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| __NOTOC__
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| To go to the COVID-19 project topics list, click '''[[COVID-19 Project Topics|here]]'''.
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| {{CMG}} {{AE}} {{SaraH}}{{mitra}}{{MC}}{{TAM}}{{AyeshaFJ}}{{MRV}}
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| ==Overview==
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| ==Complications==
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| ===Myocardial injury===
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| *COVID-19 patients with cardiovascular comorbidities have higher mortality.
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| *Hospitalized patients with COVID-19 and Cardiovascular disease seem to be more prevalent in both the USA and China. <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>
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| *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.
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| * It seems to be advisable to triage patients with COVID-19 based on their underlying CVD for a more aggressive treatment plan.
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| *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.<ref name="pmid32219356">{{cite journal| author=Guo T, Fan Y, Chen M, Wu X, Zhang L, He T | display-authors=etal| title=Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219356 | doi=10.1001/jamacardio.2020.1017 | pmc=7101506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219356 }} </ref>
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| ===Acute Coronary Syndromes===
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| ====Pathophysiology====
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| The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial.
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| *SARS-CoV-2 virus attaches to ACE 2 protein for ligand binding before entering the cell via receptor-mediated endocytosis.
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| **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.
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| *The cytokine release caused by the virus may lead to vascular inflammation, plaque instability, myocardial inflammation, a hypercoagulable state, or direct myocardial suppression.
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| Pathological changes:
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| *In the level of cardiac tissue: minimal change to interstitial inflammatory infiltration and myocyte necrosis
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| *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>
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| ====Signs and Symptoms====
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| The signs and symptoms of acute coronary syndrome include:<ref name="pmid16267320">{{cite journal| author=Abidov A, Rozanski A, Hachamovitch R, Hayes SW, Aboul-Enein F, Cohen I et al.| title=Prognostic significance of dyspnea in patients referred for cardiac stress testing. | journal=N Engl J Med | year= 2005 | volume= 353 | issue= 18 | pages= 1889-98 | pmid=16267320 | doi=10.1056/NEJMoa042741 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16267320 }} [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17213112 Review in: Evid Based Med. 2006 Jun;11(3):91] </ref>
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| *[[Chest pain]]
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| :*[[Chest pain|Substernal chest pain]]
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| :*Occurs at rest or [[exertion]]
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| :*Radiation to neck, jaw, left shoulder and left arm
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| :*Aggravated by physical activity and emotional stress
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| :*Relieved by rest, [[nitroglycerin]] or both
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| *Chest discomfort described crushing, squeezing, burning, choking, tightness or aching
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| *[[Dyspnea]]
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| *[[Diaphoresis]]
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| *[[Nausea]] and [[vomiting]]
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| *[[Fatigue]]
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| *[[Syncope]]
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| ====Treatment====
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| In patients with ACS, and COVID-19, treatment should follow the guidelines of the updated Society for Cardiovascular Angiography and Interventions.<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> <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>
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| ===ST-Elevation Myocardial Infarction (STEMI)===
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| A US model from 9 major centers showed a 38% drop in total STEMI activations during the COVID-19 pandemic. There is a 40% reduction noted in Spain as well. there was also a delay between the first presentation to a medical encounter up to 318 min. This is important since COVID-19 can potentially be a cause of STEMI through microthrombi, cytokine storm, coronary spasm, or direct endothelial injury.<ref name="pmid32550258">{{cite journal| author=Ullah W, Sattar Y, Saeed R, Ahmad A, Boigon MI, Haas DC | display-authors=etal| title=As the COVID-19 pandemic drags on, where have all the STEMIs gone? | journal=Int J Cardiol Heart Vasc | year= 2020 | volume= 29 | issue= | pages= 100550 | pmid=32550258 | doi=10.1016/j.ijcha.2020.100550 | pmc=7261452 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32550258 }} </ref>
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| *Potential etiologies for the reduction in STEMI PPCI activations:
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| **avoidance of medical care due to social distancing or concerns of contracting COVID-19 in the hospital
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| **STEMI misdiagnosis
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| **increased use of pharmacological reperfusion due to COVID-19
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| It is very important to realize if patients' anxiety is the reason behind decreasing the presentation of STEMI to U.S. hospitals.<ref name="pmid32283124">{{cite journal| author=Garcia S, Albaghdadi MS, Meraj PM, Schmidt C, Garberich R, Jaffer FA | display-authors=etal| title=Reduction in ST-Segment Elevation Cardiac Catheterization Laboratory Activations in the United States During COVID-19 Pandemic. | journal=J Am Coll Cardiol | year= 2020 | volume= 75 | issue= 22 | pages= 2871-2872 | pmid=32283124 | doi=10.1016/j.jacc.2020.04.011 | pmc=7151384 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32283124 }} </ref>
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| *Treatment of STEMI & COVID-19: The specific protocols for the treatment have been evolving. Early recommendations showed intravenous thrombolysis as first-line therapy for STEMI patients with confirmed COVID-19 since most hospitals do not have protected cardiac catheterization labs.<ref name="pmid32550258">{{cite journal| author=Ullah W, Sattar Y, Saeed R, Ahmad A, Boigon MI, Haas DC | display-authors=etal| title=As the COVID-19 pandemic drags on, where have all the STEMIs gone? | journal=Int J Cardiol Heart Vasc | year= 2020 | volume= 29 | issue= | pages= 100550 | pmid=32550258 | doi=10.1016/j.ijcha.2020.100550 | pmc=7261452 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32550258 }} </ref>
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| ===Heart Failure===
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| ====Pathophysiology====
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| *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.
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| *Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
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| *Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>
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| **Acute exacerbation of chronic heart failure
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| **Acute myocardial injury (which in turn can be caused by several mechanisms)
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| **Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
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| **Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
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| **Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)
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| ====Symptoms and signs====
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| *Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
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| *Lower limb edema
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| *Orthopnea
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| *Paroxysmal nocturnal dyspnea
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| *Confusion and altered mentation
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| *Cool extremities
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| *Cyanosis
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| *Syncope
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| *Fatigue
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| *Hemoptysis
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| *Palpitations
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| *Weakness
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| *Wheezing or cardiac asthma
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| *Distended jugular veins
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| *Crackles on auscultation
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|
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| ====Electrocardiography (ECG)====
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| *There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
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| *The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
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| *These ECG findings may include:
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| **Low QRS Voltage
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| **Left ventricular hypertrophy
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| **Left atrial enlargement
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| **Left bundle branch block
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| **Poor R progression
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| **ST-T changes
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| ====Chest x-ray (CXR)====
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| *The Chest x-ray may show evidence of:
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| **Cardiomegaly
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| **Pulmonary congestion
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| **Increased pulmonary vascular markings.
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| *Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
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| ====Echocardiography====
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| *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.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
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| *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.
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| *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:
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| **Cardiac point-of-care ultrasound (POCUS)
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| **Focused cardiac ultrasound study (FoCUS)
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| **Critical care echocardiography
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| *Cardiac ultrasound can help in assessing the following parameters:
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| **Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
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| **Left ventricular diastolic function
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| **Left ventricular structural abnormalities, including LV size and LV wall thickness
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| **Left atrial size
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| **Right ventricular size and function
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| **Detection and quantification of valvular abnormalities
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| **Measurement of systolic pulmonary artery pressure
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| **Detection and quantification of pericardial effusion
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| **Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia
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|
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| ====Cardiac biomarkers====
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| *Cardiac Troponins:
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| **Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
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| **Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>
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| *Natriuretic Peptides:
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| **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.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
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| **Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
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| **Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
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| **Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
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| **However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
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| **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.
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|
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| ====Treatment====
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| *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. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
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| *Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
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| **Fluid restriction
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| **Diuretic therapy
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| **Vasopressors and/or inotropes
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| **Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
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| *Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
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| *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.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
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| ===Cardiogenic Shock===
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| ===Myocarditis===
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|
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| ====Pathophysiology====
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|
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| *Studies have demonstrated that [[COVID-19]] interacts with the [[cardiovascular system]], thereby causing myocardial injury and dysfunction as well as increasing [[morbidity]] among patients with underlying [[cardiovascular]] conditions. Among patients with [[COVID-19]], there is a high [[prevalence]] of the [[cardiovascular]] disease, and >7% of patients experience [[myocardial]] injury from the [[infection]].<ref name="ClerkinFried2020">{{cite journal|last1=Clerkin|first1=Kevin J.|last2=Fried|first2=Justin A.|last3=Raikhelkar|first3=Jayant|last4=Sayer|first4=Gabriel|last5=Griffin|first5=Jan M.|last6=Masoumi|first6=Amirali|last7=Jain|first7=Sneha S.|last8=Burkhoff|first8=Daniel|last9=Kumaraiah|first9=Deepa|last10=Rabbani|first10=LeRoy|last11=Schwartz|first11=Allan|last12=Uriel|first12=Nir|title=COVID-19 and Cardiovascular Disease|journal=Circulation|volume=141|issue=20|year=2020|pages=1648–1655|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.120.046941}}</ref>
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| *[[Myocarditis]] is an [[inflammatory]] disease of the heart characterized by [[inflammatory]] infiltrates and [[myocardial]] injury without an [[Ischemia|ischemic]] cause.<ref name="EsfandiareiMcManus2008">{{cite journal|last1=Esfandiarei|first1=Mitra|last2=McManus|first2=Bruce M.|title=Molecular Biology and Pathogenesis of Viral Myocarditis|journal=Annual Review of Pathology: Mechanisms of Disease|volume=3|issue=1|year=2008|pages=127–155|issn=1553-4006|doi=10.1146/annurev.pathmechdis.3.121806.151534}}</ref>
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| **The major cause of [[myocarditis]] in the United States and other developed countries is viral.<ref name="CaforioPankuweit2013">{{cite journal|last1=Caforio|first1=A. L. P.|last2=Pankuweit|first2=S.|last3=Arbustini|first3=E.|last4=Basso|first4=C.|last5=Gimeno-Blanes|first5=J.|last6=Felix|first6=S. B.|last7=Fu|first7=M.|last8=Helio|first8=T.|last9=Heymans|first9=S.|last10=Jahns|first10=R.|last11=Klingel|first11=K.|last12=Linhart|first12=A.|last13=Maisch|first13=B.|last14=McKenna|first14=W.|last15=Mogensen|first15=J.|last16=Pinto|first16=Y. M.|last17=Ristic|first17=A.|last18=Schultheiss|first18=H.-P.|last19=Seggewiss|first19=H.|last20=Tavazzi|first20=L.|last21=Thiene|first21=G.|last22=Yilmaz|first22=A.|last23=Charron|first23=P.|last24=Elliott|first24=P. M.|title=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|journal=European Heart Journal|volume=34|issue=33|year=2013|pages=2636–2648|issn=0195-668X|doi=10.1093/eurheartj/eht210}}</ref> <ref name="KociolCooper2020">{{cite journal|last1=Kociol|first1=Robb D.|last2=Cooper|first2=Leslie T.|last3=Fang|first3=James C.|last4=Moslehi|first4=Javid J.|last5=Pang|first5=Peter S.|last6=Sabe|first6=Marwa A.|last7=Shah|first7=Ravi V.|last8=Sims|first8=Daniel B.|last9=Thiene|first9=Gaetano|last10=Vardeny|first10=Orly|title=Recognition and Initial Management of Fulminant Myocarditis|journal=Circulation|volume=141|issue=6|year=2020|issn=0009-7322|doi=10.1161/CIR.0000000000000745}}</ref>
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| **Number of cases of [[myocarditis]] have been reported in [[COVID-19]] patients.<ref name="ZengLiu2020">{{cite journal|last1=Zeng|first1=Jia-Hui|last2=Liu|first2=Ying-Xia|last3=Yuan|first3=Jing|last4=Wang|first4=Fu-Xiang|last5=Wu|first5=Wei-Bo|last6=Li|first6=Jin-Xiu|last7=Wang|first7=Li-Fei|last8=Gao|first8=Hong|last9=Wang|first9=Yao|last10=Dong|first10=Chang-Feng|last11=Li|first11=Yi-Jun|last12=Xie|first12=Xiao-Juan|last13=Feng|first13=Cheng|last14=Liu|first14=Lei|title=First case of COVID-19 complicated with fulminant myocarditis: a case report and insights|journal=Infection|year=2020|issn=0300-8126|doi=10.1007/s15010-020-01424-5}}</ref><ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref><ref name="HanKim2020">{{cite journal|last1=Han|first1=Seongwook|last2=Kim|first2=Hyun Ah|last3=Kim|first3=Jin Young|last4=Kim|first4=In-Cheol|title=COVID-19-related myocarditis in a 21-year-old female patient|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1859–1859|issn=0195-668X|doi=10.1093/eurheartj/ehaa288}}</ref><ref name="EspositoGodino2020">{{cite journal|last1=Esposito|first1=Antonio|last2=Godino|first2=Cosmo|last3=Basso|first3=Cristina|last4=Cappelletti|first4=Alberto Maria|last5=Tresoldi|first5=Moreno|last6=De Cobelli|first6=Francesco|last7=Vignale|first7=Davide|last8=Villatore|first8=Andrea|last9=Palmisano|first9=Anna|last10=Gramegna|first10=Mario|last11=Peretto|first11=Giovanni|last12=Sala|first12=Simone|title=Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1861–1862|issn=0195-668X|doi=10.1093/eurheartj/ehaa286}}</ref> It has also been reported as the cause of death in some [[COVID-19]] patients.<ref name="RuanYang2020">{{cite journal|last1=Ruan|first1=Qiurong|last2=Yang|first2=Kun|last3=Wang|first3=Wenxia|last4=Jiang|first4=Lingyu|last5=Song|first5=Jianxin|title=Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China|journal=Intensive Care Medicine|volume=46|issue=5|year=2020|pages=846–848|issn=0342-4642|doi=10.1007/s00134-020-05991-x}}</ref>
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| *Proposed pathophysiology of [[SARS-CoV-2]] [[myocarditis]]
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| **[[SARS-CoV-2]] infection is caused by binding of the viral surface spike [[protein]] (primed by [[TMPRSS2]], which is a transmembrane protease, [[serine]] 2) to the human [[angiotensin-converting enzyme 2 (ACE2) receptor]].<ref name="HoffmannKleine-Weber2020">{{cite journal|last1=Hoffmann|first1=Markus|last2=Kleine-Weber|first2=Hannah|last3=Schroeder|first3=Simon|last4=Krüger|first4=Nadine|last5=Herrler|first5=Tanja|last6=Erichsen|first6=Sandra|last7=Schiergens|first7=Tobias S.|last8=Herrler|first8=Georg|last9=Wu|first9=Nai-Huei|last10=Nitsche|first10=Andreas|last11=Müller|first11=Marcel A.|last12=Drosten|first12=Christian|last13=Pöhlmann|first13=Stefan|title=SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor|journal=Cell|volume=181|issue=2|year=2020|pages=271–280.e8|issn=00928674|doi=10.1016/j.cell.2020.02.052}}</ref>
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| **ACE2 is expressed in the [[lung]], principally type II [[alveolar]] cells which appears to be the principal portal of entry.<ref name="ZhaoZhao2020">{{cite journal|last1=Zhao|first1=Yu|last2=Zhao|first2=Zixian|last3=Wang|first3=Yujia|last4=Zhou|first4=Yueqing|last5=Ma|first5=Yu|last6=Zuo|first6=Wei|year=2020|doi=10.1101/2020.01.26.919985}}</ref> [[ACE2]] is highly expressed in the [[heart]] as well.<ref name="TikellisThomas2012">{{cite journal|last1=Tikellis|first1=Chris|last2=Thomas|first2=M. C.|title=Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease|journal=International Journal of Peptides|volume=2012|year=2012|pages=1–8|issn=1687-9767|doi=10.1155/2012/256294}}</ref>
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| **[[Naive T cell|Naive]] [[T lymphocytes]] can be primed for viral [[antigens]] via [[antigen-presenting cells]] and cardio-[[tropism]] by the heart-produced [[hepatocyte growth factor (HGF)]] which binds [[c-Met]], an HGF receptor on T lymphocytes.<ref name="KomarowskaCoe2015">{{cite journal|last1=Komarowska|first1=Izabela|last2=Coe|first2=David|last3=Wang|first3=Guosu|last4=Haas|first4=Robert|last5=Mauro|first5=Claudio|last6=Kishore|first6=Madhav|last7=Cooper|first7=Dianne|last8=Nadkarni|first8=Suchita|last9=Fu|first9=Hongmei|last10=Steinbruchel|first10=Daniel A.|last11=Pitzalis|first11=Costantino|last12=Anderson|first12=Graham|last13=Bucy|first13=Pat|last14=Lombardi|first14=Giovanna|last15=Breckenridge|first15=Ross|last16=Marelli-Berg|first16=Federica M.|title=Hepatocyte Growth Factor Receptor c-Met Instructs T Cell Cardiotropism and Promotes T Cell Migration to the Heart via Autocrine Chemokine Release|journal=Immunity|volume=42|issue=6|year=2015|pages=1087–1099|issn=10747613|doi=10.1016/j.immuni.2015.05.014}}</ref>
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| **The viral RNAs of [[Middle East Respiratory Syndrome coronavirus]] [[(MERS-CoV)]] and [[SARS-CoV]] were found in the heart tissues of infected animals, suggesting that these [[Coronavirus|corona viruses]] possess [[cardiotropism]].<ref name="AgrawalGarron2015">{{cite journal|last1=Agrawal|first1=Anurodh Shankar|last2=Garron|first2=Tania|last3=Tao|first3=Xinrong|last4=Peng|first4=Bi-Hung|last5=Wakamiya|first5=Maki|last6=Chan|first6=Teh-Sheng|last7=Couch|first7=Robert B.|last8=Tseng|first8=Chien-Te K.|last9=García-Sastre|first9=A.|title=Generation of a Transgenic Mouse Model of Middle East Respiratory Syndrome Coronavirus Infection and Disease|journal=Journal of Virology|volume=89|issue=7|year=2015|pages=3659–3670|issn=0022-538X|doi=10.1128/JVI.03427-14}}</ref><ref name="SchaecherStabenow2008">{{cite journal|last1=Schaecher|first1=Scott R.|last2=Stabenow|first2=Jennifer|last3=Oberle|first3=Christina|last4=Schriewer|first4=Jill|last5=Buller|first5=R. Mark|last6=Sagartz|first6=John E.|last7=Pekosz|first7=Andrew|title=An immunosuppressed Syrian golden hamster model for SARS-CoV infection|journal=Virology|volume=380|issue=2|year=2008|pages=312–321|issn=00426822|doi=10.1016/j.virol.2008.07.026}}</ref>
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| **The primed CD8+ T lymphocytes migrate to the cardiomyocytes and through [[cell-mediated cytotoxicity]], cause myocardial [[inflammation]]. In the [[cytokine storm syndrome]], proinflammatory [[cytokines]] such as [[Interleukin-6]] ([[IL-6]]) are released into the circulation, which further augments [[T-lymphocytes|T-lymphocyte]] activation and causes the release of more [[Cytokine|cytokines]].<ref name="ZhouYu2020">{{cite journal|last1=Zhou|first1=Fei|last2=Yu|first2=Ting|last3=Du|first3=Ronghui|last4=Fan|first4=Guohui|last5=Liu|first5=Ying|last6=Liu|first6=Zhibo|last7=Xiang|first7=Jie|last8=Wang|first8=Yeming|last9=Song|first9=Bin|last10=Gu|first10=Xiaoying|last11=Guan|first11=Lulu|last12=Wei|first12=Yuan|last13=Li|first13=Hui|last14=Wu|first14=Xudong|last15=Xu|first15=Jiuyang|last16=Tu|first16=Shengjin|last17=Zhang|first17=Yi|last18=Chen|first18=Hua|last19=Cao|first19=Bin|title=Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study|journal=The Lancet|volume=395|issue=10229|year=2020|pages=1054–1062|issn=01406736|doi=10.1016/S0140-6736(20)30566-3}}</ref>
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| **Cytokine storms result in increased vascular wall permeability and myocardial edema.<ref name="HanKim2020">{{cite journal|last1=Han|first1=Seongwook|last2=Kim|first2=Hyun Ah|last3=Kim|first3=Jin Young|last4=Kim|first4=In-Cheol|title=COVID-19-related myocarditis in a 21-year-old female patient|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1859–1859|issn=0195-668X|doi=10.1093/eurheartj/ehaa288}}</ref><ref name="ZengLiu2020">{{cite journal|last1=Zeng|first1=Jia-Hui|last2=Liu|first2=Ying-Xia|last3=Yuan|first3=Jing|last4=Wang|first4=Fu-Xiang|last5=Wu|first5=Wei-Bo|last6=Li|first6=Jin-Xiu|last7=Wang|first7=Li-Fei|last8=Gao|first8=Hong|last9=Wang|first9=Yao|last10=Dong|first10=Chang-Feng|last11=Li|first11=Yi-Jun|last12=Xie|first12=Xiao-Juan|last13=Feng|first13=Cheng|last14=Liu|first14=Lei|title=First case of COVID-19 complicated with fulminant myocarditis: a case report and insights|journal=Infection|year=2020|issn=0300-8126|doi=10.1007/s15010-020-01424-5}}</ref>
| |
| **Thus a positive feedback loop of immune activation and [[myocardial]] damage is established.<ref name="pmid409380">{{cite journal| author=Iakimov VP| title=[F. Engels' theory of the origin of man and modern anthropologic findings]. | journal=Arkh Anat Gistol Embriol | year= 1977 | volume= 72 | issue= 6 | pages= 5-11 | pmid=409380 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=409380 }} </ref><ref name="EsfandiareiMcManus2008">{{cite journal|last1=Esfandiarei|first1=Mitra|last2=McManus|first2=Bruce M.|title=Molecular Biology and Pathogenesis of Viral Myocarditis|journal=Annual Review of Pathology: Mechanisms of Disease|volume=3|issue=1|year=2008|pages=127–155|issn=1553-4006|doi=10.1146/annurev.pathmechdis.3.121806.151534}}</ref>
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| *Pathological changes in the myocardium
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| **They could be due to viral replication in the myocardium or immune responses caused by the infection or due to systemic responses to respiratory failure.
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| **Mononuclear inflammatory infiltration has been observed in the heart tissue in COVID-19 autopsy studies.<ref name="XuShi2020">{{cite journal|last1=Xu|first1=Zhe|last2=Shi|first2=Lei|last3=Wang|first3=Yijin|last4=Zhang|first4=Jiyuan|last5=Huang|first5=Lei|last6=Zhang|first6=Chao|last7=Liu|first7=Shuhong|last8=Zhao|first8=Peng|last9=Liu|first9=Hongxia|last10=Zhu|first10=Li|last11=Tai|first11=Yanhong|last12=Bai|first12=Changqing|last13=Gao|first13=Tingting|last14=Song|first14=Jinwen|last15=Xia|first15=Peng|last16=Dong|first16=Jinghui|last17=Zhao|first17=Jingmin|last18=Wang|first18=Fu-Sheng|title=Pathological findings of COVID-19 associated with acute respiratory distress syndrome|journal=The Lancet Respiratory Medicine|volume=8|issue=4|year=2020|pages=420–422|issn=22132600|doi=10.1016/S2213-2600(20)30076-X}}</ref>
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|
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| ====Signs and symptoms====
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|
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| Clinical presentation of [[SARS-CoV-2]] [[myocarditis]] varies among cases from mild to severe to fulminant.
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| *Mild - fatigue and [[dyspnea]],<ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref><ref name="HanKim2020">{{cite journal|last1=Han|first1=Seongwook|last2=Kim|first2=Hyun Ah|last3=Kim|first3=Jin Young|last4=Kim|first4=In-Cheol|title=COVID-19-related myocarditis in a 21-year-old female patient|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1859–1859|issn=0195-668X|doi=10.1093/eurheartj/ehaa288}}</ref>, [[chest pain]] or chest tightness on exertion.<ref name="ZengLiu2020">{{cite journal|last1=Zeng|first1=Jia-Hui|last2=Liu|first2=Ying-Xia|last3=Yuan|first3=Jing|last4=Wang|first4=Fu-Xiang|last5=Wu|first5=Wei-Bo|last6=Li|first6=Jin-Xiu|last7=Wang|first7=Li-Fei|last8=Gao|first8=Hong|last9=Wang|first9=Yao|last10=Dong|first10=Chang-Feng|last11=Li|first11=Yi-Jun|last12=Xie|first12=Xiao-Juan|last13=Feng|first13=Cheng|last14=Liu|first14=Lei|title=First case of COVID-19 complicated with fulminant myocarditis: a case report and insights|journal=Infection|year=2020|issn=0300-8126|doi=10.1007/s15010-020-01424-5}}</ref><ref name="EspositoGodino2020">{{cite journal|last1=Esposito|first1=Antonio|last2=Godino|first2=Cosmo|last3=Basso|first3=Cristina|last4=Cappelletti|first4=Alberto Maria|last5=Tresoldi|first5=Moreno|last6=De Cobelli|first6=Francesco|last7=Vignale|first7=Davide|last8=Villatore|first8=Andrea|last9=Palmisano|first9=Anna|last10=Gramegna|first10=Mario|last11=Peretto|first11=Giovanni|last12=Sala|first12=Simone|title=Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1861–1862|issn=0195-668X|doi=10.1093/eurheartj/ehaa286}}</ref>
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| *Severe - Many patients deteriorate and show symptoms of [[tachycardia]] and [[heart failure|acute-onset heart failure]] with [[cardiogenic shock]].<ref name="ZengLiu2020">{{cite journal|last1=Zeng|first1=Jia-Hui|last2=Liu|first2=Ying-Xia|last3=Yuan|first3=Jing|last4=Wang|first4=Fu-Xiang|last5=Wu|first5=Wei-Bo|last6=Li|first6=Jin-Xiu|last7=Wang|first7=Li-Fei|last8=Gao|first8=Hong|last9=Wang|first9=Yao|last10=Dong|first10=Chang-Feng|last11=Li|first11=Yi-Jun|last12=Xie|first12=Xiao-Juan|last13=Feng|first13=Cheng|last14=Liu|first14=Lei|title=First case of COVID-19 complicated with fulminant myocarditis: a case report and insights|journal=Infection|year=2020|issn=0300-8126|doi=10.1007/s15010-020-01424-5}}</ref><ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref><ref name="HanKim2020">{{cite journal|last1=Han|first1=Seongwook|last2=Kim|first2=Hyun Ah|last3=Kim|first3=Jin Young|last4=Kim|first4=In-Cheol|title=COVID-19-related myocarditis in a 21-year-old female patient|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1859–1859|issn=0195-668X|doi=10.1093/eurheartj/ehaa288}}</ref> They may also present with signs of [[heart failure|right-sided heart failure]], including raised [[jugular venous pressure]], right upper quadrant pain, and [[peripheral edema]].<ref name="KociolCooper2020">{{cite journal|last1=Kociol|first1=Robb D.|last2=Cooper|first2=Leslie T.|last3=Fang|first3=James C.|last4=Moslehi|first4=Javid J.|last5=Pang|first5=Peter S.|last6=Sabe|first6=Marwa A.|last7=Shah|first7=Ravi V.|last8=Sims|first8=Daniel B.|last9=Thiene|first9=Gaetano|last10=Vardeny|first10=Orly|title=Recognition and Initial Management of Fulminant Myocarditis|journal=Circulation|volume=141|issue=6|year=2020|issn=0009-7322|doi=10.1161/CIR.0000000000000745}}</ref>
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| *Fulminant - [[Fulminant myocarditis]] is defined as [[ventricular dysfunction]] and [[heart failure]] within 2–3 weeks of infection.<ref name="EsfandiareiMcManus2008">{{cite journal|last1=Esfandiarei|first1=Mitra|last2=McManus|first2=Bruce M.|title=Molecular Biology and Pathogenesis of Viral Myocarditis|journal=Annual Review of Pathology: Mechanisms of Disease|volume=3|issue=1|year=2008|pages=127–155|issn=1553-4006|doi=10.1146/annurev.pathmechdis.3.121806.151534}}</ref><ref name="Irabien-OrtizCarreras-Mora2020">{{cite journal|last1=Irabien-Ortiz|first1=Ángela|last2=Carreras-Mora|first2=José|last3=Sionis|first3=Alessandro|last4=Pàmies|first4=Julia|last5=Montiel|first5=José|last6=Tauron|first6=Manel|title=Fulminant myocarditis due to COVID-19|journal=Revista Española de Cardiología (English Edition)|volume=73|issue=6|year=2020|pages=503–504|issn=18855857|doi=10.1016/j.rec.2020.04.005}}</ref><ref name="FangWei2020">{{cite journal|last1=Fang|first1=Yuan|last2=Wei|first2=Xin|last3=Ma|first3=Fenglian|last4=Hu|first4=Hongde|title=Coronavirus fulminant myocarditis treated with glucocorticoid and human immunoglobulin|journal=European Heart Journal|year=2020|issn=0195-668X|doi=10.1093/eurheartj/ehaa190}}</ref><ref name="WangLi2018">{{cite journal|last1=Wang|first1=Daowen|last2=Li|first2=Sheng|last3=Jiang|first3=Jiangang|last4=Yan|first4=Jiangtao|last5=Zhao|first5=Chunxia|last6=Wang|first6=Yan|last7=Ma|first7=Yexin|last8=Zeng|first8=Hesong|last9=Guo|first9=Xiaomei|last10=Wang|first10=Hong|last11=Tang|first11=Jiarong|last12=Zuo|first12=Houjuan|last13=Lin|first13=Li|last14=Cui|first14=Guanglin|title=Chinese society of cardiology expert consensus statement on the diagnosis and treatment of adult fulminant myocarditis|journal=Science China Life Sciences|volume=62|issue=2|year=2018|pages=187–202|issn=1674-7305|doi=10.1007/s11427-018-9385-3}}</ref> The early signs resemble those of [[sepsis]]: fever, low [[pulse pressure]], cold extremities, and [[sinus tachycardia]].<ref name="KociolCooper2020">{{cite journal|last1=Kociol|first1=Robb D.|last2=Cooper|first2=Leslie T.|last3=Fang|first3=James C.|last4=Moslehi|first4=Javid J.|last5=Pang|first5=Peter S.|last6=Sabe|first6=Marwa A.|last7=Shah|first7=Ravi V.|last8=Sims|first8=Daniel B.|last9=Thiene|first9=Gaetano|last10=Vardeny|first10=Orly|title=Recognition and Initial Management of Fulminant Myocarditis|journal=Circulation|volume=141|issue=6|year=2020|issn=0009-7322|doi=10.1161/CIR.0000000000000745}}</ref><ref name="ZengLiu2020">{{cite journal|last1=Zeng|first1=Jia-Hui|last2=Liu|first2=Ying-Xia|last3=Yuan|first3=Jing|last4=Wang|first4=Fu-Xiang|last5=Wu|first5=Wei-Bo|last6=Li|first6=Jin-Xiu|last7=Wang|first7=Li-Fei|last8=Gao|first8=Hong|last9=Wang|first9=Yao|last10=Dong|first10=Chang-Feng|last11=Li|first11=Yi-Jun|last12=Xie|first12=Xiao-Juan|last13=Feng|first13=Cheng|last14=Liu|first14=Lei|title=First case of COVID-19 complicated with fulminant myocarditis: a case report and insights|journal=Infection|year=2020|issn=0300-8126|doi=10.1007/s15010-020-01424-5}}</ref>
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| According to a study, [[ventricular arrhythmias]] are also seen in the patients of myocarditis.<ref name="PerettoSala2020">{{cite journal|last1=Peretto|first1=Giovanni|last2=Sala|first2=Simone|last3=Rizzo|first3=Stefania|last4=Palmisano|first4=Anna|last5=Esposito|first5=Antonio|last6=De Cobelli|first6=Francesco|last7=Campochiaro|first7=Corrado|last8=De Luca|first8=Giacomo|last9=Foppoli|first9=Luca|last10=Dagna|first10=Lorenzo|last11=Thiene|first11=Gaetano|last12=Basso|first12=Cristina|last13=Della Bella|first13=Paolo|title=Ventricular Arrhythmias in Myocarditis|journal=Journal of the American College of Cardiology|volume=75|issue=9|year=2020|pages=1046–1057|issn=07351097|doi=10.1016/j.jacc.2020.01.036}}</ref>
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| ===Pericarditis===
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|
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| ===Arrhythmias ===
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|
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| ==== Pathophysiology: ====
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| Respiratory disease is the chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|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 [[Endothelium|endothelial cells]]. [[Hypoxemia|Hypoxia]] and [[Electrolyte disturbance|electrolyte abnormalities]] that are common in the acute phase of severe [[COVID-19]] can potentiate [[Cardiac arrhythmia|cardiac arrhythmias]]. Binding of SARS-CoV-2 to ACE2 receptors can result into [[hypokalemia]] which causes various types of [[Cardiac arrhythmia|arrhythmia]]. Elevated levels of [[Cytokine|cytokines]] as a result of the [[Systemic inflammatory response syndrome|systemic inflammatory response]] of the severe [[COVID-19|Coronavirus disease 2019]] (COVID-19) can cause injury to multiple organs, including [[Cardiac muscle|cardiac myocytes]]. According to the data based on studies on previous [[Severe acute respiratory syndrome]] ([[Severe acute respiratory syndrome|SARS]]) and the [[Middle East respiratory syndrome coronavirus infection|Middle East respiratory syndrome]] ([[Middle East respiratory syndrome coronavirus infection|MERS]]) epidemic and the ongoing [[COVID-19]] outbreak, multiple mechanisms have been suggested for cardiac damage.<ref name="WangHu2020">{{cite journal|last1=Wang|first1=Dawei|last2=Hu|first2=Bo|last3=Hu|first3=Chang|last4=Zhu|first4=Fangfang|last5=Liu|first5=Xing|last6=Zhang|first6=Jing|last7=Wang|first7=Binbin|last8=Xiang|first8=Hui|last9=Cheng|first9=Zhenshun|last10=Xiong|first10=Yong|last11=Zhao|first11=Yan|last12=Li|first12=Yirong|last13=Wang|first13=Xinghuan|last14=Peng|first14=Zhiyong|title=Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China|journal=JAMA|volume=323|issue=11|year=2020|pages=1061|issn=0098-7484|doi=10.1001/jama.2020.1585}}</ref><ref name="XuShi2020">{{cite journal|last1=Xu|first1=Zhe|last2=Shi|first2=Lei|last3=Wang|first3=Yijin|last4=Zhang|first4=Jiyuan|last5=Huang|first5=Lei|last6=Zhang|first6=Chao|last7=Liu|first7=Shuhong|last8=Zhao|first8=Peng|last9=Liu|first9=Hongxia|last10=Zhu|first10=Li|last11=Tai|first11=Yanhong|last12=Bai|first12=Changqing|last13=Gao|first13=Tingting|last14=Song|first14=Jinwen|last15=Xia|first15=Peng|last16=Dong|first16=Jinghui|last17=Zhao|first17=Jingmin|last18=Wang|first18=Fu-Sheng|title=Pathological findings of COVID-19 associated with acute respiratory distress syndrome|journal=The Lancet Respiratory Medicine|volume=8|issue=4|year=2020|pages=420–422|issn=22132600|doi=10.1016/S2213-2600(20)30076-X}}</ref><ref name="ChenPrendergast2020">{{cite journal|last1=Chen|first1=Mao|last2=Prendergast|first2=Bernard|last3=Redwood|first3=Simon|last4=Xiong|first4=Tian-Yuan|title=Coronaviruses and the cardiovascular system: acute and long-term implications|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1798–1800|issn=0195-668X|doi=10.1093/eurheartj/ehaa231}}</ref><ref name="ClerkinFried2020">{{cite journal|last1=Clerkin|first1=Kevin J.|last2=Fried|first2=Justin A.|last3=Raikhelkar|first3=Jayant|last4=Sayer|first4=Gabriel|last5=Griffin|first5=Jan M.|last6=Masoumi|first6=Amirali|last7=Jain|first7=Sneha S.|last8=Burkhoff|first8=Daniel|last9=Kumaraiah|first9=Deepa|last10=Rabbani|first10=LeRoy|last11=Schwartz|first11=Allan|last12=Uriel|first12=Nir|title=COVID-19 and Cardiovascular Disease|journal=Circulation|volume=141|issue=20|year=2020|pages=1648–1655|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.120.046941}}</ref>
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| ==== Signs and Symptoms: ====
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| 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).
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| *'''Palpitations:''' According to a study done in Hubei province,[[Palpitation|palpitations]] were reported as a presenting symptom by 7.3 percent of patients.<ref name="pmid32044814">{{cite journal| author=Liu K, Fang YY, Deng Y, Liu W, Wang MF, Ma JP | display-authors=etal| title=Clinical characteristics of novel coronavirus cases in tertiary hospitals in Hubei Province. | journal=Chin Med J (Engl) | year= 2020 | volume= 133 | issue= 9 | pages= 1025-1031 | pmid=32044814 | doi=10.1097/CM9.0000000000000744 | pmc=7147277 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32044814 }} </ref><ref name="pmid32201335">{{cite journal| author=Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G | display-authors=etal| title=Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the COVID-19 Pandemic. | journal=J Am Coll Cardiol | year= 2020 | volume= 75 | issue= 18 | pages= 2352-2371 | pmid=32201335 | doi=10.1016/j.jacc.2020.03.031 | pmc=7198856 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32201335 }} </ref>
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| *'''Prolong QT Interval:''' According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had [[QT interval|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.<ref name="pmid32320003">{{cite journal| author=Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW | display-authors=etal| title=Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. | journal=JAMA | year= 2020 | volume= | issue= | pages= | pmid=32320003 | doi=10.1001/jama.2020.6775 | pmc=7177629 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32320003 }} </ref><ref name="GiudicessiNoseworthy2020">{{cite journal|last1=Giudicessi|first1=John R.|last2=Noseworthy|first2=Peter A.|last3=Friedman|first3=Paul A.|last4=Ackerman|first4=Michael J.|title=Urgent Guidance for Navigating and Circumventing the QTc-Prolonging and Torsadogenic Potential of Possible Pharmacotherapies for Coronavirus Disease 19 (COVID-19)|journal=Mayo Clinic Proceedings|volume=95|issue=6|year=2020|pages=1213–1221|issn=00256196|doi=10.1016/j.mayocp.2020.03.024}}</ref>
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| *'''Atrial Arrhythmia:''' According to a study, among 393 patients with COVID-19, [[Cardiac arrhythmia|atrial arrhythmias]] were more common among patients requiring invasive [[mechanical ventilation]] than noninvasive [[mechanical ventilation]] (17.7 versus 1.9 percent).<ref name="GoyalChoi2020">{{cite journal|last1=Goyal|first1=Parag|last2=Choi|first2=Justin J.|last3=Pinheiro|first3=Laura C.|last4=Schenck|first4=Edward J.|last5=Chen|first5=Ruijun|last6=Jabri|first6=Assem|last7=Satlin|first7=Michael J.|last8=Campion|first8=Thomas R.|last9=Nahid|first9=Musarrat|last10=Ringel|first10=Joanna B.|last11=Hoffman|first11=Katherine L.|last12=Alshak|first12=Mark N.|last13=Li|first13=Han A.|last14=Wehmeyer|first14=Graham T.|last15=Rajan|first15=Mangala|last16=Reshetnyak|first16=Evgeniya|last17=Hupert|first17=Nathaniel|last18=Horn|first18=Evelyn M.|last19=Martinez|first19=Fernando J.|last20=Gulick|first20=Roy M.|last21=Safford|first21=Monika M.|title=Clinical Characteristics of Covid-19 in New York City|journal=New England Journal of Medicine|volume=382|issue=24|year=2020|pages=2372–2374|issn=0028-4793|doi=10.1056/NEJMc2010419}}</ref>
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| *'''Ventricular Arrhythmia:''' According to a study done in Wuhan, China. among 187 hospitalized patients with [[COVID-19]], 11 patients (5.9 percent) developed [[Ventricular arrhythmias|ventricular tachyarrhythmias]].<ref name="pmid32219356">{{cite journal| author=Guo T, Fan Y, Chen M, Wu X, Zhang L, He T | display-authors=etal| title=Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219356 | doi=10.1001/jamacardio.2020.1017 | pmc=7101506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219356 }} </ref>
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| *'''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%).<ref name="BaldiSechi2020">{{cite journal|last1=Baldi|first1=Enrico|last2=Sechi|first2=Giuseppe M.|last3=Mare|first3=Claudio|last4=Canevari|first4=Fabrizio|last5=Brancaglione|first5=Antonella|last6=Primi|first6=Roberto|last7=Klersy|first7=Catherine|last8=Palo|first8=Alessandra|last9=Contri|first9=Enrico|last10=Ronchi|first10=Vincenza|last11=Beretta|first11=Giorgio|last12=Reali|first12=Francesca|last13=Parogni|first13=Pierpaolo|last14=Facchin|first14=Fabio|last15=Bua|first15=Davide|last16=Rizzi|first16=Ugo|last17=Bussi|first17=Daniele|last18=Ruggeri|first18=Simone|last19=Oltrona Visconti|first19=Luigi|last20=Savastano|first20=Simone|title=Out-of-Hospital Cardiac Arrest during the Covid-19 Outbreak in Italy|journal=New England Journal of Medicine|year=2020|issn=0028-4793|doi=10.1056/NEJMc2010418}}</ref><ref name="ShaoXu2020">{{cite journal|last1=Shao|first1=Fei|last2=Xu|first2=Shuang|last3=Ma|first3=Xuedi|last4=Xu|first4=Zhouming|last5=Lyu|first5=Jiayou|last6=Ng|first6=Michael|last7=Cui|first7=Hao|last8=Yu|first8=Changxiao|last9=Zhang|first9=Qing|last10=Sun|first10=Peng|last11=Tang|first11=Ziren|title=In-hospital cardiac arrest outcomes among patients with COVID-19 pneumonia in Wuhan, China|journal=Resuscitation|volume=151|year=2020|pages=18–23|issn=03009572|doi=10.1016/j.resuscitation.2020.04.005}}</ref>
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| ==== Diagnostic Testing: ====
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|
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| *'''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.<ref name="GandhiSolomon2020">{{cite journal|last1=Gandhi|first1=Rajesh T.|last2=Solomon|first2=Caren G.|last3=Lynch|first3=John B.|last4=del Rio|first4=Carlos|title=Mild or Moderate Covid-19|journal=New England Journal of Medicine|year=2020|issn=0028-4793|doi=10.1056/NEJMcp2009249}}</ref><ref name="ChangSaleh2020">{{cite journal|last1=Chang|first1=David|last2=Saleh|first2=Moussa|last3=Gabriels|first3=James|last4=Ismail|first4=Haisam|last5=Goldner|first5=Bruce|last6=Willner|first6=Jonathan|last7=Beldner|first7=Stuart|last8=Mitra|first8=Raman|last9=John|first9=Roy|last10=Epstein|first10=Laurence M.|title=Inpatient Use of Ambulatory Telemetry Monitors for COVID-19 Patients Treated With Hydroxychloroquine and/or Azithromycin|journal=Journal of the American College of Cardiology|volume=75|issue=23|year=2020|pages=2992–2993|issn=07351097|doi=10.1016/j.jacc.2020.04.032}}</ref>
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| *'''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.<ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref>
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| ==== Treatment:====
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|
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| *'''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.<ref name="PanchalBerg2018">{{cite journal|last1=Panchal|first1=Ashish R.|last2=Berg|first2=Katherine M.|last3=Kudenchuk|first3=Peter J.|last4=Del Rios|first4=Marina|last5=Hirsch|first5=Karen G.|last6=Link|first6=Mark S.|last7=Kurz|first7=Michael C.|last8=Chan|first8=Paul S.|last9=Cabañas|first9=José G.|last10=Morley|first10=Peter T.|last11=Hazinski|first11=Mary Fran|last12=Donnino|first12=Michael W.|title=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|journal=Circulation|volume=138|issue=23|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000613}}</ref>
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| **'''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.
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| **'''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.<ref name="TzivoniBanai1988">{{cite journal|last1=Tzivoni|first1=D|last2=Banai|first2=S|last3=Schuger|first3=C|last4=Benhorin|first4=J|last5=Keren|first5=A|last6=Gottlieb|first6=S|last7=Stern|first7=S|title=Treatment of torsade de pointes with magnesium sulfate.|journal=Circulation|volume=77|issue=2|year=1988|pages=392–397|issn=0009-7322|doi=10.1161/01.CIR.77.2.392}}</ref><ref name="NeumarOtto2010">{{cite journal|last1=Neumar|first1=R. W.|last2=Otto|first2=C. W.|last3=Link|first3=M. S.|last4=Kronick|first4=S. L.|last5=Shuster|first5=M.|last6=Callaway|first6=C. W.|last7=Kudenchuk|first7=P. J.|last8=Ornato|first8=J. P.|last9=McNally|first9=B.|last10=Silvers|first10=S. M.|last11=Passman|first11=R. S.|last12=White|first12=R. D.|last13=Hess|first13=E. P.|last14=Tang|first14=W.|last15=Davis|first15=D.|last16=Sinz|first16=E.|last17=Morrison|first17=L. J.|title=Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care|journal=Circulation|volume=122|issue=18_suppl_3|year=2010|pages=S729–S767|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.110.970988}}</ref>
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| *'''Other Cardiac arrhythmia:''' The treatment for other arrhythmias in COVID-19 patients is the same as in patients with arrhythmias without COVID-19 infection.
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| ===Out-of-hospital cardiac arrest and Sudden Cardiac Death===
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|
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| ===Spontaneous Coronary Artery Dissection===
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| ====Pathophysiology====
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| * 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.
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|
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| ====Signs and symptoms====
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| ====Treatment====
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|
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| ==References==
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| {{reflist|2}}
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| <references />
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