|Year : 2021 | Volume
| Issue : 1 | Page : 24-30
COVID-19 and cardiac health: A review
Avinash Mani1, Vineeta Ojha2, Manoj Kumar Dubey3
1 Department of Cardiology, Sreechitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram, Kerala, India
2 Department of Cardiovascular Radiology and Endovascular Interventions, All India Institute of Medical Sciences, New Delhi, India
3 Department of Medicine, Patliputra Medical College and Hospital, Dhanbad, Jharkhand, India
|Date of Submission||10-Sep-2020|
|Date of Decision||22-Feb-2021|
|Date of Acceptance||25-Mar-2021|
|Date of Web Publication||24-Apr-2021|
Department of Cardiology, Sreechitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram - 695 011, Kerala
Source of Support: None, Conflict of Interest: None
The ongoing novel coronavirus pandemic has caused a serious impact on patients suffering from cardiovascular disorders as they are predisposed to COVID infection as well as to exacerbation of their preexisting conditions which can prove to be fatal. Novel coronavirus disease-2019 (nCOVID-19) has a varied effect on the cardiac system ranging from myocardial injury to thromboembolic complications. A significant proportion of patients are noted to have comorbidities. Human angiotensin-converting enzyme 2 (ACE 2) receptor is considered the target of the severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2). SARS-Cov-2 leads to imbalance in RAAS activity which is responsible for target organ damage. Recombinant ACE 2 has been shown to restore ACE 2 levels in explanted hearts and restore balanced RAAS activity. nCOVID-19 can have varied cardiac manifestations ranging from acute coronary syndrome to heart failure, arrhythmias, pulmonary thromboembolism, and pericarditis. The current nCOVID-19 pandemic has led to changes in management strategies for cardiovascular diseases. Patients with ST-elevation myocardial infarction can be fibrinolysed when a primary percutaneous coronary intervention facility with adequate protection is not available. Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker needs to be continued in patients with hypertension. Continuity of care for patients with chronic cardiovascular illness needs to be maintained. Management of cardiovascular emergencies needs to be done in a way which ensures the safety of health-care professionals and prevents infection transmission. Strict prevention of infection and health control measures will help to prevent spread of infection and reduce disease incidence.
Keywords: Acute coronary syndrome, COVID-19, heart failure
|How to cite this article:|
Mani A, Ojha V, Dubey MK. COVID-19 and cardiac health: A review. J Pract Cardiovasc Sci 2021;7:24-30
| Introduction|| |
The ongoing novel coronavirus disease-2019 (nCOVID-19) pandemic has affected around 200 countries throughout the world. It is the worst pandemic the world has seen since the Spanish Flu in 1918. As the pandemic continues for more than 1 year now, with fresh surge of cases noted in different parts of the world, health-care professionals and facilities are working at maximum capacity to ensure optimum care to patients who have been affected by this deadly disease.
In the current scenario, when critical care for nCOVID-19 affected patients is of utmost importance, we need to ensure continuity of care to patients suffering from chronic illness who are predisposed to contract nCOVID-19 infection. The same holds true for patients suffering from cardiovascular disorders, who are predisposed to nCOVID-19 infection which can prove to be fatal. Patients with cardiac disease can develop new manifestations related to nCOVID-19 illness or may have exacerbation of their preexisting condition. These situations require prompt recognition and management so that adverse events can be prevented. All health-care professionals need to ensure that patients with cardiovascular disease (CVD) are able to avail their routine health care. In this article, we aim to identify the major cardiovascular manifestations of nCOVID-19 and how established management strategies need to be altered for these patients during this pandemic situation.
| Methodology|| |
An extensive literature search was done on PubMed/Medline and Google Scholar/Google using the keywords: nCOVID-19, myocardial infarction (MI), acute coronary syndrome (ACS), heart failure (HF), myocarditis, arrhythmias, pulmonary embolism, deep venous thrombosis, pericardial effusion, percutaneous coronary intervention (PCI), hypertension, echocardiography, and infection control. All articles were reviewed for suitability and relevant original studies, systematic review, and case reports were used for the purpose of this narrative review.
| Cardiovascular Involvement in Novel Coronavirus Disease-2019|| |
nCOVID-19 has varied presentations. Patients usually have constitutional symptoms such as fever, malaise, and body ache. Some patients may also remain asymptomatic or have minimal symptoms while remaining infective. Respiratory involvement is most common, which usually manifests in the form of pneumonia and can progress to acute respiratory distress syndrome (ARDS) in severe cases. nCOVID-19 has varied effect on the heart, ranging from myocardial injury to thromboembolic complications. Patients with nCOVID-19 usually have associated comorbidities which is likely makes them susceptible. In a study of around 1100 confirmed nCOVID-19 patients (both outpatient and inpatient) from China, around 24% of patients had comorbidities-2.5% had known coronary artery disease, 7.4% were diabetics whereas 15% had hypertension. A meta-analysis which involved 8 studies conducting in China, including 46,248 infected patients, showed that hypertension (17 ± 7%) and diabetes (8 ± 6%) were the most common risk factors.
| Pathophysiology|| |
Human angiotensin-converting enzyme 2 (ACE 2) receptor is considered to be the target of the severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2). ACE 2 is present on a variety of tissues including the heart, lung alveolar epithelial cells, kidney, and gastrointestinal system. ACE 2 enzyme degrades angiotensin II into angiotensin,,,,,, thereby attenuating the deleterious effects of vasoconstriction, sodium restriction and fibrosis. During SARS-Cov-2 infection, the viral glycoproteins bind with the ACE-2 receptor, leading to internalization of the viral particle. SARS-Cov-2 infection also leads to downregulation of ACE 2 enzyme activity. This causes unopposed angiotensin-II activity and tissue damage. Dysregulated ACE 2 activity leads to attenuated cardioprotection during SARS-Cov-2 infection due to unopposed angiotensin II activity. ACE 2 also has a well-documented role in myocardial injury and recovery – ACE 2 knockout animal models had showed adverse ventricular remodeling. In autopsy studies of patients who had died from SARS, 35% of cardiac samples were positive for viral RNA, which was associated with reduced ACE2 protein expression. SARS-Cov-2 leads to imbalance in RAAS activity which is responsible for target organ damage. Recombinant ACE 2 has been shown to restore ACE 2 levels in explanted hearts and restore balanced RAAS activity.
| Clinical Presentation|| |
nCOVID-19 can have varied cardiac manifestation ranging from ACS to HF and pericarditis [Figure 1].
|Figure 1: Different manifestations of cardiovascular involvement by severe acute respiratory syndrome coronavirus 2.|
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Acute coronary syndrome
Patients with SARS-Cov-2 infection can present with either unstable angina/NSTEMI or ST-elevation MI (STEMI). These events are either Type 1 MI, which occurs as a result of vulnerable plaque rupture due to heightened sympathetic stimulation or Type 2 MI resulting from a demand/supply mismatch due to reduced coronary reserve (pre-existing coronary artery disease). These patients will present with features of typical angina associated with ST/T changes on electrocardiogram (ECG). They will have elevated cardiac biomarkers (creatine kinase-MB, Trop T, Trop I) and cardiac catheterization will show the presence of obstructive coronary disease. There is another group of patients who can present with typical features of ACS including symptoms, ECG changes and troponin elevation but will have normal coronaries on cardiac catheterization.
In a study, which included 18 patients of nCOVID-19 who presented with STEMI, coronary angiography was performed in 9 patients. 30% of these patients were found to have normal coronaries whereas others had obstructive lesions and underwent angioplasty. Another study of 28 STEMI patients with nCOVID-19 infection showed that culprit lesion was found in 60% whereas the rest had nonobstructive CAD indicating type 2 MI. Patients with nCOVID-19, who had STEMI, were noted to have higher thrombus burden, higher incidence of stent thrombosis, and multivessel thrombus. Intensive care unit (ICU) admission and total duration of hospital stay was longer in STEMI patients with nCOVID-19, whereas in-hospital mortality was similar. Rarely, patients with nCOVID-19 can present with typical ST elevation on ECG without serial troponin elevations– pseudo-acute MI.
SARS-Cov-2 infection causes myocardial injury which leads to HF. In a study of 416 confirmed nCOVID-19 patients, 19.7% had evidence of myocarditis as evidenced by elevated cardiac troponins. In another cohort study of 187 patients by Guo et al., 27.8% of patients were found to have elevated cardiac troponin levels. Risk factors for the development of myocardial injury were likely older age, presence of comorbidities like diabetes and hypertension, along with preexisting CVDs. Myocardial injury in nCOVID-19 can be due to direct and indirect mechanisms. The direct mechanism involves viral entry into cardiac myocytes causing cell death and necrosis. Indirect injury is mediated by excess stimulation of sympathetic and RAAS systems in nCOVID-19 along with pro-inflammatory cytokines which can lead to cytokine storm.
nCOVID-19 patients can have varied presentations-
- Acute decompensated HF – Patients develop hemodynamically unstable HF, associated with elevated cardiac troponins and natriuretic peptides. They have left ventricular (LV) dysfunction (ejection fraction <40%) and global hypokinesia on echocardiography suggestive of acute myocarditis. The true incidence of myocarditis in nCOVID-19 patients is not known. Patients with COVID-19 can have persistently rising troponin levels, which is in contrast to the rapid rise and fall seen in patients with ischemic injury. This reflects a state of heightened inflammatory activity in these patients. Cardiac imaging can play an important role in identifying patients with myocardial injury
- Exacerbation of chronic HF – Patients with preexisting chronic HF present with exacerbation of preexisting symptoms when there is an added myocardial insult in the form of nCOVID-19 infection
- Cardiogenic shock – Patients with nCOVID-19 can also present with hypotension and cardiogenic shock after a short period of flu-like symptoms. These patients will likely require ECMO/ventricular assist devices to tide over the crisis
- Stress cardiomyopathy – Patients with nCOVID-19 can present with acute onset LV dysfunction with typical apical ballooning and basal hyperkinesia on echocardiogram suggestive of stress cardiomyopathy. Increased neurohormonal stimulation seen in nCOVID-19 is likely responsible for the development of stress cardiomyopathy.
Troponin elevation is quite commonly seen in patients affected with nCOVID-19. The incidence varies depending on the type of assays used. Depending on the level of troponin elevation, these patients can be categorized as having a chronic myocardial injury, acute nonischemic myocardial injury, and acute MI. Chronic myocardial injury is usually seen in the elderly, with multiple comorbidities, who have mild elevation of troponins which remains stable over time. Acute nonischemic myocardial injury is the most common pattern seen in nCOVID-19 patients. They have dynamic rise and fall in troponin levels without any evidence of myocardial ischemia. It can be due to cardiac etiologies such as acute HF, myocarditis, or extracardiac causes like pulmonary thromboembolism.
Myocardial injury can be associated with multi-organ damage. In this setting, the myocardial injury probably results from a dysregulated immune system producing a cytokine storm rather than direct affliction of cardiac tissue with virus. Patients with elevated troponin levels have been found to have significantly elevated levels of high sensitivity C-reactive protein (CRP), myoglobin, and NT-ProBNP suggesting the presence of a heightened systemic inflammatory response. Patients with myocardial injury are likely to be associated with more systemic complications during hospitalization as compared to those without myocardial injury. In the cohort studied by Guo et al., patients who had myocardial injury developed more frequent complications in form of ARDS (57.7% vs. 11.9%), acute kidney injury (36.8% vs. 4.7%), and coagulopathy (65.8% vs. 20.0%). Cardiac complications in the form of malignant arrhythmias (VT/VF) were also higher in patients with myocardial injury (11.5% vs. 5.2%). This reflects that elevated troponin levels are associated with more severe systemic viral infection. Mortality rates were highest among patients with previous CVD and elevated troponins (69.44%). Even patients without previous CVD having elevated troponins had significantly high mortality (37.5%). Patients with/without CVD and having normal troponins had considerably lower mortality (13.3% and 7.6%). Thus, myocardial injury is considered to be a predictor of in-hospital mortality. Progressively rising troponins and natriuretic peptides during hospital stay was a bad prognostic marker.
SARS-Cov-2 involvement of the heart can predispose to arrhythmia. Arrhythmias were noted in 17% of total hospitalized nCOVID-19 patients in a cohort of 138 patients. The exact nature of arrhythmias is not clearly known. Malignant VT/VF was noted in 5.9% in a cohort of 189 patients. These arrhythmic events can be the result of direct myocardial injury, microvascular ischemia, pericardial inflammation, or gap junction dysfunction due to pro-inflammatory state.
Patients with inherited arrhythmic syndromes are also at risk of developing lethal arrhythmias due to COVID-19 infection. nCOVID-19 patients most commonly develop fever which can be detrimental in patients with underlying Brugada syndrome. Dyselectrolytemia associated with renal/hepatic dysfunction can lead to QTc prolongation which can be lethal in patients with inherited long QT syndromes. The use of various antiviral drugs can also lead to prolongation of QT interval in these patients.
Pericardial involvement in nCOVID-19 can manifest as pericardial effusion. These cases can have associated myocarditis, thus constituting “myopericarditis.” Cardiac tamponade can occur in nCOVID-19 patients presenting with myopericarditis, which can lead to acute hemodynamic collapse.
Pulmonary thromboembolism and deep vein thrombosis
nCOVID-19 is associated with systemic inflammation and predisposes to the development of a hypercoagulable state. D-dimer levels have been shown to be significantly higher in patients with severe disease as in comparison to patients with mild disease. Patients are thus vulnerable to a variety of thromboembolic complications. Acute pulmonary embolism has been reported in nCOVID-19 patients presenting with acute respiratory distress. Pulmonary thromboembolism could be related to in situ thrombosis developing due to hypercoagulability or upstream embolism from deep vein thrombosis.
| Diagnosis|| |
nCOVID-19 can present as an acute cardiovascular emergency or exacerbation of preexisting CVD. There can be considerable overlap in presenting symptoms of cardiac disorders and nCOVID-19. Symptoms of chest pain and dyspnea in these patients can be related to ACS or nCOVID-19 itself. ECG and echocardiography will help in the diagnosis of cardiac involvement in these patients. 12 lead ECG will show ischemic changes in patients presenting with ACS (ST elevation in STEMI, ST depression, and T wave inversion in UA/NSTEMI). Echocardiography can show reduced LV ejection fraction with global hypokinesia or regional wall motion abnormalities. Elevated troponins (trop T/I) and natriuretic peptides (BNP, NT-ProBNP) have been shown to correlate with the degree of myocardial injury. In hemodynamically stable patients, cardiac magnetic resonance imaging (MRI) can be done to establish the diagnosis of myocarditis according to the updated Lake-Louise criteria. A study performed cardiac MRI in nCOVID-19 recovered patients, to look for evidence of myocardial involvement. Out of 26 patients, half of the patients had myocardial edema and 30% had late gadolinium enhancement (LGE) on MRI. Another cardiac MRI study of 100 asymptomatic COVID-19 recovered patients showed presence of cardiac abnormalities in the form of elevated T1/T2 mapping values or LGE in about 78% patients. A systematic review of 34 studies on cardiac MRI in nCOVID-19 patients revealed that myocarditis was seen in about 40% of patients. T1 and T2 abnormalities were seen in 73% and 63% of patients, respectively, whereas edema and LGE were noted in 51% and 43% of patients. All these evidence points to myocardial damage inflicted by nCOVID-19. As nCOVID-19 is generally associated with systemic inflammation, inflammatory markers like ESR, CRP, and serum ferritin are elevated and can act as prognostic markers. D-dimer levels are elevated in patients with nCOVID-19, which points toward a hypercoagulable state.
| Management|| |
Management of cardiovascular disorders in nCOVID-19 requires a two-pronged approach involving diagnosis and management along with the implementation of measures for the prevention of infection. The current nCOVID-19 scenario has led to changes in management strategies for CVDs while ensuring proper utilization of health resources and protection of health-care workers.
Coronary artery disease
Patients with nCOVID-19 and STEMI present a real challenge. The time to first medical contact after symptom onset can be affected during the present routines to disruption of regular health services. In a study of STEMI patients, who underwent primary PCI in China, it was seen that the average time to first medical contact after symptom onset was higher during the present time in comparison to previous pre-COVID times (318 min vs. 82.5 min). A number of challenges are posed in providing care to STEMI patients during the nCOVID pandemic. Availability of emergency services and prolonged emergency department evaluations can cause delay in treatment. Availability of well-sanitized catheterization labs with adequate protective equipment is also a prerequisite. Screening of every patient is a prerequisite to determine the risk status of the patient. Rapid antigen tests can be used to determine the infective status of the patients, but it can cause delay in treatment. The benefits of immediate invasive therapy need to be balanced against the risks of exposure and contact of health-care professionals.
ACC/SCAI have come up with a joint statement regarding the use of cardiac catheterization lab facilities in patients infected with nCOVID-19. Consensus statement for the management of STEMI patients in the Indian setting has also been developed. Patients with STEMI should be assessed for hemodynamic stability and presence of mechanical complications as well as the territory involved. Patients with extensive anterior wall STEMI are at high risk of developing cardiogenic shock. A proposed treatment algorithm is shown in [Figure 2]. In patients with STEMI who are hemodynamically stable and present to a non-PCI capable hospital, fibrinolysis is a good option with a pharmaco-invasive strategy. Primary PCI is the treatment of choice in patients with STEMI who are hemodynamically unstable or as rescue therapy in patients who have had a failed fibrinolysis. Patients presenting to a PCI-capable hospital can be taken up for either primary PCI or receive fibrinolysis depending on the institutional protocol. Cardiac catheterization labs need to be modified for the purpose of doing interventions on nCOVID patients. Normally, catheterization labs have a positive pressure ventilation system. Converting this into a negative-pressure ventilation system can help in the reduction of risk of transmission. If negative pressure ventilation systems are not available, the air conditioner system in the cath lab should ideally be turned off in order to prevent transmission.
|Figure 2: Proposed algorithm for the management of ST-elevation myocardial infarction patients in the COVID era.|
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Patients who present with NSTEMI may be managed conservatively if they are hemodynamically stable and do not have any high-risk features. Majority of these patients do not have any obstructive coronary lesions and belong to the category of Type 2 MI. Cardiac catheterization will be required in patients who are unstable with high likelihood of having obstructive CAD. Patients with stable CAD who are planned for elective PCI should be continued on optimal medical therapy at present and their procedures may be deferred, if possible. This will prevent patients from nosocomial infection and also help in better utilization of hospital resources for more critical patients.
Management strategies for arrhythmias include the use of antiarrhythmic drugs for rate and rhythm control. nCOVID-19 patients being treated with antiviral agents like lopinavir/ritonavir, hydroxychloroquine (HCQS), azithromycin require regular monitoring of QTc interval as combination of these drugs can lead to marked QTc prolongation and torsade de pointes. The presence of electrolyte abnormalities may also compound the effect of these drugs on QTc interval.
HCQS is being extensively used for the purpose of severe nCOVID-19 infections. This drug has a mild risk of causing QT prolongation and should be used with caution in the elderly, patients with hepatic and renal dysfunction. Patients with chronic use of drug (>5 years) are more prone to develop these complications and short-term usage, as in nCOVID-19, is usually uneventful. However, the use of HCQS in combination with other drugs like azithromycin can lead to marked QTc prolongation and adverse events on short-term usage. Thus, caution needs to be exercised during usage.
Electrophysiological testing and procedures may be done in emergency cases as identified by the Heart Rhythm Society COVID-19 Task Force. Some of these conditions include – VT ablation in medically uncontrolled VT storm, catheter ablation for WPW syndrome presenting with syncope/cardiac arrest, pacemaker implant for the complete atrioventricular block (AVB), high-grade AVB or sinus node dysfunction, pulse generator change for patients, and ICD implant for secondary prevention.
Patients with HF are at considerable risk during the nCOVID-19 pandemic. Delay in the initiation of therapy and disruption in the chain of health care can affect these patients significantly. Patients with recent-onset HF should be initiated on HF-directed therapy without any delay. Temporary mechanical circulatory support may be required in patients of acute HF who have severe cardiopulmonary failure. Guideline-directed medical therapy with angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB) must be continued for patients with chronic HF. Discontinuation of drug therapy can lead to sudden exacerbation of HF in patients with nCOVID-19. Patients should have regular monitoring of QT interval. Patients with HF and nCOVID-19 are at increased risk of thrombosis. Patients with HF, who are already on oral anticoagulants (OAC), should be continued on anticoagulants during the entire duration of hospitalization. In hospitalized HF patients who are not on OAC, prophylactic anticoagulation should be started. Continued delivery of HF care to patients should be ensured by using telemedicine. All HF patients should be immunized against seasonal viral infections to boost their immune status.
nCOVID-19 predisposes to a hypercoagulable state. All patients admitted with COVID-19 should be started on low molecular weight heparin prophylaxis. Patients with elevated D-dimer levels should be initiated on enoxaparin 1 mg/kg twice daily. Patients admitted to ICU may require continuous heparin infusion to maintain APTT in the therapeutic range of 60–90. Patients already on OACs must continue their drugs without any discontinuation.
Patients should continue antihypertensive drugs without any discontinuation/change as fluctuations in blood pressure may be deleterious. Recently concerns were raised about intake of ACEI/ARB in connection with possibility of increasing susceptibility to viral infection due to effect on ACE 2. There are no conclusive data at present to suggest that these drugs predispose individuals to more severe viral infection. On the contrary, some believe that the use of ACEI/ARB may be helpful in reducing the severity of the target organ damage from nCOVID-19. The ESC Hypertension Council has stated in a position statement that the use of antihypertensive drugs including ACEI/ARB should be continued in patients and there is no evidence pointing toward harmful effect of ACEI/ARB.
Implementation of infection prevention and control measures
Along with the management of diseases, prevention of infection spread and reducing exposure to health-care workers is also necessary.
- Patients in outpatient departments should be screened for fever before entry. There should be adequate distancing between patients in the waiting area. Doctors should wear appropriate protective equipment while examining outpatients
- Echocardiograms should be performed in patients where they are likely to help in diagnosis or alter the management plan. Transesophageal echocardiograms have high risk of aerosol generation and should be used only in very special circumstances. Echocardiograms of suspected/positive patients may be performed in isolated rooms and specific echocardiography machines may be kept dedicated for this sole purpose. Focused examination needs to be done which includes necessary views to make the diagnosis while ensuring that no important detail is missed. Doctors need to wear appropriate personal protective equipment (PPE) while doing echocardiograms especially transesophageal echocardiography
- In the cardiac catheterization lab, all personnel are required to don PPE. Use of powered air-purifying respirator system is recommended in cases where the patient is vomiting and is hemodynamically unstable. Cath labs need to undergo terminal clean up after every procedure to prevent any cross infection
- In critical patients, the threshold for intubation should be low so as to avoid any emergency intubation in the catheterization lab which produces significant exposure to health-care staff. Open circuit suctions should be avoided as it generates lots of aerosol. Cardiopulmonary resuscitation may also be initiated only in those patients who are likely to recover as it is an aerosol-generating procedure and can cause widespread exposure to health-care staff.
| Conclusion|| |
nCOVID-19 has been a deadly pandemic with a high mortality rate. Patients with preexisting comorbidities are predisposed to infection and poorer outcomes. Patients with CVDs need to be managed while ensuring the safety of health-care providers and preventing nosocomial spread. Strict infection prevention and control measures will help to prevent the spread of infection and reduce disease incidence.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Guan WJ, Ni ZY, Hu Y, Liang WH, Ou CQ, He JX, et al
. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med 2020;382:1708-20.
Yang J, Zheng Y, Gou X, Pu K, Chen Z, Guo Q, et al
. Prevalence of comorbidities and its effects in patients infected with SARS-CoV-2: A systematic review and meta-analysis. Int J Infect Dis 2020;94:91-5.
Kassiri Z, Zhong J, Guo D, Basu R, Wang X, Liu PP, et al
. Loss of angiotensin-converting enzyme 2 accelerates maladaptive left ventricular remodeling in response to myocardial infarction. Circ Heart Fail 2009;2:446-55.
Oudit GY, Kassiri Z, Jiang C, Liu PP, Poutanen SM, Penninger JM, et al
. SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS. Eur J Clin Invest 2009;39:618-25.
Basu R, Poglitsch M, Yogasundaram H, Thomas J, Rowe BH, Oudit GY. Roles of angiotensin peptides and recombinant human ACE2 in heart failure. J Am Coll Cardiol 2017;69:805-19.
Bangalore S, Sharma A, Slotwiner A, Yatskar L, Harari R, Shah B, et al
. ST-segment elevation in patients with Covid-19-A case series. N Engl J Med 2020;382:2478-80.
Stefanini GG, Montorfano M, Trabattoni D, Andreini D, Ferrante G, Ancona M, et al
. ST-elevation myocardial infarction in patients with COVID-19: Clinical and angiographic outcomes. Circulation 2020;141:2113-6.
Choudry FA, Hamshere SM, Rathod KS, Akhtar MM, Archbold RA, Guttmann OP, et al
. High thrombus burden in patients with COVID-19 presenting with ST-segment elevation myocardial infarction. J Am Coll Cardiol 2020;76:1168-76.
Loghin C, Chauhan S, Lawless SM. Pseudo-acute myocardial infarction in a young COVID-19 patient. JACC Case Rep 2020;2:1284-8.
Shi 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.
Guo 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.
Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D, et al
. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:819-24.
Tavazzi G, Pellegrini C, Maurelli M, Belliato M, Sciutti F, Bottazzi A, et al
. Myocardial localization of coronavirus in COVID-19 cardiogenic shock. Eur J Heart Fail 2020;22:911-5.
Minhas AS, Scheel P, Garibaldi B, Liu G, Horton M, Jennings M, et al
. Takotsubo syndrome in the setting of COVID-19 infection. Am Coll Cardiol Case Rep 2020;2:1321-5.
Wang 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.
Siripanthong B, Nazarian S, Muser D, Deo R, Santangeli P, Khanji MY, et al
. Recognizing COVID-19-related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management. Heart Rhythm 2020;17:1463-71.
Hua A, O'Gallagher K, Sado D, Byrne J. Life-threatening cardiac tamponade complicating myo-pericarditis in COVID-19. Eur Heart J 2020;41:2130.
Danzi GB, Loffi M, Galeazzi G, Gherbesi E. Acute pulmonary embolism and COVID-19 pneumonia: A random association? Eur Heart J 2020;41:1858.
Bonow RO, Fonarow GC, O'Gara PT, Yancy CW. Association of coronavirus disease 2019 (COVID-19) with myocardial injury and mortality. JAMA Cardiol 2020;5:751-3.
Ferreira VM, Schulz-Menger J, Holmvang G, Kramer CM, Carbone I, Sechtem U, et al
. Cardiovascular magnetic resonance in nonischemic myocardial inflammation: Expert recommendations. J Am Coll Cardiol 2018;72:3158-76.
Huang L, Zhao P, Tang D, Zhu T, Han R, Zhan C, et al
. Cardiac involvement in patients recovered from COVID-2019 identified using magnetic resonance imaging. JACC Cardiovasc Imaging 2020;13:2330-9.
Puntmann VO, Carerj ML, Wieters I, Fahim M, Arendt C, Hoffmann J, et al
. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:1265-73.
Ojha V, Verma M, Pandey NN, Mani A, Malhi AS, Kumar S, et al
. Cardiac magnetic resonance imaging in coronavirus disease 2019 (COVID-19): A systematic review of cardiac magnetic resonance imaging findings in 199 patients. J Thorac Imaging 2021;36:73-83.
Yu B, Li X, Chen J, Ouyang M, Zhang H, Zhao X, et al
. Evaluation of variation in D-dimer levels among COVID-19 and bacterial pneumonia: A retrospective analysis. J Thromb Thrombolysis 2020;50:548-57.
Tam CF, Cheung KS, Lam S, Wong A, Yung A, Sze M, et al
. Impact of coronavirus disease 2019 (COVID-19) outbreak on ST-segment-elevation myocardial infarction care in Hong Kong, China. Circ Cardiovasc Qual Outcomes 2020;13:e006631.
Welt FG, Shah PB, Aronow HD, Bortnick AE, Henry TD, Sherwood MW, et al
. Catheterization laboratory considerations during the coronavirus (COVID-19) pandemic: From the ACC's Interventional Council and SCAI. J Am Coll Cardiol 2020;75:2372-5.
Chopra HK, Hiremath SM, Wander GS, Kumar AS, Naik S. Consensus on STEMI management in the era of COVID-19. J Assoc Physicians India 2020;68:76-81.
Truesdell M, Guttman P, Clarke B, Wagner S, Bloom J, DuShane J, et al
. Conversion of positive-pressure cardiac catheterization and electrophysiology laboratories to a novel 2-zone negative-pressure system during COVID-19 pandemic. J Cardiovasc Electrophysiol 2020;31:1901-3.
DeFilippis EM, Reza N, Donald E, Givertz MM, Lindenfeld J, Jessup M. Considerations for heart failure care during the COVID-19 pandemic. JACC Heart Fail 2020;8:681-91.
Atallah B, Mallah SI, AlMahmeed W. Anticoagulation in COVID-19. Eur Heart J Cardiovasc Pharmacother 2020;6:260-1.
Bozkurt B, Kovacs R, Harrington B. Joint HFSA/ACC/AHA statement addresses concerns Re: Using RAAS antagonists in COVID-19. J Card Fail 2020;26:370.
Kirkpatrick JN, Mitchell C, Taub C, Kort S, Hung J, Swaminathan M. ASE statement on protection of patients and echocardiography service providers during the 2019 novel coronavirus outbreak: Endorsed by the American College of Cardiology. J Am Soc Echocardiogr 2020;33:648-53.
[Figure 1], [Figure 2]