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 Table of Contents  
Year : 2021  |  Volume : 41  |  Issue : 3  |  Page : 107-115

Burden of Coronavirus Disease-19 on cardiovascular system

Department of Cardiology, BLK Superspeciality Hospital, New Delhi, India

Date of Submission29-Jul-2020
Date of Decision01-Sep-2020
Date of Acceptance02-Nov-2020
Date of Web Publication03-Feb-2021

Correspondence Address:
Dr. Amit Goel
Superspeciality Hospital, Pusa Road, New Delhi - 110 005
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmedsci.jmedsci_236_20

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The rapid emergence and spread of coronavirus disease-19 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into a worldwide pandemic has caused unprecedented crisis on already overwhelmed healthcare system and global economy leading to healthcare and social emergency. Since its outbreak, the disease prognosis has largely been influenced by multisystem involvement. Comorbid conditions such as cardiovascular diseases have been the most common risk factor for its severity and outcome. Although the exact mechanism of myocardial involvement in patients with COVID-19 is unknown, several plausible mechanisms have been proposed, of which uncontrolled and dysregulated immune response is most implicated in its causation. In the present article, an attempt has been made to summarize the literature available on COVID-19 and its impact on the cardiovascular system.

Keywords: Coronavirus disease.19, severe acute respiratory syndrome coronavirus 2, pandemic, cardiovascular disease

How to cite this article:
Goel A, Madaan A, Singh S, Chandra S. Burden of Coronavirus Disease-19 on cardiovascular system. J Med Sci 2021;41:107-15

How to cite this URL:
Goel A, Madaan A, Singh S, Chandra S. Burden of Coronavirus Disease-19 on cardiovascular system. J Med Sci [serial online] 2021 [cited 2022 Aug 19];41:107-15. Available from: https://www.jmedscindmc.com/text.asp?2021/41/3/107/308687

  Introduction Top

The cataclysmic coronavirus disease-19 (COVID-19) outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly grown into a global pandemic and has also challenged the overwhelmed public health care system. In December 2019, first case of novel coronavirus disease was reported from Hubei province, China, which subsequently was identified as its origin.[1] On January 30, 2020, the World Health Organization (WHO) declared the outbreak of SARS-CoV-2, a Public Health Emergency of international concern.[2] India has recorded its first case of COVID-19 disease on January 30, 2020 and ever since the country has witnessed 8.0 lakh cases, as on July 10, 2020. Although the virus has predisposition for the lungs, where it causes bilateral pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organ systems, particularly the cardiovascular system and often requires care from a multidisciplinary team.[3],[4] Majority of cardiovascular events in patients with COVID-19 infections are as a result of severe inflammatory and hemodynamic changes in patients with extensive respiratory involvement. Cardiovascular manifestations of COVID-19 are complex and include acute coronary syndrome (ACS), myocarditis simulating ST-elevation myocardial infarction (STEMI mimicker), nonspecific myocardial injury, stress-induced cardiomyopathy, arrhythmias, and thromboembolic complications.[4] The preexisting conditions associated with cardiovascular disease (CVD) are known to increase the risk for serious outcomes of the infection.[5],[6] Therefore, understanding of the damage caused by SARS-CoV-2 to the cardiovascular system and its underlying mechanism is of utmost importance, so that the treatment of such patients can be timely initiated to ensure effective therapeutic response.

  Severe Acute Respiratory Syndrome Coronavirus 2, Mechanism of Cardiac Involvement and its Prognostic Impact Top

Coronaviruses are a large family of single positive-stranded, nonsegmented, enveloped RNA viruses that can affect human beings and various animal species. Several different epidemics have been caused by its family members in the last two decades. The first epidemic was caused by SARS-CoV from 2002 to 2003, followed by Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012.[7],[8] An unidentified pathogen had infected several individuals in December 2019, in Wuhan, China, which was later identified as a novel member belonging to Beta-CoV family.[1] On January 12, 2020, the WHO named the virus as 2019-novel coronavirus (2019-nCoV) which was subsequently officially named as SARS-CoV-2 owing to its genetic homology with human SARS-CoV.[9] The “hotspot” for the origin of the said virus has been identified as a seafood market in Wuhan, Hubei district, in Mainland China. Later, on March 11, 2020, the WHO declared the disease as the first-ever pandemic caused by any CoV till date.[10]

According to the current evidence, COVID-19 is a bat-borne novel zoonotic virus illness which is primarily transmitted among people through respiratory droplets from infected persons and fomite transmission is also known to occur. Although respiratory symptoms predominate the clinical picture of infections caused by coronaviruses, some patients still developed severe cardiovascular damage which prognosticates the course of illness. In patients with SARS and MERS, CVD or its risk factors were commonly observed. In SARS, about 8% and 11% of cases had CVD or diabetes mellitus respectively, and a 12-fold higher mortality risk was observed in the presence of either of the two risk factors.[11],[12] However, in MERS, the prevalence of cardiovascular comorbidities was even higher, estimated to be 30%.[13] Similarly, studies from China have also supported the notion that patients with underlying CVD or its risk factors are at higher risk of developing COVID-19, especially its most severe manifestations. A systematic review of 3470 COVID-19 patients from 72 studies mostly from China reported the prevalence of CVD, hypertension and diabetes as 8.3%, 13.3% and 7.3% respectively.[14] More recently, data from Italy, the first western country to get affected by COVID-19, had emerged where 96.7% of deceased patients had atleast one comorbidity.[15] The prevalence of hypertension, diabetes, ischemic heart disease, atrial fibrillation, and heart failure was present in 70%, 32%, 28%, 23%, and 16%, respectively of patients in the study group.

The exact pathogenic mechanisms of cardiovascular involvement of SARS-CoV-2 are unknown, but most researchers believe that it might be similar to SARS-CoV due to its structural homology. Cardiac involvement in COVID-19 can occur through the following plausible mechanisms: (1) direct invasion of the virus into cardiomyocytes (2) indirect injury due to increased immunoinflammatory response and higher number of cytokines secretion (cytokine storm), and (3) damage to the pneumocytes from the virus causing hypoxia leading to oxidative stress and injury to cardiomyocytes.[16],[17],[18]

Angiotensin-converting enzyme-2 (ACE-2) has been recognized as a functional receptor for coronaviruses for its pathogenicity, which acts as a portal of entry into the host cells.[19] The virus mediates its virulence after adhesion to the host cell expressing the ACE-2 receptor by means of spike (S) glycoprotein present on its surface. ACE-2 receptors are expressed in abundance mainly in endothelial cells of arteries and veins, arterial smooth muscles, respiratory tract epithelium, epithelial cells of heart, intestine, and kidney. SARS-CoV-2 results in predominant respiratory symptoms mainly by invasion of alveolar epithelial cells of respiratory tract. It is uncertain if SARS-CoV-2 binding changes the ACE-2 expression or causes abnormal regulation of the renin–angiotensin–aldosterone system (RAAS).[18] The binding of the virus to the ACE-2 receptor causes downregulation of ACE-2 activity, leading to inappropriate and uninhibited action of the angiotensin-II protein.[20] This protein has immense negative effects at the local and systemic levels. It induces vasoconstriction and oxidative organ damage and also has proatherosclerotic, prothrombotic, and inflammatory action leading to various systemic complications and multiorgan dysfunction.

Another mechanism by which COVID-19 can cause cardiovascular involvement is by cellular-mediated immunity which triggers uncontrolled and dysregulated immune response resulting in a cytokine storm. There are activation and proliferation of T helper 1 (TH1) and T helper 2 (TH2) cells leading to uninhibited secretion of cytokines which causes myocardial injury by mechanisms of apoptosis and necrosis of myocardial cells.[1] Due to these, reduction in coronary blood flow, decrease in oxygen supply, destabilization of coronary plaque, and microthrombogenesis are observed. Pro-inflammatory cytokines, such as interleukin (IL)-2, IL-10, monocyte chemoattractant protein-1, macrophage inflammatory protein-1α, and tumor necrosis factor-alpha are seen raised in critically ill patients.[1] Chronic CVD also may become unstable as a consequence of imbalance between infection-induced increased metabolic demand and reduced cardiac reserve. Acute coronary event in COVID-19 patients may result from the significant increase in myocardial demand triggered by infections that precipitate myocardial injury and infarct, similar to type 2 MI.[21] The symptoms are more evident in patients with CVD, which is linked with increased expression of ACE-2 receptors in these patients compared with healthy individuals. There are concerns regarding the use of ACE inhibitor (ACEI)/angiotensin receptor blocker (ARB) in patients with COVID-19 and coexisting CVD because as mentioned in the previous discussion that SARS-CoV-2 enters the human cells by binding to ACE-2 receptor and severity of infection may get potentiated with upregulation of ACE-2 receptors.[22]

The various risk factors, pathophysiological mechanisms, and cardiovascular manifestations are highlighted in [Figure 1].
Figure 1: Risk factors, pathophysiological mechanisms and cardiovascular manifestations of coronavirus disease-19

Click here to view

  Cardiovascular Manifestation in Coronavirus Disease-19 Top

Myocardial injury

Patients with underlying CVD and associated comorbid conditions are more vulnerable to experience myocardial injury during the course of COVID-19 illness. In about 1/3 of the patients with SARS-CoV infection, the SARS-CoV genome could be positively detected in the heart, which raises the possibility of direct cardiomyocytes damage by the virus and demonstrates the propensity for the SARS coronavirus subfamily to infect and modulate cardiac tissue potentiating myocardial damage.[23] Several mechanisms of myocardial injury have been postulated which include direct damage to the cardiomyocytes, systemic inflammation, myocardial interstitial fibrosis, interferon-mediated immune response, exaggerated cytokine response by T cells, and hypoxia. Because of the genome homology in SARS-CoV-2 and SARS-CoV, the same mechanism of action could be extrapolated for both types of viruses.[9],[24] Huang et al. highlighted that in COVID-19 patients, the TH1/TH2 cellular dysbalance results in a cytokine storm, which might be a contributor to myocardial injury.[1] The cytokine storm may cause damage to myocardial cells, paucity in coronary blood flow, and coronary plaque destabilization. A procoagulant state in COVID-19 patients has been also reported.[25] This might lead to endothelial, macrophage, tissue factor, and platelet activation enhancing the risk of ACS. Excessive intracellular calcium deposition results in cell necrosis, thereby leading to myocardial damage. The resultant oxygen demand supply mismatch exacerbates further damage.

Myocarditis is a clinical syndrome of myocardial damage and can be diagnosed based on clinical presentation as well as diagnostic criterion like elevated troponin T (TnT) or troponin I (TnI). Two patterns of myocardial injury are described based on initial reports from China. In primary myocardial injury, predominantly cardiac symptoms are present instead of respiratory symptomatology. It can manifest as acute MI (type 1, Fourth Universal Definition of MI), viral myocarditis, and stress-induced left ventricular (LV) dysfunction. Secondary myocardial injury is known to occur when the patient develops cardiovascular symptoms after the development of respiratory features. The virus can directly invade the cardiomyocytes through ACE-2 receptors, producing myocardial inflammation and damage and can be diagnosed with reliability on magnetic resonance imaging findings of marked biventricular myocardial interstitial edema and late gadolinium enhancement.[26],[27] However, it is true that incidence is unknown in patients with COVID-19 as data pertaining to cardiac imaging or biopsies are sparse.

In a study by Chen et al., NT-Pro-BNP, TnI, and D-dimer levels were found elevated as the markers of myocardial injury and were also significantly correlated with severe disease.[28] Huang et al. had reported increased levels of high sensitive troponin I (hs-cTnI) levels (>28 pg/ml) in 5 of 41 COVID-19 patients, and also increased intensive care unit (ICU) admission rates were observed in these patients.[1] In a similar study conducted in Wuhan, of 416 hospitalized patients, only 82 patients showed myocardial injury through the same surrogate markers and the mortality rate was higher in this group of patients.[29] Zhou et al. had also reported that the incidence of elevation in hs-cTnI (>28 pg/mL) was 17%, and it was significantly higher among nonsurvivors.[30] The trend in the rise of hs-cTnI was in synchrony with the increase of inflammatory biomarkers (IL-6, D-dimer, ferritin, and lactate dehydrogenase). It was observed by Guo et al. that patients with elevated troponin levels had a higher incidence of complications such as ARDS, malignant ventricular tachyarrhythmia, acute renal injury, and acute coagulopathy.[31] Interestingly, the mortality was highest in patients with myocardial injury and underlying CVD (69.4%). However, the mortality also was observed considerably high in cases with myocardial injury but without prior CVD (37.5%). On the other hand, patients with prior CVD without acute myocardial injury had a relatively favorable prognosis (mortality of 13.3%).[31] Hence, troponin estimation has an important role in risk stratification of patients and also it helps in defining prognosis.

Fulminant myocarditis has also been found in association with COVID-19.[32] Pericardial involvement is also known to occur in COVID-19 patients either in association with myocarditis or standalone. Pericardial effusion with or without tamponade has been reported too.[33]

Acute coronary syndrome

As mentioned in the foregoing discussion, severe systemic inflammation along with a procoagulant state increases the risk of atherosclerotic plaque disruption and acute MI in COVID-19 disease. The majority of MI are type 2 (Fourth Universal Definition of MI), which are consequent to mismatch between oxygen supply and demand.[21] The case volumes of ACS have shown a different pattern across the world, whereas more studies are in favor of reduction in the incidence of ACS in the COVID-19 era, some had recorded a comparable case volume as in the non-COVID.[34] Multiple studies have found that the incidence of hospitalization for acute MI has decreased by as much as 40%–50% during the pandemic.[35],[36] A study from North California compared the weekly incidence rate of hospitalization for acute MI (STEMI and non-STEMI [NSTEMI]) before and after March 2020.[35] The data were compared with available data from the same time period in 2019. The weekly rate of hospitalization was declined by 48% during the COVID-19 period. Compared with 2019, the incidence of hospitalization for acute MI was significantly lower in 2020 post March, demonstrating that decrease could not be explained by seasonal variation alone. Similarly, a study from Italy compared the admission rate for acute MI from March 12 to 19 in 2020 with the corresponding week in 2019.[36] There was a 49.9% reduction (P < 0.001), and it was significant for both STEMI and NSTEMI.

A possible explanation for the decreased hospitalization rate includes patient fear of being infected with COVID-19 virus while seeking medical help at emergency departments, strict travel restriction imposed during nationwide lockdown laid by various governments, and redistribution of the health-care system due to over occupancy of hospitals with patients with COVID-19.[37] Last but not the least, the economic effect of pandemic has forced many patients to stay at home for minor symptoms which may be the preceding symptoms of major cardiac event. As a result, more patients with late presentation and ACS-related complications such as extensive infarcts, cardiogenic shock complicating MI, high coronary thrombus burden, and no reflow were often seen.[37] These patients will suffer increased morbidity and mortality without proper or due to delayed ACS management. The Italian investigators had observed that the STEMI case fatality rate was higher in 2020 as compared to 2019 (risk ratio 3.3, 95% confidence interval 1.7–6.6).[36] Health-care providers should make every effort to persuade patients with complaints suggestive of ACS to seek early medical aid to prevent from deadly consequences. It is prudent to note that all patients should be screened for COVID-19, regardless of the primary complaint.

Acute heart failure and cardiomyopathy

Acute heart failure can be the primary presentation of COVID-19 disease. In a study conducted on 191 patients, acute heart failure was seen in 23% of patients on the initial presentation of COVID-19 disease.[30] Chen et al. had reported that the incidence of heart failure was 24% in their study group and that had caused greater mortality.[28] A significant majority of COVID-19 patients presenting with heart failure lacked the history of classical risk factors for heart failure such as hypertension, diabetes mellitus, or CVD.[28] The possible mechanisms can be exacerbation of preexisting LV dysfunction, new-onset myocarditis, drug induced, ACS, and dysrhythmias. Stress-induced cardiomyopathy is another important cause of heart failure in COVID-19 patients, which can mimic COVID-19 myocarditis.[38] The incidence of right heart failure with pulmonary hypertension is high in seriously/critically ill COVID-19 patients with ARDS.[39],[40] Aggressive fluid replacement needs to be avoided in view of both pulmonary hypertension and existence of left heart failure.


Cardiac arrhythmias are the common cardiac manifestation in COVID-19 patients. Liu et al. found that among 137 hospitalized COVID-19 patients, 7.3% of patients had nonspecific palpitations as the presenting symptom.[41] In another study, about 44% of the patients admitted in the ICU with COVID-19 had arrhythmia in comparison to 6.9% of those in non-ICU care.[42] Most commonly encountered arrhythmia was sinus tachycardia.[39] The relationship of COVID-19 to increased arrhythmia occurrence can be attributed to fever, ACS, systemic inflammation, metabolic disturbances (particularly hypokalemia), neurohormonal dysregulation, myocardial ischemia/injury, and hypoxia.[43] Drugs, which are empirically being used in the management of COVID-19, predispose the patients for various types of brady/tachyarrhythmias. Of particular mention is the QTc prolongation by azithromycin and hydroxychloroquine (HCQ). In the presence of troponin elevation, dysrhythmias should raise the suspicion of myocardial injury, ACS, and fulminant myocarditis.[39] Finally, arrhythmia management in COVID-19 patients depends on the primary cause and should be treated in the same way as non-COVID patients.

Thromboembolic events

Patients with COVID-19 are at high risk of developing arterial or venous thromboembolic events (VTE).[44],[45] Pulmonary embolism (PE) is the most frequent thrombotic complication. The contributing factors for these complications are systemic inflammatory syndrome, procoagulant state, endothelial dysfunction, and multiorgan dysfunction.[1],[30],[44],[45] Prolonged immobilization in critically ill patients also predisposes to VTE. Coagulation pathway alterations were found in COVID-19 patients, evident by elevated fibrin degradation products and D-dimer levels, which, in turn, were associated with the development of disseminated intravascular coagulation and increased in-hospital mortality.[1],[30],[44],[45] A study by Chen et al., of 25 COVID-19 pneumonitis patients noticed that an elevated D-dimer level was present in all patients and the same study also concluded the incidence of PE diagnosed on CTPA in 40% of the patients.[46] Therefore, if a COVID-19 hospitalized patient demonstrates sudden clinical deterioration evidenced by hemodynamic instability, sinus tachycardia, worsening dyspnea or hypoxia, acute PE should always be kept in mind as the differential diagnosis. A study by Tang et al. made an observation that anticoagulation with low molecular weight heparin may be associated with reduced mortality in severe COVID-19 infections or those with raised D-dimer values.[47] Hence, the thromboprophylaxis is indicated in all patients admitted in the ICU or seriously ill COVID-19 patients with standard societal guidelines due to lack of validated regimen till date.

Drugs interactions and coronavirus disease-19 treatment

Many of the drugs used to treat COVID-19 patients exhibit serious cardiovascular side effects and have an interaction with other cardiovascular drugs. HCQ sulfate is currently one of the most commonly recommended drugs for the treatment of COVID-19. It acts by change in endosomal/organelle pH, which results in electrolyte abnormality and cardiotoxicity. Furthermore, it is known to cause AV blocks and prolonged QTc interval/Torsades de pointes (Tdp). Concomitant use of beta-blockers or nondihydropyridine calcium channel blockers with HCQ can lead to severe bradycardia/AV blocks.[48] Azithromycin (a macrolide antibiotic) has been combined with HCQ for improved symptoms recovery based on the result of a small French trial.[49],[50] This particular drug is also known to prolong QTc, like HCQ. Hence, currently, it is recommended to assess QTc before the initiation of these medications and followed by close monitoring in patients.[51]

There is a particular concern in COVID-19 regarding hypokalemia, due to the interaction of SARS-CoV2 with the ACE-2 receptor.[17],[52] This electrolyte disturbance is a well-known risk factor for the development of tachyarrhythmias by prolonging QTc, and thus, serum K+ and QTc need close monitoring in COVID-19 patients.

Lopinavir and ritonavir are Food and Drug Administration approved protease inhibitors for the treatment of HIV-1 infection. They run the risk of prolongation of PR and QTc intervals. These drugs are also known to augment the effects of factor Xa inhibitors and antiplatelets like ticagrelor through CYP3A4 inhibition. Hence, caution is needed in patients on multiple CVD-related medicines.[53] However, these drugs are not recommended for the treatment of COVID-19 patients.

Favipiravir is a prodrug which was approved in Japan for influenza in 2014. The drug acts by selective inhibition of viral RNA-dependent RNA polymerase and induces lethal RNA transversion mutations, producing a nonviable viral phenotype.[54],[55] It is known to interact with various cardiovascular drugs such as anticoagulants, statins, and antiarrhythmics. Hemolytic anemia can be caused by its use. The Drug Controller General of India has approved its use in mild to moderate COVID-19 cases.

Remdesivir is a novel antiviral drug which interferes with the action of viral RNA-dependent RNA polymerase and evades proofreading, causing thereby, decrease in viral RNA production. A recent trial by Grein et al. of 61 seriously ill COVID-19 patients showed clinical improvement in 68% of patients.[56] There is paucity of data on its safety profile effects, however hypotension and hypokalemia were observed.

The use of corticosteroids in the treatment of COVID-19 is highlighted in few trials. Initial clinical data from the United Kingdom showed that dexamethasone can be lifesaving for critically ill/serious COVID-19 patients.[57] For patients on ventilators, the treatment was shown to reduce mortality by one-third, and for patients requiring only oxygen, mortality was cut by one-fifth, according to preliminary findings shared with the WHO. These agents can cause fluid retention, hypertension, and dyselectrolytemia. Hence, corticosteroids should be used with caution in COVID-19 patients due to its side effects in patients with cardiovascular involvement. Also to mention, the drugs should be avoided in mild to moderate cases of COVID-19 because of the fear of viral shedding.[58],[59]

The anti-IL-6 antibody tocilizumab is currently on clinical trials for COVID-19 seriously ill/critical patients. The drug is thought to inhibit the inflammatory response and the cytokine storm and hence preventing ARDS/mortality.[1] The cardiovascular safety profile data are limited, however can cause hypotension and arrhythmias.

Colchicine is an anti-inflammatory drug, indicated for pericarditis associated with transmural infarction. It has immunomodulatory activities like the nonselective inhibition of NLRP3 inflammasome, which is considered as a major pathophysiological component of ARDS. Therefore, it has been thought that colchicine may improve the clinical course and prevent complications in patients with COVID-19 disease.[60]

  Treatment of Cardiovascular Complications of Coronavirus Disease-19 Top

The mainstay treatment of COVID-19 is generally symptomatic and supportive management along with the treatment of its associated complications. Although there are no specific guidelines regarding the prevention and treatment of cardiovascular complications of COVID-19 disease, some considerations should be kept in mind while treating such patients. All patients presenting to emergency with cardiorespiratory symptoms should be considered as COVID-19 suspected patients unless proven otherwise and adequate precautions should be taken to prevent the spread of nosocomial infection due to the prevalence of asymptomatic carrier state. The new rapid COVID-19 testing should be expeditiously disseminated to all hospitals involved in the care of such patients.

At the present stage of the COVID-19 pandemic, it is imperative to triage patients with COVID-19 according to the presence of underlying CVD and evidence of myocardial injury to prioritize treatment strategies. Abnormal troponin values are common among patients of COVID-19 particularly when testing with high sensitivity cardiac troponin. This is more common due to myocarditis or type 2 MI caused by demand and supply mismatch seen in COVID-19 infections. Type 1 MI due to plaque rupture triggered by infection is uncommon. Furthermore, the American College of Cardiology (ACC) has recommended to assess troponin levels only if the diagnosis of MI is being considered on clinical grounds and disregard casually ordered abnormal troponin value.[61],[62] Therefore, estimation of cardiac biomarkers such as troponin and NT-Pro-BNP is justified in patients with prior CVD or its risk factors or in patients with evidence of cardiac injury. ECG is vital for documenting QTc or any arrhythmic potential before initiating specific therapy for COVID-19.

There are concerns regarding the use of ACEI/ARB in patients with COVID-19 and coexisting CVD or its risk factors. It is based on the fact that SARS-CoV-2 enters the human cells by binding to the ACE-2 receptor and upregulation of these receptors has been implicated in the pathogenesis of the disease. The well-studied reduction in mortality conferred by these drugs and its beneficial effects for patients with diabetes and chronic kidney disease currently outweighs the theoretical risks. The council of hypertension of the European College of Cardiology has released a position statement on continued use of ACEI/ARB due to lack of scientific evidence and clinical data that these drugs may increase the risk of infection and its severity.[63] Similarly, ACC/AHA has recommended the continued use of RAAS antagonists for patients who are currently prescribed such agents.[64]

There is high likelihood of developing arterial or VTEs in critically ill COVID-19 patients which pose risk of mortality. However, there are no specific societal guidelines for the use of thromboprophylaxis in such scenario. Therefore, low molecular weight heparin or unfractionated heparin is widely used to prevent such life-threatening events in patients with considerably elevated D-dimer levels.[65]

Clinical discernment is of utmost importance in diagnosing STEMI as myocarditis may mimic myocardial infarction. Patients need to be isolated because of the prevalence of asymptomatic carrier state with SARS-CoV-2 infection, with the aim to reduce the risk of infection spreading within the hospital. Wherever it is possible, a catheterization laboratory with negative pressure ventilation should be isolated for dedicated use in cases of suspected or confirmed COVID-19 patients to prevent nosocomial as well as community spread of infection. It is important to note that some of the patients may have a STEMI mimicker such as myocarditis or stress cardiomyopathy which is known to be associated with COVID-19.[66],[67] Fibrinolysis of such patients would provide no benefit to the patient and may incur bleeding risk. Hence, differentiation between the type 2 MI and primary ACSs is important.

For the confirmed or suspected COVID-19 patients with STEMI, primary percutaneous coronary intervention (PCI) should be preferred if performed with the necessary precautions and preparedness. Fibrinolysis is advisable where PCI may not be feasible due to logistic issues in performing timely PCI. Post fibrinolysis, around 50% of patients require rescue PCI due to failed fibrinolysis.[68] In the presence of hemodynamic compromise, PCI would be an ideal option. It is noteworthy that the procedure should be performed with minimum number of trained personnel in the catheterization laboratory to reduce the risk of nosocomial infection and with adequate personal protective equipment (PPE). For the stable NSTEMI patients, coronary angiography and revascularization should be preferably deferred until a COVID-19 negative test result has been obtained. After obtaining negative test result and in absence of infection, coronary angiography and revascularization may be performed in a catheterization laboratory reserved for SARS-CoV-2 negative patients.

The intubation threshold should be kept lower to avoid emergent intubation and aerosol generation. Patient transportation from the ward to the catheterization laboratory may carry the risk of in-hospital infection transmission; some of the procedures routinely performed in the catheterization laboratory (e.g., pericardiocentesis and intra-aortic balloon pump) can be considered for bedside performance.

  Conclusion Top

COVID-19 disease caused by SARS-CoV-2 has rapidly emerged as a global health concern with almost every country in the world been affected. The understanding of this novel coronavirus and its pathogenic mechanisms causing cardiovascular complications is largely unknown but is rapidly unfolding. Patients with underlying CVD are at increased risk of complications and death caused by COVID-19. At the same time, COVID-19 is a high inflammatory state that itself leads to various cardiovascular complications. Standard of procedure and care for treating CVDs should be developed by every institution treating COVID-19 patients. Social distancing is the cornerstone to curb the spread of the disease, but at the same time it should not prevent patients from seeking medical care. Emphasis should be given on a registry database of patients with COVID-19 with a systematic recording of all clinical variables that will be helpful in developing a risk model for early identification of cardiovascular complications so as to enhance therapeutic efforts and monitor its response.

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Conflicts of interest

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