patients with stress cardiomyopathy undergo cardiac catheterization, the following findings are usually reported:[9][11][7]
- 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
- 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:[5][9]
- 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.[5]
Treatment
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..
- 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- and beta blockers is reasonable.[8]
Treatment of Complications
The following interventions are performed if their associated complications arise:[8][9][11]
- Cardiogenic shock is treated with intraaortic balloon pump
- Pulmonary edema is treated by advising the patient to adopt an upright position, supplementation of oxygen, and administration of diuretics, morphine and sedatives
- Heart failure is managed ACE inhibitors, ARBs, diuretics and nitrates
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 if a patient has acquired COVID-19 infection.
- 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
- ↑ Roca E, Lombardi C, Campana M, Vivaldi O, Bigni B, Bertozzi B; et al. (2020). "Takotsubo Syndrome Associated with COVID-19". Eur J Case Rep Intern Med. 7 (5): 001665. doi:10.12890/2020_001665. PMC 7213829 Check
|pmc=value (help). PMID 32399453 Check|pmid=value (help). - ↑ Pasqualetto MC, Secco E, Nizzetto M, Scevola M, Altafini L, Cester A; et al. (2020). "Stress Cardiomyopathy in COVID-19 Disease". Eur J Case Rep Intern Med. 7 (6): 001718. doi:10.12890/2020_001718. PMC 7279910 Check
|pmc=value (help). PMID 32523926 Check|pmid=value (help). - ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Jabri A, Kalra A, Kumar A, Alameh A, Adroja S, Bashir H; et al. (2020). "Incidence of Stress Cardiomyopathy During the Coronavirus Disease 2019 Pandemic". JAMA Netw Open. 3 (7): e2014780. doi:10.1001/jamanetworkopen.2020.14780. PMC 7348683 Check
|pmc=value (help). PMID 32644140 Check|pmid=value (help). - ↑ Hendren NS, Drazner MH, Bozkurt B, Cooper LT (2020). "Description and Proposed Management of the Acute COVID-19 Cardiovascular Syndrome". Circulation. 141 (23): 1903–1914. doi:10.1161/CIRCULATIONAHA.120.047349. PMC 7314493 Check
|pmc=value (help). PMID 32297796 Check|pmid=value (help). - ↑ 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). "Takotsubo cardiomyopathy: a new form of acute, reversible heart failure". Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
- ↑ 6.0 6.1 6.2 6.3 6.4 6.5 Prasad A, Lerman A, Rihal CS (2008). "Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction". Am. Heart J. 155 (3): 408–17. doi:10.1016/j.ahj.2007.11.008. PMID 18294473.
- ↑ 7.0 7.1 7.2 7.3 7.4 7.5 Tsai TT, Nallamothu BK, Prasad A, Saint S, Bates ER (2009). "Clinical problem-solving. A change of heart". N. Engl. J. Med. 361 (10): 1010–6. doi:10.1056/NEJMcps0903023. PMID 19726776.
- ↑ 8.0 8.1 8.2 8.3 Omerovic E (2011). "How to think about stress-induced cardiomyopathy?--Think "out of the box"!". Scand. Cardiovasc. J. 45 (2): 67–71. doi:10.3109/14017431.2011.565794. PMID 21401402.
- ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 Brenner ZR, Powers J (2008). "Takotsubo cardiomyopathy". Heart Lung. 37 (1): 1–7. doi:10.1016/j.hrtlng.2006.12.003. PMID 18206521.
- ↑ 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 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.
- ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 11.9 Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS (2004). "Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction". Ann. Intern. Med. 141 (11): 858–65. PMID 15583228.
- ↑ 12.0 12.1 Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I (2001). "Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan". J. Am. Coll. Cardiol. 38 (1): 11–8. PMID 11451258.
- ↑ 13.0 13.1 13.2 13.3 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.
- ↑ 14.0 14.1 Desmet WJ, Adriaenssens BF, Dens JA (2003). "Apical ballooning of the left ventricle: first series in white patients". Heart. 89 (9): 1027–31. PMC 1767823. PMID 12923018.
- ↑ 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.
- ↑ 16.0 16.1 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.
- ↑ Y-Hassan S, Yamasaki K (2013). "History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies". Int. J. Cardiol. 166 (3): 736–7. doi:10.1016/j.ijcard.2012.09.183. PMID 23073280.
- ↑ 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.
- ↑ 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.
- ↑ 21.0 21.1 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.