Anesthesia: Essays and Researches

: 2020  |  Volume : 14  |  Issue : 3  |  Page : 359--365

Cardiovascular complications related to COVID-19 disease

Raed A Alsatli 
 Department of Anesthesia, Section Cardiac Anesthesia, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

Correspondence Address:
Dr. Raed A Alsatli
Department of Anesthesia, King Faisal Specialist Hospital and Research Centre, Zahrawi Street, Al Maather, Al Maazer, P O Box 3354, Riyadh 11211
Saudi Arabia


Coronavirus disease-2019 (COVID-19) is a world epidemic disease and is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). In addition to the respiratory manifestations, it may also cause cardiovascular complications, such as, myocarditis, arrhythmias, myocardial infarction, heart failure, and venous thromboembolic events. This review article will discuss in detail pathophysiology, manifestations, and management of these cardiac complications. A literature review was performed, it included meta-analyses studies, cohort studies, publications, and case series from the largest COVID-19 outbreak centers around the world. Cardiac complications of COVID-19 disease can lead to significant cardiovascular morbidity and mortality. It is important to recognize and treat these complications as early as possible.

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Alsatli RA. Cardiovascular complications related to COVID-19 disease.Anesth Essays Res 2020;14:359-365

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Alsatli RA. Cardiovascular complications related to COVID-19 disease. Anesth Essays Res [serial online] 2020 [cited 2021 Apr 20 ];14:359-365
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Literature search was performed to review articles with the keywords: COVID-19, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), cardiovascular, myocardial injury, myocarditis, heart failure (HF), hypertension, acute myocardial injury, dysrhythmias, coagulopathy, drug side effect, venous thromboembolism, anesthetic management, and airway management in COVID-19. This search included meta-analyses, major publications from the largest COVID-19 outbreak centers, published in the English language.


Coronaviruses are enveloped single-stranded ribonucleic acid (RNA) viruses with surface projections that correspond to surface spike proteins.[1] SARS-CoV-2 is highly virulent with a higher infectivity rate than the SARS virus (outbreak in 2003). There are a high number of viruses in the sputum of infected people (up to a billion RNA copies/mL of sputum). In addition, this virus has a long-term stability on contaminated surfaces (up to 72 h on plastic and stainless-steel surfaces).[2]

The incubation period is 2–14 days (mostly 3–7 days).[2],[3] During the latency period, the virus is already contagious. SARS-CoV-2 virus can be detected 1–2 days before the onset of upper respiratory tract symptoms. While mild cases were found to have early viral clearance and a negative reverse transcriptase–polymerase chain reaction (RT-PCR) by day 10 post onset, all severe cases were tested positive at or beyond day 10 after symptom onset.[4] The median duration of viral shedding was 20 days (interquartile range: 17–24) in survivors. The longest observed duration of viral shedding in survivors was 37 days.[5]

After the first reported cases in Wuhan (China, December 31, 2019), COVID-19 was declared by the World Health Organization as a Pandemic in March 2020. The responsible pathogen was identified as a novel coronavirus by the Chinese Center for Disease Control and Prevention. Then, it was called SARS-CoV-2 by the International Committee on Taxonomy of Viruses.

The main organ affected by SARS-CoV-2 is the respiratory system. However, the myocardium can be involved as well in the form of myocarditis, myocardial injury, myocardial infarction (MI), HF, and arrhythmias leading to an increase in morbidity and mortality. Myocardial injury in COVID-19 patients can lead to poor outcomes. Furthermore, mortality rate among patients with underlying cardiovascular disease (CVD) has been reported to reach 10.5%.[6]

This article will discuss the cardiovascular complications of COVID-19. In addition, it will demonstrate the current practice for airway management in COVID-19 patients. Finally, we put a summary of our experience in the anesthetic management of cardiac patients having COVID-19 infection and undergoing cardiac and noncardiac surgery.

Cardiac implications

Myocardial infiltration with interstitial mononuclear inflammatory cells has been found in the autopsies of patients with COVID-19. In addition, myocardial injury in the form of myocarditis, myocardial ischemia, and infarction was associated with increased cardiac biomarkers levels.[7],[8],[9],[10]

The study of Shi et al. included 416 COVID-19 patients, 57 of them passed away. Cardiac injury was reported in 19.7% of them, coronary artery disease (CAD) in 10.6%, HF in 4.1%, and cerebrovascular disease in 5.3%.[9] In addition, cardiac injury was significantly and independently associated with a mortality hazard ratio of 4.6.

Another study showed that elevated troponin levels due to myocardial injury were associated with significantly increased mortality. Those patients were older in age, male gender, hypertensive, and had a history of CAD.[8]


Cardiovascular involvement could be either primary or secondary. Primary cardiac injury can be related to direct infection of the myocytes or ischemic myocardial injury. Secondary cardiac involvement may happen after pulmonary injury leading to an abnormal coupling between the pulmonary vascular bed and the heart, particularly in patients with the above-mentioned comorbidities.

The pathobiology of coronavirus infection involves SARS-COV-2 binding via its SPIKE protein to the host receptor angiotensin-converting enzyme 2 (ACE2). It is part of the renin-angiotensin system (RAS) that mediates the entry into cells and is expressed in the lungs, heart, vessels, and gastrointestinal tract.[11],[12]

SARS-CoV2 will lead to dysregulation of the RAS/ACE2 system which normally has a cardiovascular protective effect[13] that leads to cardiovascular complications.

Cytokine storm originating from the imbalance of T-cell activation with dysregulated release of interleukin (IL)-6, 7, and 22 and other cytokines may contribute to CVD in COVID-19. Immune system activation alone may result in plaque instability, contributing to the development of acute coronary events.

ACE2 is a protein found on the surface of lung alveolar epithelial cells and enterocytes of the small intestine, heart, and blood vessels. These have been confirmed as the most important entry sites for SARS-CoV-2.[11] ACE2 converts angiotensin 2 into angiotensin 1–7 and angiotensin 1 into angiotensin (1–9). It plays an important role in the pathogenesis of SARS-CoV2, as it facilitates entry of the virus into the host cell by combining to the protein spikes on the surface of the virus, which will replicate intracellularly. The viral RNA is released and processed in the sarcoplasmic reticulum and replicates leading to a newly formed genomic RNA. This is processed into virion-containing vesicles, which will fuse with the cell membrane to release the virus to the epithelial surfaces. This promotes local tissue injury, such as lung injury, which can lead in severe cases to respiratory failure and end-organ failure.

Endothelial inflammation promotes variable degrees of microvascular and macrovascular dysfunction, depending on virus dose and host immune responses. Acute coronary syndromes (ACSs) can develop due to atherosclerotic plaque destabilization after immune hyperreactivity. The development of the so-called “cytokine storm” is associated with an exaggerated immune response and high levels of IL-6, IL-7, IL-22, and C-X-C motif chemokine 10 (CXCL10).

In addition to myocarditis due to direct invasion of the myocardium by the virus, fulminant myocarditis and myocardial damage (increased troponin I, creatine kinase, and lactate dehydrogenase) may happen after T-cell and macrophages invasion of the myocardium. Myocarditis can lead to arrhythmias severe cardiac dysfunction and HF.[14]

A study of 44,672 patients with COVID-19 found that a history of CVD was associated with a nearly fivefold increase in the case fatality rate when compared with patients without CVD (10.5% vs. 2.3%).[6]

Cardiovascular complication of COVID-19

Patients who are at higher baseline risk (older age, comorbidities including CVD, lung and renal disease, diabetes, and disorders of hemostasis) at the time of COVID-19 infection are more prone to develop complications, such as myocarditis, myocardial tissue injury, ST elevation acute myocardial infarction (AMI), HF, arrhythmias, cardiac arrest, cardiogenic shock, and venous thromboembolic events (VTE).[6],[15],[16],[17],[18]

Myocarditis and myocardial injury

Myocarditis and myocardial injury may reflect several pathologic mechanisms: direct viral invasion of the myocardium, also T-cells, macrophages, and mononuclear infiltrates, may attack the myocardium. In addition, cytokines storm (IL 6, 7, and 22 and CXCL10 mediated), and other hyperimmune activation may also potentiate myocardial inflammatory injury.

Myocarditis should be suspected in any COVID-19 patient presenting with an ACS, HF, or dysrhythmias, even if there was no preceding cardiac history. First reports documenting cardiovascular complications came from Wuhan (China) where 12% of the patients infected with COVID-19 developed myocardial injury with increased levels of troponin I. Later reports indicated that 7%–17% of hospitalized patients and 22%–31% of COVID-19 patients admitted in the intensive care unit (ICU) developed myocardial injury with increased level of troponin I.[5],[19],[20] About 7% of deaths due to COVID-19 were found to be secondary to myocarditis.[16]

COVID-19 patients with myocarditis may present with typical anginal manifestations, such as chest pain radiating to the left arm, tightness of the chest, dysrhythmias, dyspnea, and left ventricular dysfunction. In addition to the electrocardiogram (EKG) abnormalities that mimic ACS like ST and T changes), elevated troponin levels can be detected as well.[5],[6],[16],[19],[20]

Echocardiography is an important diagnostic tool in differentiating between ACS and myocarditis. While in ACS focal wall-motion abnormalities may happen, global wall-motion dysfunction can be found in severe myocarditis.[15],[21]

Significant EKG and echocardiography findings combined with elevated serum troponin I level were found to be significantly correlated with worse outcomes and higher mortality rates in COVID-19 patients.[8],[9],[22]

Coronary computed tomography angiogram (CCTA) is the preferred test for ruling out CAD. However, cardiac magnetic resonance imaging has been used as well.[23]

In a published case report of 38-year-old patient who developed COVID-19 myocarditis, the patient presented with chest pain, ST-segment elevation, hypotension, bilateral pneumonia, and pleural effusion. However, the patient had normal coronary morphology on CCTA. Troponin and B-type natriuretic peptide (BNP) were highly increased. Echocardiography showed significant left ventricular dilatation and reduced function. The patient improved after high-dose intravenous glucocorticoid and immunoglobulin infusion.[23]

Acute myocardial infarction

Hypercoagulability and severe inflammation can also lead to AMI.[15],[21] Inflammation itself can contribute to atheroma formation and plaque disruption inside the coronary arteries leading to AMI.[23],[24] This pattern of plaque disruption has been observed in other severe forms of viral-mediated inflammation, such as influenza which increased the risk of AMI 6.2 fold in severe cases.[24]

Management of AMI in COVID-19 patients depends on the type of AMI, as explained in the guidelines of the American College of Cardiology.

Low-risk ST elevation myocardial infarction (STEMI) is defined as inferior MI without the involvement of the right or left ventricle and no hemodynamic instability. In these patients, fibrinolysis can be performed, but percutaneous coronary intervention (PCI) remains the treatment of choice. Full precautions should be followed in COVID-19 patients undergoing PCI, personal protective equipment (PPE) should be performed by the catheterization laboratory staff. The desired maximum time interval between STEMI diagnosis and PCI is 120 min. However, a delay of up to 60 min can be added for preparation of protective measures in the pandemic era.[25] If the target time cannot be met and fibrinolysis is not contraindicated, then fibrinolysis should be undertaken without any unnecessary delay.

It is important to consider any patient presenting with a STEMI as potentially COVID-19 positive. Diagnostic PCR testing should be done as early as possible, preferably at the first medical contact, irrespective of the subsequent medical management plan. If COVID-19 status could not be assessed due to hemodynamic instability at the time of presentation, then it should be pursued at the time of ICU admission after PCI. Cardiac catheterization laboratory staff should be aware, trained, adhere to safe measures, and precautions to reduce the risk of COVID-19 transmission.

In case of non-STEMI (NSTEMI) patients who are COVID-19 positive, if the patient is stable, medical management can be conservative. If the patient is unstable, then management should be the same as in STEMI patients.[21] In low-risk NSTEMI patients who are stable but have elevated troponin level, it is advised to perform noninvasive imaging (CCTA), avoid invasive approach, and arrange for an early discharge.

In high-risk Non ST elevation myocardial infarction, it is important to do the RT-PCR test and if positive, then transfer the patient to COVID-19 equipped ward or hospital. High-risk NSTEMI should be treated as STEMI patients.[26]

Acute heart failure and cardiomyopathy

It is not clear whether this is secondary to myocarditis or an exacerbation of a previously unrecognized impaired myocardial function.[27],[28] They tend to have a high subsequent mortality rate.[27]

Acute HF in COVID-19 patients may complicate acute myocardial ischemia, MI, acute respiratory distress syndrome (ARDS), stress-induced cardiomyopathy, tachyarrhythmia, acute kidney injury, or severe hypovolemia.

COVID-19 pneumonia leading to hypoxemia or hypoperfusion may further compromise the hemodynamic condition in these patients. Elevated biomarkers BNP and N-terminal BNP (NT-proBNP) may indicate acute HF, or only myocardial injury. This can be further assessed with transthoracic echocardiography.

In a meta-analysis, it was concluded that patients with severe COVID-19 infection have higher level of high sensitivity cardiac troponin. This indicates acute myocardial injury compared to patients with mild COVID-19 infection.[29]


A variety of dysrhythmias may occur in COVID-19 infection. These include tachyarrhythmias, such as supraventricular tachycardia, atrial fibrillation, flutter, ventricular arrhythmias, sustained ventricular tachycardia, ventricular fibrillation, and atrial or ventricular ectopy. Acute management is similar to that in non-COVID 19 patients.[30] The most commonly encountered dysrhythmia is sinus tachycardia. This is usually multifactorial related to inflammation, fever, anxiety, and hypoxia.[15]

In a retrospective study including 138 COVID-19 patients, cardiac arrhythmias occurred in 16.7% of hospitalized patients and in 44% of patients admitted to the ICU. In the same study, acute myocardial infarction (AMI defined as an elevated troponin level, new ST, T changes on the EKG, and wall-motion abnormalities were found in 7.2% of patients.[20]

In a cohort study including over 137 COVID-19 patients, palpitation was the presenting symptom in 7.3% of them.[31] If there is an increased level of troponin in association with dysrhythmia, this can be related to AMI or acute myocarditis.[15] In a retrospective study from Italy, 24.5% of COVID-19 dead patients had a prior history of atrial fibrillation. This was especially common in older COVID-19 patients with pneumonia, ARDS, and sepsis.[32]

New onset of malignant ventricular arrhythmia signals acute myocardial injury and may necessitate more aggressive antiviral and immunosuppressive treatment.[8]

As it will be shown later in this article, some of the medications used in COVID-19 treatment may induce or potentiate arrhythmias, such as the macrolides (azithromycin) and fluoroquinolones. They act through QT-interval prolongation and predispose to polymorphic ventricular tachyarrhythmia.[33],[34] The well-known antimalarial medication chloroquine/hydroxychloroquine was used initially in the management of COVID-19.[35],[36] However, they have a severe and irreversible cardiotoxicity including arrhythmia and HF.[37]


The reported association between hypertension, morbidity, and mortality in COVID-19 patients is confounded by the lack of adjustment for age and other comorbidities. There is currently no evidence that hypertension by itself is an independent risk factor for the development of severe complications or death.[38] Treatment of hypertension with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin-receptor blockers (ARBs) did not lead to an increase in serum ACE2 levels. Studies concluded that such antihypertensive medications have not produced an upregulation of ACE2 in human tissues.[39]

Prior use of ACEI/ARBs was not found to increase the mortality rate among hypertensive patients having COVID-19. These findings do not support discontinuation of ACEI/ARB medications that are clinically indicated in the context of the COVID-19 pandemic.[40]

Another study from Wuhan that included 1128 hospitalized patients found that treatment with ACEI or ARBs was associated with a lower risk of COVID-19 infection, serious complications, or death.[38],[40],[41],[42],[43],[44],[45],[46]

In the study of de Abajo et al., neither ACEIs, nor ARBs increased the risk of hospital admission in COVID-19 patients, even after adjustment for age, sex, and cardiovascular risk. Surprisingly, these antihypertensive medications reduced the severity of infection and played a protective role in diabetic patients.[42]

Side effects and drugs interactions of COVID-19 medications


It is a nucleotide-analog inhibitor of RNA polymerases. It may cause hypotension and arrhythmias.[47],[48]


It inhibits RNA and RNA-dependent polymerases. It interacts with anticoagulants, statins, antiarrhythmics, and may cause severe hemolytic anemia.[47],[48],[49]

Chloroquine and hydroxychloroquine

They change endosomal pH. They interact with antiarrhythmics and may cause direct myocardial toxicity and worsen cardiomyopathy. Furthermore, they alter cardiac conduction, resulting in bundle branch block, AV block, ventricular arrhythmias, and torsades de pointes.[50],[51]


It interferes with protein synthesis and binds to 50 s ribosome. It interacts with anticoagulants, statins, antiarrhythmics, and other QT-prolonging agents. It may result in dysrhythmias, prolonged QTc, and torsades de pointes.


It is responsible for immune system activation. It may cause direct myocardial toxicity, worsen cardiomyopathy, and alter cardiac conduction. In addition, it can cause hypotension or cardiac ischemia.


It reduces inflammation. It interacts with anticoagulants and may cause fluid retention, hypertension, and electrolyte changes.[51]

Venous thromboembolic events

Hemostatic inflammatory activation in combination with a microvascular injury can result in an increased risk of venous thromboembolic events (VTE) in COVID-19 patients. This is exacerbated in the presence of multiorgan dysfunction.[52-54] Disseminated intravascular coagulopathy may develop, and coagulation factors are often consumed in the lung parenchyma. A prospective management trial used the 'YEARS' clinical decision rule, which consists of three clinical items of the Wells score: signs of deep vein thrombosis (DVT), hemoptysis, and pulmonary embolism (PE) is the most likely diagnosis, plus D-dimer concentrations. in this study which included 2946 patients, PE was considered to be excluded in patients without clinical items and D-dimer levels <1000 ng/mL, or in patients with one or more clinical items and D-dimer levels <500 ng/mL. All other patients underwent computed tomography pulmonary angiography (CTPA).[55] A D-dimer level above 1 microgram/ml in COVID-19 infection is associated with an increased mortality rate (odds ratio18.4).[5] Anticoagulation with low molecular weight heparin (LMWH) has reduced the mortality rate in patients with severe COVID-19 infections, or when D-dimer is elevated.[20]

Airway management in emergency procedures

Airway management should be done by the most experienced person:

Endotracheal intubation prevents viral spread and it is preferred over supraglottic airway[56]Endotracheal intubation and extubation are aerosol-generating procedures with an increased risk of transmission of infection. Thus, a high level PPE is necessary[56],[57]It is recommended to use a video laryngoscope to improve the success rate and reduce the exposure timePerform rapid sequence induction and intubation to minimize the need for ventilation, and thereby prevent the aerosol spread of virus[58]Critically ill patients are prone to develop hypoxia during endotracheal intubation. Therefore, preoxygenation with a tight face mask for 5 min is recommended[59]When possible, intubate in a negative pressure operating room (OR)Anesthesia circuit and filters should be discarded, and anesthesia machines should undergo complete disinfection after the procedure. Electrostatic heat and moisture exchange filter should be used in the anesthesia circuit. Its virus filtration efficacy reaches 99.99%

It is important to reduce the number of staff in the OR to minimum, which will reduce the exposure of personnel as low as possible.[60]

Anesthetic considerations in cardiac patients having COVID-19 disease and undergoing cardiac surgery in our tertiary hospital

In addition to the above-mentioned points:

Careful preoperative evaluation considering all the above-mentioned cardiac complications of COVID-19, particularly viral myocardial damage, HF, and hypoxia-induced myocardial injury

Implement invasive arterial, central venous pressures monitoring, and pulmonary artery catheter if a patient has pulmonary hypertension. In addition, transesophageal echocardiography can help in assessing heart function and volume status inside the heart

Inotropic and vasoactive medications should be prepared

Ventricular assist device, intra-aortic balloon pump, and extracorporeal membrane oxygenator should be ready if indicated

Coagulation condition should be properly checked before surgery. It is important to implement blood conservation strategies (cell saver, antifibrinolytics therapy) intraoperatively to reduce blood and blood products transfusion, to avoid transfusion-related lung injury.[61]

If these patients who have cardiac complications and undergo non cardiac surgery, points 1, 3, and 5 should be implemented.

Regarding invasive monitoring (arterial line and central venous catheter), it depends on the severity of the disease and patient's condition. This is also the same consideration for point 4, regarding circulatory assist devices.


COVID-19 disease has become a global disease of epidemic proportion. It can cause cardiovascular complications, such as myocarditis, myocardial injury, infarction, and HF.

In addition, it may lead to venous thromboembolism due to hemostatic activation. The last complication can progress to disseminated intravascular coagulation during the hyperinflammatory state, resulting in serious complications or death. Awareness of such complications and prompt intervention by medical team, emergency room, and intensive care physicians may help to reduce the morbidity and mortality burden of this devastating disease.

It is important to follow the guidelines for airway management in these patients. Finally, we described our experience in the anesthetic management of COVID-19 cardiac patients, undergoing cardiac and noncardiac surgery.


The author thanks Dr. Adel Aly and Dr. Gruschen Veldtman and Miss Ola Alsatli for their kind support and assistance during preparation of this article.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Cui J, Li F, Shi ZL. Origin and evolution of pathogenic coronaviruses. Nat Rev Microbiol 2019;17:181-92.
2Van Doremalen N, Bushmaker T, Morris DH, Holbrook MG, Gamble A, Williamson BN, et al. Aerosol and surface stability of SARS-CoV-2 as compared with SARS-CoV-1. N Engl J Med 2020;382:1564-7.
3Guo YR, Cao QD, Hong ZS, Tan YY, Chen SD, Jin HJ, et al. The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak-An update on the status. Mil Med Res 2020;7:1-10.
4Liu Y, Yang Y, Zhang C, Huang F, Wang F, Yuan J, et al. Clinical and biochemical indexes from 2019-nCoV infected patients linked to viral loads and lung injury. Sci China Life Sci 2020;63:364-74.
5Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet 2020;395:1054-62.
6Wu Z, McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72314 cases from the Chinese Center for Disease Control and Prevention. JAMA 2020;323:1239-42.
7Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med 2020;8:420-2.
8Guo T, Fan Y, Chen M, Wu X, Zhang L, He T, et al. Cardiovascular Implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:811-8.
9Shi S, Qin M, Shen B, Cai Y, Liu T, Yang F, et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol 2020;5:802-10.
10Madjid M, Safavi-Naeini P, Solomon SD, Vardeny O. Potential effects of coronaviruses on the cardiovascular system: A review. JAMA Cardiol 2020;5:831-40.
11Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol 2004;203:631-7.
12Zou X, Chen K, Zou J, Han P, Hao J, Han Z. Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection. Front Med 2020;14:185-92.
13Wu Y. Compensation of ACE2 function for possible clinical management of 2019-nCoV-induced acute lung injury. Virol Sin 2020;35:256-8.
14Guzik TJ, Mohiddin SA, Dimarco A, Patel V, Savvatis K, Marelli-Berg FM, et al. COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. Cardiovasc Res 2020;116:1666-87.
15Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G, et al. Cardiovascular considerations for patients, health care workers, and health systems during the coronavirus disease 2019 (COVID-19) pandemic. J Am Coll Cardiol 2020;75:2352-71.
16Ruan Q, Yang K, Wang W, Jiang L, Song J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med 2020;46:846-8.
17Li B, Yang J, Zhao F, Zhi L, Wang X, Liu L, et al. Prevalence and impact of cardiovascular metabolic diseases on COVID-19 in China. Clin Res Cardiol 2020;109:531-8.
18Murthy S, Gomersall CD, Fowler RA. Care for critically Ill patients with COVID-19. JAMA 2020;323:1499-500.
19Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020;395:497-506.
20Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA 2020;323:1061-9.
21Welt FG, Shah PB, Aronow HD, Bortnick AE, Henry TD, Sherwood MW, et al. From the American College of Cardiology's (ACC) Interventional Council and the Society of Cardiovascular Angiography and Intervention (SCAI). Catheterization laboratory considerations during the coronavirus (COVID-19) pandemic: From ACC's Interventional Council and SCAI. JACC 2020;75:2372-5.
22Chen C, Zhou Y, Wang DW. SARS-CoV-2: A potential novel etiology of fulminant myocarditis. Herz 2020;45:230-2.
23Hu H, Ma F, Wei X, Fang Y. Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin. Eur Heart J 2020;42:206.
24Kwong JC, Schwartz KL, Campitelli MA, Chung H, Crowcroft NS, Karnauchow T, et al. Acute myocardial infarction after laboratory-confirmed influenza infection. N Engl J Med 2018;378:345-53.
25Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The task force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39:119-77.
26Kucharski AJ, Russell TW, Diamond C, Liu Y, Edmunds J, Funk S, et al. Centre for mathematical modelling of infectious diseases C-wg. Early dynamics of transmission and control of COVID-19: A mathematical modelling study. Lancet Infect Dis 2020;20:553-8.
27Chen T, Wu D, Chen H, Chen H, Yan W, Yang D, et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: Retrospective study. BMJ 2020;368:m1091.
28Buzon J, Roignot O, Lemoine S, Perez P, Kimmoun A, Levy B, et al. Takotsubo Cardiomyopathy triggered by influenza a virus. Intern Med 2015;54:2017-9.
29Lippi G, Lavie CJ, Sanchis-Gomar F. Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): Evidence from a meta-analysis. Prog Cardiovasc Dis 2020;63:390-1.
30Boriani G, Fauchier L, Aguinaga L, Beattie JM, Blomstrom Lundqvist C, Cohen A, et al. European Heart Rhythm Association (EHRA) consensus document on management of arrhythmias and cardiac electronic devices in the critically ill and post-surgery patient, endorsed by Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm (APHRS), Cardiac Arrhythmia Society of Southern Africa (CASSA), and Latin American Heart Rhythm Society (LAHRS). Europace 2019;21:7-8.
31Liu K, Fang YY, Deng Y, Liu W, Wang MF, Ma JP, et al. Clinical characteristics of novel coronavirus cases in tertiary hospitals in Hubei Province. Chin Med J (Engl) 2020;133:1025-31.
32Onder G, Rezza G, Brusaferro S. Case-Fatality rate and characteristics of patients dying in relation to COVID-19 in Italy. JAMA 2020;323:1775-6.
33Shah S, McArthur E, Farag A, Nartey M, Fleet JL, Knoll GA, et al. Risk of hospitalization for community acquired pneumonia with renin-angiotensin blockade in elderly patients: A population-based study. PLoS One 2014;9:e110165.
34Falagas ME, Rafailidis PI, Rosmarakis ES. Arrhythmias associated with fluoroquinolone therapy. Int J Antimicrob Agents 2007;29:374-9.
35Gao J, Tian Z, Yang X. Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies. Biosci Trends 2020;14:72-3.
36Gautret P, Lagier JC, Parola P, et al. Hydroxychloroquine and azithromycin as a treatment of COVID-19: Results of an open-label non-randomized clinical trial. Int J Antimicrob Agents 2020;56:105949.
37Chatre C, Roubille F, Vernhet H, Jorgensen C, Pers YM. Cardiac complications attributed to chloroquine and hydroxychloroquine: A systematic review of the literature. Drug Saf 2018;41:919-31.
38Williams B, Zhang Y. Hypertension, renin-angiotensin-aldosterone system inhibition, and COVID-19. Lancet 2020;395:1671-3.
39Vaduganathan M, Vardeny O, Michel T, McMurray JJ, Pfeffer MA, Solomon SD. Renin-angiotensin-aldosterone system inhibitors in patients with Covid-19. N Engl J Med 2020;382:1653-9.
40Fosbøl EL, Butt JH, Østergaard L, Andersson C, Selmer C, Kragholm K, et al. Association of angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use with COVID-19 diagnosis and mortality. JAMA 2020;324:168-177.
41Bean D, Kraljevic Z, Searle T, Bendayan R, Pickles A, Folarin A, et al. ACE-inhibitors and angiotensin-2 receptor blockers are not associated with severe SARS- COVID19 infection in a multi-site UK acute hospital trust. Eur J Heart Fail 2020;22:967-74.
42de Abajo FJ, Rodríguez-Martín S, Lerma V, Mejía-Abril G, Aguilar M, García-Luque A, et al. Use of renin–angiotensin–aldosterone system inhibitors and risk of COVID-19 requiring admission to hospital: A case-population study. Lancet 2020; 395:1705-14.
43Li J, Wang X, Chen J, Zhang H, Deng A. Association of renin-angiotensin system inhibitors with severity or risk of death in patients with hypertension hospitalized for coronavirus disease 2019 (COVID-19) infection in Wuhan, China. JAMA Cardiol 2020;5:825-30.
44Mancia G, Rea F, Ludergnani M, Apolone G, Corrao G. Renin-Angiotensin-aldosterone system blockers and the risk of Covid-19. N Engl J Med 2020;382:2431-40.
45Reynolds HR, Adhikari S, Pulgarin C, Troxel AB, Iturrate E, Johnson SB, et al. Renin-angiotensin-aldosterone system inhibitors and risk of Covid-19. N Engl J Med 2020;382:2441-8.
46Zhang P, Zhu L, Cai J, Lei F, Qin JJ, Xie J, et al. Association of inpatient use of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers with mortality among patients with hypertension hospitalized with COVID-19. Circ Res 2020;126:1671-81.
47Chavez S, Long B, Koyfman A, Liang S. Coronavirus disease (COVID-19): A primer for emergency physicians. Am J Emerg Med 2020. [doi: 10.1016/j.ajem. 2020.03.036].
48Elfiky AA. Anti-HCV, nucleotide inhibitors, repurposing against COVID-19. Life Sci 2020;248:117477.
49Chu CM, Cheng VC, Hung IF, Wong MM, Chan KH, Chan KS, et al. Role of lopinavir/ritonavir in the treatment of SARS: Initial virological and clinical findings. Thorax 2004;59:252-6.
50Page RL 2nd, O'Bryant CL, Cheng D, Dow TJ, Ky B, Stein CM, Spencer AP, et al. Drugs that may cause or exacerbate heart failure: A scientific statement from the American Heart Association. Circulation 2016;134:32-69.
51Tönnesmann E, Kandolf R, Lewalter T. Chloroquine cardiomyopathy – A review of the literature. Immunopharmacol Immunotoxicol 2013;35:434-42.
52Xie Y, Wang X, Yang P, Zhang S. COVID-19 complicated by acute pulmonary embolism. Radiol Cardiothorac Imaging 2020;2. Published Online Mar 16. Available from: [Last accessed on 2021 Jan 29].
53Danzi GB, Loffi M, Galeazzi G, Gherbesi E. Acute pulmonary embolism and COVID-19 pneumonia: A random association?. Eur Heart J 2020;41:1858.
54Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost 2020;18:844-7.
55van der Hulle T, Cheung WY, Kooij S, Beenen LFM, van Bemmel T, van Es J, et al. (Years Study Group). Simplified diagnostic management of suspected pulmonary embolism (the YEARS study): A prospective, multicentre, cohort study. LANCET 2017;390:289-97.
56Canelli R, Connor CW, Gonzalez M, Nozari A, Ortega R. Barrier enclosure during endotracheal intubation. N Engl J Med 2020;382:1957-8.
57Tran K, Cimon K, Severn M, Pessoa-Silva CL, Conly J. Aerosol generating procedures and risk of transmission of acute respiratory infections to healthcare workers: A systematic review. PLoS One 2012;7:e35797.
58Schumacher J, Arlidge J, Dudley D, Sicinski M, Ahmad I. The impact of respiratory protective equipment on difficult airway management: A randomised, crossover, simulation study. Anaesthesia 2020;75:1301-6.
59Yao W, Wang T, Jiang B, Gao F, Wang L, Zheng H, et al. Emergency tracheal intubation in 202 patients with COVID-19 in Wuhan, China: Lessons learnt and international expert recommendations. Br J Anaesth 2020;125:e28-37.
60Eldawlatly A, El Tahan1 MR, Abdulmomen A, Kattan M, Ahmad AE. Anesthesia management of thoracic surgery in a patient with anesthesia management of thoracic surgery in a patient with suspected confirmed COVID-19: Interim Saudi Anesthesia Society Guidelines. Saudi J Anaesth 2020;14:383-6.
61He Y, Wei J, Bian J, Guo K, Lu J, Mei W, et al. Chinese society of anesthesiology expert consensus on anesthetic management of cardiac surgical patients with suspected or confirmed coronavirus disease 2019. J Cardiothorac Vasc Anesth 2020;34:1397-401.