Cardiovascular Disorders and COVID-19: Difference between revisions

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*In the level of cardiac tissue: minimal change to interstitial inflammatory infiltration and myocyte necrosis
*In the level of cardiac tissue: minimal change to interstitial inflammatory infiltration and myocyte necrosis
*In the level of vasculature: micro-thrombosis and vascular inflammation<ref name="pmid32354800">{{cite journal| author=Kang Y, Chen T, Mui D, Ferrari V, Jagasia D, Scherrer-Crosbie M | display-authors=etal| title=Cardiovascular manifestations and treatment considerations in covid-19. | journal=Heart | year= 2020 | volume=  | issue=  | pages=  | pmid=32354800 | doi=10.1136/heartjnl-2020-317056 | pmc=7211105 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32354800  }} </ref>
*In the level of vasculature: micro-thrombosis and vascular inflammation<ref name="pmid32354800">{{cite journal| author=Kang Y, Chen T, Mui D, Ferrari V, Jagasia D, Scherrer-Crosbie M | display-authors=etal| title=Cardiovascular manifestations and treatment considerations in covid-19. | journal=Heart | year= 2020 | volume=  | issue=  | pages=  | pmid=32354800 | doi=10.1136/heartjnl-2020-317056 | pmc=7211105 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32354800  }} </ref>
====Treatment====
In patients with ACS, and COVID-19 treatment should follow the guideline of the updated Society for Cardiovascular Angiography and Interventions guidelines.<ref name="pmid32212409">{{cite journal| author=Szerlip M, Anwaruddin S, Aronow HD, Cohen MG, Daniels MJ, Dehghani P | display-authors=etal| title=Considerations for cardiac catheterization laboratory procedures during the COVID-19 pandemic perspectives from the Society for Cardiovascular Angiography and Interventions Emerging Leader Mentorship (SCAI ELM) Members and Graduates. | journal=Catheter Cardiovasc Interv | year= 2020 | volume=  | issue=  | pages=  | pmid=32212409 | doi=10.1002/ccd.28887 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32212409  }} </ref>


===Heart Failure===
===Heart Failure===

Revision as of 00:58, 21 June 2020

To go to the COVID-19 project topics list, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]Mandana Chitsazan, M.D. [3]Tayyaba Ali, M.D.[4]Ayesha Javid, MBBS[5] Sara Haddadi, M.D.[6]

Overview

Complications

Myocardial injury

  • COVID-19 patients with cardiovascular comorbidities have higher mortality.
  • Hospitalized patients with COVID-19 and Cardiovascular disease seem to be more prevalent in both the USA and China. [1]
  • In a case series with 187 patients who had confirmed COVID-19, 27.8% of patients had a myocardial injury, which caused cardiac dysfunction and arrhythmias. The result was significantly higher mortality among patients with myocardial injury.
  • It seems to be advisable to triage patients with COVID-19 based on their underlying CVD for a more aggressive treatment plan.
  • The mortality during hospitalization was shown to be 7.62% for patients without underlying CVD and normal TnT levels, 13.33% for those with underlying CVD and normal TnT levels, 37.50% for those without underlying CVD but elevated TnT levels, and 69.44% for those with underlying CVD and elevated TnTs.[2]

Acute Coronary Syndromes

Pathophysiology

The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial.

  • SARS-CoV-2 virus attaches to ACE 2 protein for ligand binding before entering the cell via receptor-mediated endocytosis.
    • Based on single-cell RNA sequencing more than 7.5% of myocardial cells have positive ACE2 expression. This protein can mediate the entry of SARS-CoV-2 and result in direct cardiotoxicity.
  • The cytokine release caused by the virus may lead to vascular inflammation, plaque instability, myocardial inflammation, a hypercoagulable state, or direct myocardial suppression.

Pathological changes:

  • In the level of cardiac tissue: minimal change to interstitial inflammatory infiltration and myocyte necrosis
  • In the level of vasculature: micro-thrombosis and vascular inflammation[1]

Treatment

In patients with ACS, and COVID-19 treatment should follow the guideline of the updated Society for Cardiovascular Angiography and Interventions guidelines.[3]

Heart Failure

Pathophysiology

  • Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
  • Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
  • Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:[4] [5] [6] [7] [8]
    • Acute exacerbation of chronic heart failure
    • Acute myocardial injury (which in turn can be caused by several mechanisms)
    • Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
    • Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
    • Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)

Symptoms and signs

  • Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
  • Lower limb edema
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Confusion and altered mentation
  • Cool extremities
  • Cyanosis
  • Syncope
  • Fatigue
  • Hemoptysis
  • Palpitations
  • Weakness
  • Wheezing or cardiac asthma
  • Distended jugular veins
  • Crackles on auscultation

Electrocardiography (ECG)

  • There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
  • The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
  • These ECG findings may include:
    • Low QRS Voltage
    • Left ventricular hypertrophy
    • Left atrial enlargement
    • Left bundle branch block
    • Poor R progression
    • ST-T changes

Chest x-ray (CXR)

  • The Chest x-ray may show evidence of:
    • Cardiomegaly
    • Pulmonary congestion
    • Increased pulmonary vascular markings.
  • Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

Echocardiography

  • A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.[9]
  • To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
  • In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
    • Cardiac point-of-care ultrasound (POCUS)
    • Focused cardiac ultrasound study (FoCUS)
    • Critical care echocardiography
  • Cardiac ultrasound can help in assessing the following parameters:
    • Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
    • Left ventricular diastolic function
    • Left ventricular structural abnormalities, including LV size and LV wall thickness
    • Left atrial size
    • Right ventricular size and function
    • Detection and quantification of valvular abnormalities
    • Measurement of systolic pulmonary artery pressure
    • Detection and quantification of pericardial effusion
    • Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia

Cardiac biomarkers

  • Cardiac Troponins:
    • Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
    • Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.[10]
  • Natriuretic Peptides:
    • Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.[11]
    • Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
    • Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
    • Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.[12] [13]
    • However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.[14] [15] [16] [17] [18]
    • Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

Treatment

  • Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. [19]
  • Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
    • Fluid restriction
    • Diuretic therapy
    • Vasopressors and/or inotropes
    • Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
  • Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.[20]
  • Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.[21]

Cardiogenic Shock

Myocarditis

Pathophysiology

Pericarditis

Arrhythmias

Pathophysiology:

Respiratory disease is the chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including arrhythmia. According to a study done in Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had arrhythmias. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Type 1 and type 2 pneumocytes exhibit ACE 2 receptors in the lung. Studies report that coronary endothelial cells in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the renin-angiotensin system. The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and endothelial cells. Hypoxia and electrolyte abnormalities that are common in the acute phase of severe COVID-19 can potentiate cardiac arrhythmias. Binding of SARS-CoV-2 to ACE2 receptors can result into hypokalemia which causes various types of arrhythmia. Elevated levels of cytokines as a result of the systemic inflammatory response of the severe Coronavirus disease 2019 (COVID-19) can cause injury to multiple organs, including cardiac myocytes. According to the data based on studies on previous Severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS) epidemic and the ongoing COVID-19 outbreak, multiple mechanisms have been suggested for cardiac damage.[39][40][41][22]

Signs and Symptoms:

Arrhythmia or conduction system disease is the nonspecific clinical presentation of COVID-19. Patients may be tachycardic (with or without palpitations) in the setting of other COVID-19-related symptoms (eg, fever, shortness of breath, pain, etc).

  • Palpitations: According to a study done in Hubei province,palpitations were reported as a presenting symptom by 7.3 percent of patients.[42][43]
  • Prolong QT Interval: According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had corrected QT interval (QTc) >500 milliseconds at the time of admittance. However, in another study that involved 84 patients who got hydroxychloroquine and azithromycin, the baseline QTc interval was 435 milliseconds before receiving these medications.[44][45]
  • Atrial Arrhythmia: According to a study, among 393 patients with COVID-19, atrial arrhythmias were more common among patients requiring invasive mechanical ventilation than noninvasive mechanical ventilation (17.7 versus 1.9 percent).[46]
  • Ventricular Arrhythmia: According to a study done in Wuhan, China. among 187 hospitalized patients with COVID-19, 11 patients (5.9 percent) developed ventricular tachyarrhythmias.[47]
  • Cardiac Arrest: According to a Lombardia Cardiac Arrest Registry (Lombardia CARe) of the region Lombardia in Italy. Out of 9806 cases of COVID-19, 362 cases of out-of-hospital cardiac arrest were reported during the study time frame in 2020. During a similar period in 2019, 229 cases of out-of-hospital cardiac arrest were reported, which means an increment of 58% was observed in 2020 among COVID-19 patients. According to the records from a tertiary care hospital in Wuhan. Out of 761 patients with severe COVID-19, 151 patients developed in-hospital cardiac arrest. 136 patients received resuscitation. Out of 136 patients, 119 patients had a respiratory cause. 10 patients had a cardiac cause. 7 patients had other causes. Ventricular fibrillation or pulseless ventricular tachycardia was observed in 8 patients (5.9%), Pulseless electrical activity in 6 patients (4.4%), and asystole in 122 COVID-19 patients (89.7%).[48][49]

Diagnostic Testing:

  • ECG: Most patients with the severe COVID-19, and especially patients who receive QT-prolonging medications, should have a baseline electrocardiogram (ECG) performed at the time of admission to the hospital.The best technique to get the QT interval is with a 12-lead electrocardiogram (ECG). However, to scale back exposure to hospital workers, this could not perpetually be possible. A single-lead ECG might underestimate the QT interval, and there ought to be an effort to use a multiple-lead telemetry system to observe the QT interval.[50][51]
  • Transthoracic echocardiography: Transthoracic echocardiography is recommended for an inpatient with heart failure, arrhythmia, ECG changes, or newly diagnosed cardiomegaly on chest x-ray or CT-chest.[27]

Treatment:

  • Polymorphic Ventricular Tachycardia (torsades de pointes): All patients with torsades de pointes (TdP) should be determined if they are hemodynamically stable or unstable through immediate evaluation of the symptoms, vital signs, and level of consciousness.[52]
    • Unstable patients: Patients with COVID-19 with sustained torsades de pointes (TdP) usually become hemodynamically unstable, severely symptomatic because of perfusion failure, or pulseless and should be treated according to standard resuscitation algorithms, including cardioversion/defibrillation. Initial treatment with antiarrhythmic medications is not indicated for hemodynamically unstable or pulseless patients except intravenous (IV) magnesium.
    • Stable patients: In a patient with a single episode of TdP, treatment with IV magnesium along with correction of metabolic/electrolyte disturbances or removal of any inciting medications may be sufficient. The patient should be kept under observation until the electrolytes, and the QT interval nearly normalizes. An IV bolus of 2-gram magnesium sulfate is the standard therapy for an adult. This is equivalent to a dose of 8.12 mmol of magnesium. The clinical situation of a patient determines the rate of magnesium infusion. Infusion occurs over one to two minutes in patients with pulseless cardiac arrest. The infusion should occur over 15 minutes in patients without cardiac arrest as a rapid IV bolus of magnesium can result in hypotension and asystole. Some patients are given a continuous bolus of IV magnesium at a rate of 3 to 20 mg/min until the QT interval is below 0.50 seconds.[53][54]
  • Other Cardiac arrhythmia: The treatment for other arrhythmias in COVID-19 patients is the same as in patients with arrhythmias without COVID-19 infection.

Out-of-hospital cardiac arrest and Sudden Cardiac Death

Spontaneous Coronary Artery Dissection

Pathophysiology

  • In patients with an inflammatory overload, a localized inflammation of the coronary adventitia and periadventitial fat can occur. This could lead to the development of sudden coronary artery dissection in a susceptible patient.

Signs and symptoms

Treatment

References

  1. ↑ 1.0 1.1 Kang Y, Chen T, Mui D, Ferrari V, Jagasia D, Scherrer-Crosbie M; et al. (2020). "Cardiovascular manifestations and treatment considerations in covid-19". Heart. doi:10.1136/heartjnl-2020-317056. PMC 7211105 Check |pmc= value (help). PMID 32354800 Check |pmid= value (help).
  2. ↑ "Reorganized text". JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
  3. ↑ Szerlip M, Anwaruddin S, Aronow HD, Cohen MG, Daniels MJ, Dehghani P; et al. (2020). "Considerations for cardiac catheterization laboratory procedures during the COVID-19 pandemic perspectives from the Society for Cardiovascular Angiography and Interventions Emerging Leader Mentorship (SCAI ELM) Members and Graduates". Catheter Cardiovasc Interv. doi:10.1002/ccd.28887. PMID 32212409 Check |pmid= value (help).
  4. ↑ PMID 32219357 (PMID 32219357)
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  5. ↑ PMID 32360242 (PMID 32360242)
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  6. ↑ PMID 32186331 (PMID 32186331)
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  7. ↑ PMID 30625066 (PMID 30625066)
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  8. ↑ PMID 32140732 (PMID 32140732)
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  9. ↑ PMID 32391912 (PMID 32391912)
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  10. ↑ PMID 20863950 (PMID 20863950)
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  11. ↑ PMID 28062628 (PMID 28062628)
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  12. ↑ PMID 32293449 (PMID 32293449)
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  13. ↑ PMID 32232979 (PMID 32232979)
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  14. ↑ PMID 18298480 (PMID 18298480)
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  15. ↑ PMID 16442916 (PMID 16442916)
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  16. ↑ PMID 28322314 (PMID 28322314)
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  17. ↑ PMID 23837838 (PMID 23837838)
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  18. ↑ PMID 21478812 (PMID 21478812)
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  19. ↑ PMID 31129923 (PMID 31129923)
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  20. ↑ PMID 24251454 (PMID 24251454)
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  21. ↑ PMID 12656651 (PMID 12656651)
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  22. ↑ 22.0 22.1 Clerkin, Kevin J.; Fried, Justin A.; Raikhelkar, Jayant; Sayer, Gabriel; Griffin, Jan M.; Masoumi, Amirali; Jain, Sneha S.; Burkhoff, Daniel; Kumaraiah, Deepa; Rabbani, LeRoy; Schwartz, Allan; Uriel, Nir (2020). "COVID-19 and Cardiovascular Disease". Circulation. 141 (20): 1648–1655. doi:10.1161/CIRCULATIONAHA.120.046941. ISSN 0009-7322.
  23. ↑ 23.0 23.1 Esfandiarei, Mitra; McManus, Bruce M. (2008). "Molecular Biology and Pathogenesis of Viral Myocarditis". Annual Review of Pathology: Mechanisms of Disease. 3 (1): 127–155. doi:10.1146/annurev.pathmechdis.3.121806.151534. ISSN 1553-4006.
  24. ↑ Caforio, A. L. P.; Pankuweit, S.; Arbustini, E.; Basso, C.; Gimeno-Blanes, J.; Felix, S. B.; Fu, M.; Helio, T.; Heymans, S.; Jahns, R.; Klingel, K.; Linhart, A.; Maisch, B.; McKenna, W.; Mogensen, J.; Pinto, Y. M.; Ristic, A.; Schultheiss, H.-P.; Seggewiss, H.; Tavazzi, L.; Thiene, G.; Yilmaz, A.; Charron, P.; Elliott, P. M. (2013). "Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: A position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases". European Heart Journal. 34 (33): 2636–2648. doi:10.1093/eurheartj/eht210. ISSN 0195-668X.
  25. ↑ Kociol, Robb D.; Cooper, Leslie T.; Fang, James C.; Moslehi, Javid J.; Pang, Peter S.; Sabe, Marwa A.; Shah, Ravi V.; Sims, Daniel B.; Thiene, Gaetano; Vardeny, Orly (2020). "Recognition and Initial Management of Fulminant Myocarditis". Circulation. 141 (6). doi:10.1161/CIR.0000000000000745. ISSN 0009-7322.
  26. ↑ Zeng, Jia-Hui; Liu, Ying-Xia; Yuan, Jing; Wang, Fu-Xiang; Wu, Wei-Bo; Li, Jin-Xiu; Wang, Li-Fei; Gao, Hong; Wang, Yao; Dong, Chang-Feng; Li, Yi-Jun; Xie, Xiao-Juan; Feng, Cheng; Liu, Lei (2020). "First case of COVID-19 complicated with fulminant myocarditis: a case report and insights". Infection. doi:10.1007/s15010-020-01424-5. ISSN 0300-8126.
  27. ↑ 27.0 27.1 Inciardi, Riccardo M.; Lupi, Laura; Zaccone, Gregorio; Italia, Leonardo; Raffo, Michela; Tomasoni, Daniela; Cani, Dario S.; Cerini, Manuel; Farina, Davide; Gavazzi, Emanuele; Maroldi, Roberto; Adamo, Marianna; Ammirati, Enrico; Sinagra, Gianfranco; Lombardi, Carlo M.; Metra, Marco (2020). "Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiology. doi:10.1001/jamacardio.2020.1096. ISSN 2380-6583.
  28. ↑ Han, Seongwook; Kim, Hyun Ah; Kim, Jin Young; Kim, In-Cheol (2020). "COVID-19-related myocarditis in a 21-year-old female patient". European Heart Journal. 41 (19): 1859–1859. doi:10.1093/eurheartj/ehaa288. ISSN 0195-668X.
  29. ↑ Esposito, Antonio; Godino, Cosmo; Basso, Cristina; Cappelletti, Alberto Maria; Tresoldi, Moreno; De Cobelli, Francesco; Vignale, Davide; Villatore, Andrea; Palmisano, Anna; Gramegna, Mario; Peretto, Giovanni; Sala, Simone (2020). "Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection". European Heart Journal. 41 (19): 1861–1862. doi:10.1093/eurheartj/ehaa286. ISSN 0195-668X.
  30. ↑ Ruan, Qiurong; Yang, Kun; Wang, Wenxia; Jiang, Lingyu; Song, Jianxin (2020). "Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China". Intensive Care Medicine. 46 (5): 846–848. doi:10.1007/s00134-020-05991-x. ISSN 0342-4642.
  31. ↑ Hoffmann, Markus; Kleine-Weber, Hannah; Schroeder, Simon; Krüger, Nadine; Herrler, Tanja; Erichsen, Sandra; Schiergens, Tobias S.; Herrler, Georg; Wu, Nai-Huei; Nitsche, Andreas; Müller, Marcel A.; Drosten, Christian; Pöhlmann, Stefan (2020). "SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor". Cell. 181 (2): 271–280.e8. doi:10.1016/j.cell.2020.02.052. ISSN 0092-8674.
  32. ↑ Zhao, Yu; Zhao, Zixian; Wang, Yujia; Zhou, Yueqing; Ma, Yu; Zuo, Wei (2020). doi:10.1101/2020.01.26.919985. Missing or empty |title= (help)
  33. ↑ Tikellis, Chris; Thomas, M. C. (2012). "Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease". International Journal of Peptides. 2012: 1–8. doi:10.1155/2012/256294. ISSN 1687-9767.
  34. ↑ Komarowska, Izabela; Coe, David; Wang, Guosu; Haas, Robert; Mauro, Claudio; Kishore, Madhav; Cooper, Dianne; Nadkarni, Suchita; Fu, Hongmei; Steinbruchel, Daniel A.; Pitzalis, Costantino; Anderson, Graham; Bucy, Pat; Lombardi, Giovanna; Breckenridge, Ross; Marelli-Berg, Federica M. (2015). "Hepatocyte Growth Factor Receptor c-Met Instructs T Cell Cardiotropism and Promotes T Cell Migration to the Heart via Autocrine Chemokine Release". Immunity. 42 (6): 1087–1099. doi:10.1016/j.immuni.2015.05.014. ISSN 1074-7613.
  35. ↑ Agrawal, Anurodh Shankar; Garron, Tania; Tao, Xinrong; Peng, Bi-Hung; Wakamiya, Maki; Chan, Teh-Sheng; Couch, Robert B.; Tseng, Chien-Te K.; García-Sastre, A. (2015). "Generation of a Transgenic Mouse Model of Middle East Respiratory Syndrome Coronavirus Infection and Disease". Journal of Virology. 89 (7): 3659–3670. doi:10.1128/JVI.03427-14. ISSN 0022-538X.
  36. ↑ Schaecher, Scott R.; Stabenow, Jennifer; Oberle, Christina; Schriewer, Jill; Buller, R. Mark; Sagartz, John E.; Pekosz, Andrew (2008). "An immunosuppressed Syrian golden hamster model for SARS-CoV infection". Virology. 380 (2): 312–321. doi:10.1016/j.virol.2008.07.026. ISSN 0042-6822.
  37. ↑ Zhou, Fei; Yu, Ting; Du, Ronghui; Fan, Guohui; Liu, Ying; Liu, Zhibo; Xiang, Jie; Wang, Yeming; Song, Bin; Gu, Xiaoying; Guan, Lulu; Wei, Yuan; Li, Hui; Wu, Xudong; Xu, Jiuyang; Tu, Shengjin; Zhang, Yi; Chen, Hua; Cao, Bin (2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". The Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. ISSN 0140-6736.
  38. ↑ Iakimov VP (1977). "[F. Engels' theory of the origin of man and modern anthropologic findings]". Arkh Anat Gistol Embriol. 72 (6): 5–11. PMID 409380.
  39. ↑ Wang, Dawei; Hu, Bo; Hu, Chang; Zhu, Fangfang; Liu, Xing; Zhang, Jing; Wang, Binbin; Xiang, Hui; Cheng, Zhenshun; Xiong, Yong; Zhao, Yan; Li, Yirong; Wang, Xinghuan; Peng, Zhiyong (2020). "Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China". JAMA. 323 (11): 1061. doi:10.1001/jama.2020.1585. ISSN 0098-7484.
  40. ↑ Xu, Zhe; Shi, Lei; Wang, Yijin; Zhang, Jiyuan; Huang, Lei; Zhang, Chao; Liu, Shuhong; Zhao, Peng; Liu, Hongxia; Zhu, Li; Tai, Yanhong; Bai, Changqing; Gao, Tingting; Song, Jinwen; Xia, Peng; Dong, Jinghui; Zhao, Jingmin; Wang, Fu-Sheng (2020). "Pathological findings of COVID-19 associated with acute respiratory distress syndrome". The Lancet Respiratory Medicine. 8 (4): 420–422. doi:10.1016/S2213-2600(20)30076-X. ISSN 2213-2600.
  41. ↑ Chen, Mao; Prendergast, Bernard; Redwood, Simon; Xiong, Tian-Yuan (2020). "Coronaviruses and the cardiovascular system: acute and long-term implications". European Heart Journal. 41 (19): 1798–1800. doi:10.1093/eurheartj/ehaa231. ISSN 0195-668X.
  42. ↑ Liu K, Fang YY, Deng Y, Liu W, Wang MF, Ma JP; et al. (2020). "Clinical characteristics of novel coronavirus cases in tertiary hospitals in Hubei Province". Chin Med J (Engl). 133 (9): 1025–1031. doi:10.1097/CM9.0000000000000744. PMC 7147277 Check |pmc= value (help). PMID 32044814 Check |pmid= value (help).
  43. ↑ Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G; et al. (2020). "Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the COVID-19 Pandemic". J Am Coll Cardiol. 75 (18): 2352–2371. doi:10.1016/j.jacc.2020.03.031. PMC 7198856 Check |pmc= value (help). PMID 32201335 Check |pmid= value (help).
  44. ↑ Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW; et al. (2020). "Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area". JAMA. doi:10.1001/jama.2020.6775. PMC 7177629 Check |pmc= value (help). PMID 32320003 Check |pmid= value (help).
  45. ↑ Giudicessi, John R.; Noseworthy, Peter A.; Friedman, Paul A.; Ackerman, Michael J. (2020). "Urgent Guidance for Navigating and Circumventing the QTc-Prolonging and Torsadogenic Potential of Possible Pharmacotherapies for Coronavirus Disease 19 (COVID-19)". Mayo Clinic Proceedings. 95 (6): 1213–1221. doi:10.1016/j.mayocp.2020.03.024. ISSN 0025-6196.
  46. ↑ Goyal, Parag; Choi, Justin J.; Pinheiro, Laura C.; Schenck, Edward J.; Chen, Ruijun; Jabri, Assem; Satlin, Michael J.; Campion, Thomas R.; Nahid, Musarrat; Ringel, Joanna B.; Hoffman, Katherine L.; Alshak, Mark N.; Li, Han A.; Wehmeyer, Graham T.; Rajan, Mangala; Reshetnyak, Evgeniya; Hupert, Nathaniel; Horn, Evelyn M.; Martinez, Fernando J.; Gulick, Roy M.; Safford, Monika M. (2020). "Clinical Characteristics of Covid-19 in New York City". New England Journal of Medicine. 382 (24): 2372–2374. doi:10.1056/NEJMc2010419. ISSN 0028-4793.
  47. ↑ Guo T, Fan Y, Chen M, Wu X, Zhang L, He T; et al. (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiol. doi:10.1001/jamacardio.2020.1017. PMC 7101506 Check |pmc= value (help). PMID 32219356 Check |pmid= value (help).
  48. ↑ Baldi, Enrico; Sechi, Giuseppe M.; Mare, Claudio; Canevari, Fabrizio; Brancaglione, Antonella; Primi, Roberto; Klersy, Catherine; Palo, Alessandra; Contri, Enrico; Ronchi, Vincenza; Beretta, Giorgio; Reali, Francesca; Parogni, Pierpaolo; Facchin, Fabio; Bua, Davide; Rizzi, Ugo; Bussi, Daniele; Ruggeri, Simone; Oltrona Visconti, Luigi; Savastano, Simone (2020). "Out-of-Hospital Cardiac Arrest during the Covid-19 Outbreak in Italy". New England Journal of Medicine. doi:10.1056/NEJMc2010418. ISSN 0028-4793.
  49. ↑ Shao, Fei; Xu, Shuang; Ma, Xuedi; Xu, Zhouming; Lyu, Jiayou; Ng, Michael; Cui, Hao; Yu, Changxiao; Zhang, Qing; Sun, Peng; Tang, Ziren (2020). "In-hospital cardiac arrest outcomes among patients with COVID-19 pneumonia in Wuhan, China". Resuscitation. 151: 18–23. doi:10.1016/j.resuscitation.2020.04.005. ISSN 0300-9572.
  50. ↑ Gandhi, Rajesh T.; Solomon, Caren G.; Lynch, John B.; del Rio, Carlos (2020). "Mild or Moderate Covid-19". New England Journal of Medicine. doi:10.1056/NEJMcp2009249. ISSN 0028-4793.
  51. ↑ Chang, David; Saleh, Moussa; Gabriels, James; Ismail, Haisam; Goldner, Bruce; Willner, Jonathan; Beldner, Stuart; Mitra, Raman; John, Roy; Epstein, Laurence M. (2020). "Inpatient Use of Ambulatory Telemetry Monitors for COVID-19 Patients Treated With Hydroxychloroquine and/or Azithromycin". Journal of the American College of Cardiology. 75 (23): 2992–2993. doi:10.1016/j.jacc.2020.04.032. ISSN 0735-1097.
  52. ↑ Panchal, Ashish R.; Berg, Katherine M.; Kudenchuk, Peter J.; Del Rios, Marina; Hirsch, Karen G.; Link, Mark S.; Kurz, Michael C.; Chan, Paul S.; Cabañas, José G.; Morley, Peter T.; Hazinski, Mary Fran; Donnino, Michael W. (2018). "2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 138 (23). doi:10.1161/CIR.0000000000000613. ISSN 0009-7322.
  53. ↑ Tzivoni, D; Banai, S; Schuger, C; Benhorin, J; Keren, A; Gottlieb, S; Stern, S (1988). "Treatment of torsade de pointes with magnesium sulfate". Circulation. 77 (2): 392–397. doi:10.1161/01.CIR.77.2.392. ISSN 0009-7322.
  54. ↑ Neumar, R. W.; Otto, C. W.; Link, M. S.; Kronick, S. L.; Shuster, M.; Callaway, C. W.; Kudenchuk, P. J.; Ornato, J. P.; McNally, B.; Silvers, S. M.; Passman, R. S.; White, R. D.; Hess, E. P.; Tang, W.; Davis, D.; Sinz, E.; Morrison, L. J. (2010). "Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 122 (18_suppl_3): S729–S767. doi:10.1161/CIRCULATIONAHA.110.970988. ISSN 0009-7322.
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