COVID-19-associated stress cardiomyopathy: Difference between revisions
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==Natural History, Complications, and Prognosis== | ==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.<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> | |||
A study evaluated the outcomes for patients with stress cardiomyopathy | |||
==Diagnosis== | ==Diagnosis== | ||
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==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
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="pmid214014022">{{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> | * 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="pmid214014022">{{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> | |||
====Treatment of Complications ==== | ====Treatment of Complications ==== | ||
Revision as of 23:28, 16 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 CV 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 [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].
OR
The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].
OR
The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].
OR
There are no established criteria for the diagnosis of [disease name].
History and Symptoms
The majority of patients with [disease name] are asymptomatic.
OR
The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].
Physical Examination
Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].
OR
Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
The presence of [finding(s)] on physical examination is diagnostic of [disease name].
OR
The presence of [finding(s)] on physical examination is highly suggestive of [disease name].
Laboratory Findings
- Laboratory findings consistent with the diagnosis of COVID-19-associated stress cardiomyopathy include elevated troponin and Pro-BNP.[3]
Electrocardiogram
There are no ECG findings associated with [disease name].
OR
An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
X-ray
There are no x-ray findings associated with [disease name].
OR
An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Echocardiography or Ultrasound
There are no echocardiography/ultrasound findings associated with [disease name].
OR
Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
CT scan
There are no CT scan findings associated with [disease name].
OR
[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
MRI
There are no MRI findings associated with [disease name].
OR
[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Other Imaging Findings
There are no other imaging findings associated with [disease name].
OR
[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
There are no other diagnostic studies associated with [disease name].
OR
[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
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][10]
- 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). - ↑ 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.
- ↑ 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.
- ↑ 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 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.
- ↑ Brenner ZR, Powers J (2008). "Takotsubo cardiomyopathy". Heart Lung. 37 (1): 1–7. doi:10.1016/j.hrtlng.2006.12.003. PMID 18206521.
- ↑ 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.