key: cord-1026635-nun9nh9k
authors: DeFilippis, Ersilia M.; Reza, Nosheen; Donald, Elena; Givertz, Michael M.; Lindenfeld, JoAnn; Jessup, Mariell
title: Considerations for Heart Failure Care During the Coronavirus Disease 2019 (COVID-19) Pandemic
date: 2020-06-03
journal: JACC Heart Fail
DOI: 10.1016/j.jchf.2020.05.006
sha: fb00574e5acdc7da74d23d98e209141349b721fd
doc_id: 1026635
cord_uid: nun9nh9k

Abstract The coronavirus disease 2019 (COVID-19) pandemic has affected the care of patients with HF who contract COVID-19 as well as those without COVID-19 who have been impacted by the restructuring of health care delivery. Patients with HF and other cardiovascular comorbidities are at risk for severe disease and complications of infection. Similarly, COVID-19 has been demonstrated to cause myocarditis and may be implicated in new-onset cardiomyopathy. During this pandemic, special considerations are needed for patients with advanced HF, including those supported by durable left ventricular assist devices (LVADs) and heart transplant recipients. The purpose of this review is to summarize emerging data regarding the development of HF secondary to COVID-19, COVID-19 infection in patients with advanced HF, and the implications of the pandemic on care for non-infected patients with HF.

Since the earliest cases of coronavirus disease 2019 (COVID- 19) were reported (1), our care delivery systems have been reorganized and challenged in unprecedented ways. Patients with underlying cardiovascular conditions, including heart failure (HF), are at risk for severe infection and complications (2, 3) . Special considerations are needed for patients with advanced HF, including those supported by durable left ventricular assist devices (LVADs) and heart transplant (HT) recipients. This review aims to summarize emerging data regarding the development of HF secondary to COVID-19, COVID-19 infection in patients with advanced HF, and the implications of the pandemic on care delivery for non-infected patients with HF.

COVID-19 may cause or worsen HF through a variety of mechanisms including myocardial ischemia or infarction, increased oxygen demand, elevations in pulmonary pressures, pulmonary embolism, myocarditis, stress cardiomyopathy, and diffuse cytokine release (4) (Figure 1) .

These may concurrently lead to arrhythmias, cardiogenic shock, and sudden cardiac death (2, 5) .

Patients with COVID-19 are at higher risk for thrombosis in the arterial and venous circulations due to endothelial dysfunction, inflammation, oxidative stress, and platelet activation (6) . Acute coronary syndromes with plaque rupture leading to type I myocardial infarction may occur in this setting (6) . Hypoxemic respiratory failure and increased myocardial oxygen demand may lead to oxygen supply-demand mismatch and precipitate type 2 myocardial infarction (4) . Both may trigger decompensation of pre-existing HF or development of de novo acute HF. Right ventricular failure can also develop secondary to elevated pulmonary pressures in the setting of ARDS and/or pulmonary embolism (7) .

COVID-19-associated myocarditis has been demonstrated by visualization of COVID-19 viral particles on endomyocardial biopsy and detection of diffuse myocardial edema on cardiac magnetic resonance imaging (MRI) (8, 9) . Attempted myocarditis treatment strategies have included lopinavir/ritonavir, hydroxychloroquine, systemic glucocorticoid therapy, and intravenous immunoglobulin (9, 10) .

Some data suggest that cardiomyopathy may not be uncommon in patients with COVID-19. In a U.S. report of 21 patients with severe COVID-19 disease, 7 (33%) developed cardiomyopathy, which was defined as newly decreased left ventricular systolic function with one of the following: 1) increased cardiac biomarkers, 2) decreased central venous oxygen saturation, or 3) clinical signs of shock (11) . In another cohort of patients with COVID-19 from China, HF developed in 41/83 (49%) of those who died compared to 3/94 (3%) of those who recovered (12) . Among those who developed HF, approximately 50% did not have a pre-existing history of hypertension or cardiovascular disease.

The underlying mechanisms for these cardiomyopathies are difficult to elucidate given inpatient diagnostic testing limitations. For example, the true prevalence of myocarditis secondary to COVID-19 may be hard to determine without the use of definitive endomyocardial biopsies and routine cardiac imaging in a wide cohort of infected patients. Accordingly, the diagnosis of myocarditis is often made using elevations in biomarkers, echocardiography demonstrating reduction in systolic function, and/or worsening hemodynamics or arrhythmias.

Large registries like the American Heart Association (AHA) COVID-19 CVD registry (13) will help capture the prevalence of systolic dysfunction and incidence of myocardial recovery.

Ongoing studies will also explore the pathology of myocarditis and HF more broadly in SARS-CoV-2 infection (14) .

Patients with COVID-19 can develop a cytokine release syndrome with hyperinflammation leading to progressive shock and multiorgan failure. In patients with cardiac involvement, important questions remain regarding the use and efficacy of mechanical circulatory support.

Device insertion and maintenance require significant equipment, blood products, and personnel; health systems may have limited resources to deploy these therapies, particularly in older patients with other co-morbidities.

The Extracorporeal Life Support Organization has released guidance regarding the use of ECMO for patients with COVID-19 who develop severe cardiopulmonary failure (15) . They suggest that in resource-limited settings, younger patients without comorbidities and/or health care workers should be the highest priority for support. ECMO should rarely be used in older patients with significant comorbidities and multiorgan failure (15) .

Angiotensin converting enzyme inhibitors (ACEI), angiotensin II receptor blockers (ARBs), and angiotensin receptor neprilysin inhibitors (ARNI) are principal components of guideline-directed medial therapy for patients with chronic systolic HF. The SARS-CoV-2 virus, the causative viral agent for COVID-19, uses the ACE2 receptor for cell entry (Figure 2) , and concerns have been raised regarding this interaction with respect to disease virulence (16) . Large retrospective studies have since suggested that ACEI/ARB use are not associated with increased rates of COVID-19 infection or risk of severe disease (17, 18) .

A joint statement from the Heart Failure Society of America (HFSA), American College of Cardiology (ACC) and AHA recommends continuation of RAAS antagonists in patients who are prescribed these medications for HF or other cardiovascular indications (19) .

RAAS inhibition may have potential therapeutic benefit. Data from the Severe Acute Respiratory Syndrome (SARS) epidemic demonstrated that injection of SARS-CoV-1 into mice worsened acute lung failure, which was attenuated by renin-angiotensin-aldosterone-system (RAAS) blockade (20) . In pre-clinical studies, sacubitril-valsartan has been shown to reduce levels of proinflammatory cytokines, increase lymphocyte counts (21) , and inhibit expression of proinflammatory genes including interleukin-6, a potential therapeutic target in COVID-19 (22) .

Patients with HF have pre-existing risk factors for venous thromboembolism including possible stasis of blood in the legs, heart, and endothelial injury (23, 24) . Similarly, patients with ischemic cardiomyopathy and atrial fibrillation are at risk for arterial thrombosis (23) . In women with HF, additional thrombotic risks include oral contraceptive use, hormone replacement therapy, and breast cancer (25) . In patients with durable LVAD support who are already at increased risk for thrombosis, the effects of COVID-19 infection on the risk for stroke or pump thrombosis are currently unknown.

Patients with HF on anticoagulation who require admission for COVID-19 should be continued on such agents unless a strong contraindication exists. All hospitalized HF patients with COVID-19 without a pre-existing indication should receive prophylactic doses of anticoagulation (26) .

This and other therapeutic considerations are described in the Central Illustration.

Underlying pulmonary disease is common in patients with HF. Approximately 30% of such patients have chronic obstructive lung disease which independently increases their risk for hospitalization and mortality (27) . These patients may have pulmonary hypertension as a consequence of parenchymal lung disease in addition to elevated left ventricular filling pressures (28) . In patients with COVID-19, hypoxemic respiratory failure and ARDS can exacerbate pulmonary vasoconstriction and interstitial edema, worsening pulmonary hypertension even in patients without pre-existing lung disease (29) . In patients with pre-existing biventricular failure, further elevation in pulmonary pressures secondary to ARDS can worsen right ventricular function.

Patients with advanced HF including those on durable LVAD support have severely reduced functional capacity (30, 31) , as measured by peak VO2, and impaired ability to augment cardiac output in response to physiologic stressors. These factors collectively decrease their cardiopulmonary reserve.

Despite preliminary reports suggesting that hydroxychloroquine and azithromycin may improve Both agents have been associated with QT interval prolongation, increasing the risk for arrhythmias, including Torsades de Pointes, and sudden cardiac death (34, 35) . Patients with HF often have structural and electrical abnormalities leading to delayed ventricular repolarization and QT prolongation on the surface electrocardiogram (ECG) (36) . Prolonged QTc intervals are independent predictors of adverse outcomes in patients with HF (37) . Many patients with HF may be prescribed QT-prolonging drugs as well as loop diuretics that can lead to electrolyte abnormalities and increase the risk of serious arrhythmias (38) . Additional risk factors for QT interval prolongation in hospitalized patients include female sex, older age, sepsis, and a baseline QTc >450 milliseconds on admission (39) .

Systemic inflammation underlies both acute and chronic HF (40) . The hemodynamic stress of HF stimulates the release of pro-inflammatory cytokines including tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta (40) . Furthermore, co-existing co-morbidities such as obesity, type 2 diabetes, and hypertension may perpetuate a persistent inflammatory state leading to multiorgan involvement and endothelial dysfunction (40) . Inflammatory markers used to determine COVID-19 severity such as C-reactive protein, lactate dehydrogenase, NT-proBNP, and interleukin-6 may already be elevated in HF including patients on LVAD support (40) (41) (42) .

Therefore, values obtained in the setting of COVID-19 should be compared to prior values, if available.

Despite efforts to maintain social distancing, community spread of COVID-19 is increasing.

Patients with HF who self-quarantine may still be at risk for acquiring COVID-19 as they commonly have external nursing support. Advanced care planning is critical for all HF patients including populations on LVAD support and HT recipients, particularly for patients in areas with high COVID-19 prevalence. Ideally, clinicians should initiate these conversations with patients and their caregivers at the onset of their HF diagnosis, and not at the time of emergent hospitalization. For patients with HF who develop COVID-19 and require hospital admission, care teams should involve their HF specialists in conversations regarding goals of care, including the deactivation of implantable cardioverter-defibrillators (ICDs) (43) . Patients should be encouraged to have these discussions with their families even after admission, utilizing videoconferencing technology, as institutional visitor restrictions frequently limit the bedside presence of family members.

Patients on LVAD support who contract COVID-19 are at risk for severe viral infection due to older age, comorbidities, and immunosuppressed state. They suffer from compromised cellular immunity evidenced by aberrant T-cell activation, heightened susceptibility of CD4 T cells to spontaneous apoptosis, and cytokine imbalances (44) . This "functionally immunosuppressed state" increases susceptibility to complications from opportunistic infections (45) .

Cases of COVID-19 have been reported in patients on destination therapy LVAD support who developed ARDS and multiorgan failure with evidence of cytokine release syndrome (46, 47) .

Both cases highlighted the challenges of prone positioning in LVAD patients given concerns regarding increased right ventricular pressures and right ventricular failure. While International Society for Heart and Lung Transplantation (ISHLT) guidance suggests that LVAD patients can be "proned" for the management of hypoxemic respiratory failure (48) , more data are needed.

Respiratory viruses have been shown to cause rapid progression to pneumonia, greater disease severity, and prolonged viral shedding in solid organ transplant recipients (49) . Post-transplant patients are more likely to develop bacterial or fungal superinfection due to their immunocompromised state (49) . Although the anti-inflammatory effects of immunosuppressants may mitigate disease severity through reduction in cytokine production (50, 51) , past experience with SARS and MERS showed that clinical presentations of transplant patients were similar to the general population (2) . Notably, mTOR inhibitors have been associated with increased susceptibility to viral infections (52, 53) .

Cases of COVID-19 have been reported in HT recipients (54-56) ( Table 1) . Given their immunosuppressed states, presentations may be atypical, and high suspicion for COVID-19

illness should be maintained. In the largest report of 28 HT recipients with COVID-19, 79%

were hospitalized and 25% required mechanical ventilation (56) . Mycophenolate mofetil was discontinued in 70% and calcineurin inhibitors were reduced in 26% of patients. Seven patients (25%) died.

For HT patients with COVID-19 illness, transplant teams should consider dose reducing calcineurin inhibitors and reducing or holding antimetabolites. Drug interactions between immunosuppressants and COVID-19 therapeutics should be reviewed (57) . Leukopenia is common in patients with COVID-19, although it is typically manifest by lymphopenia rather than neutropenia (58) . This should be considered in newly transplanted patients on valganciclovir and mycophenolate, which can have similar myelosuppressive effects. In patients who develop allograft dysfunction, distinguishing rejection from viral myocardial involvement may be difficult, as availability of endomyocardial biopsies may be restricted (57) .

The reorganization of healthcare structures spurred by the COVID-19 pandemic has significantly affected patients with HF (Figure 3) . To reduce SARS-CoV-2 transmission and maintain a healthy workforce, health systems have largely transitioned to non-contact care delivery methods for ambulatory care. In response to these challenges, the Centers for Medicare and Medicaid

Response Supplemental Appropriations Act in early March 2020. Under the 1135 waiver, Medicare will pay for telehealth services provided in inpatient, outpatient, and home settings by a range of providers.

Types of covered services include telehealth visits during which an audiovisual telecommunication system is used; virtual check-ins, which are brief check-ins between patient and provider via telephone or another device to decide whether additional services are needed; and e-visits, which are communications between patients and providers through an online portal (59) . Commercial payers are also reimbursing for telehealth, however policies surrounding rates and payments are evolving. Penalties against providers for violations of the Health Insurance Portability and Accountability Act are also being waived, allowing the use of more commonly available telecommunications platforms.

The feasibility and safety of telemedicine for patients with HF is well established, however its use has not yet been reliably associated with reduction in emergency department visits or Therapeutic inertia in HF care is an ongoing risk during this period. Close monitoring of electrolyte and renal function is critical to safe dose adjustment of guideline directed therapies for HF with reduced ejection fraction and diuretics (61) . However, the reduction in available laboratory services during the pandemic and patients' hesitancy to risk COVID-19 exposure may limit up-titration of RAAS antagonists.

In addition to providing standard HF care, clinicians should regularly inquire regarding dietary and lifestyle habits related to COVID-19. Due to physical and social isolation and other stresses, changes in nutritional status, food availability, alcohol intake, physical activity, and social support may occur and contribute to worsening HF. This reliance on remote care has the potential to exacerbate preexisting health inequities (62) .

Disadvantaged populations, some underrepresented racial and ethnic groups, and those with limited access to the internet and/or smart devices may not derive benefit from the expansion of these innovations. Older adults, who comprise a significant portion of the U.S. population with HF, may have educational, visual, auditory, and cognitive impairments that hinder their participation in remote care. Programs should incorporate social workers and case managers to maximize outreach to these at-risk populations. The option for in-person clinic visits should remain available for patients without access to telemedicine services, high-risk patients (e.g. patients on continuous inotropes) or those for whom physical examination is critical for clinical decision-making. Aggressive risk reduction practices should be in place during these visits.

Programs may benefit from establishing triage principles for outpatient virtual versus in-person visits. Virtual visits may be best utilized for medication titration and optimization for stable patients with ACC/AHA Stage C HF. HT recipients on stable immunosuppression at low risk for allograft rejection and hemodynamically optimized LVAD patients may be managed remotely.

In-person visits should be considered for recently hospitalized patients, patients approaching Stage D HF, on continuous inotropes, undergoing evaluation for advanced HF therapies, who are newly post-LVAD implantation/HT, and those with new-onset HF. Virtual and in-person ambulatory schedules should be constructed to accommodate both routine and urgent visits.

Given uncertainty surrounding the future course of COVID-19, telemedicine is likely to endure as an important component of advanced HF disease management. Monitoring the safety and efficacy of remote care for HF and establishing evidence-based best practices for virtual visits should become a priority for HF programs.

Additional information regarding existing platforms, workflows, and care models for telemedicine in HF is provided in a recently published statement from the HFSA (60).

Under CDC guidance, risk mitigation strategies have included the postponement and cancellation of elective diagnostic and therapeutic procedures (6, 63) . For stable patients with advanced HF, these procedures include echocardiograms, stress testing, cardiopulmonary exercise testing, right heart catheterizations, coronary angiography, and implantation or interrogation of cardiac electronic devices among others. Individualized risk assessment is needed when classifying cases as elective. The rationale for delaying procedures should be reviewed with patients and documented in the medical record (64) .

Although delay of these procedures may not immediately affect clinical outcomes, there are important long-term and indirect implications for patients with HF (62) . Patients undergoing LVAD/HT evaluation may experience delays in listing and/or surgery leading to worsening nutritional, functional, or hemodynamic status. Completion of the evaluation process can highlight opportunities for optimization of pulmonary vascular resistance, renal function, weight, and adherence.

Centers are encouraged to consider local COVID-19 disease prevalence and resource availability when deliberating the timing of LVAD implantation. Limiting implantation to patients in INTERMACS (Interagency Registry for Mechanically Assisted Circulatory Support) profiles 1-3 is a reasonable approach at this time (48) . For HT patients > 3 months post-transplant, programs may defer routine surveillance endomyocardial biopsies in those with stable allograft function with low risk of rejection. For those in the more immediate post-transplant period or at higher rejection risk, the decision to perform surveillance biopsies should be weighed against the risk of COVID-19 exposure to patient and staff (48) .

The COVID-19 pandemic has had far-reaching implications for donor selection, organ procurement organizations, wait-list candidates, and transplant programs (57) . Given the limitations of current testing and risks for asymptomatic transmission and infection, the HT community must be careful to select uninfected donors. Globally, OPOs in Canada, Italy, Spain and others have performed universal screening for all deceased donors (65) , recognizing the false negative rates of these tests. In some cases, chest computed tomography may be performed as part of donor assessment to evaluate for radiographic evidence of COVID-19 (48) . Only negative COVID-19 donors should be considered.

According to ISHLT guidance, decisions regarding transplantation should be made at the transplanting center based on COVID-19 community prevalence and potential risks and benefits to the patient (48) . In institutions with a high burden of COVID-19, transplants are being reserved for patients in highest urgency statuses whose waitlist mortality risk supersedes the risk of nosocomial infection (57) .

Beginning the week of March 15, transplant programs were able to inactivate waitlisted patients as a COVID-19 precaution (66) . Weekly national and regional data is available from the United Network for Organ Sharing (66) . Evaluation of changes in transplant volumes and outcomes over time will be necessary to understand the implications of the COVID-19 pandemic on HT candidates and recipients.

There remains much to learn about the pathophysiology of COVID-19 in patients with HF.

Concurrently, we need robust health services research focused on elucidating the impacts of telemedicine, elective care deferral, and risk aversion behaviors being practiced by patients and providers during the pandemic. These research questions and others are described in Table 2 .

The economic upheaval caused by the COVID-19 pandemic has wide-ranging health consequences, especially for those who already suffer from socioeconomic deprivation. The national burdens of incident, prevalent, and undertreated HF will likely grow as a result of new COVID-19-related heart disease, delays in the recognition and treatment of ischemic heart disease, rising unemployment, and loss of income and health benefits for large segments of the population (62).

In spite of this devastation, the COVID-19 pandemic has given the HF community opportunities to explore alternative care delivery models, optimize ancillary support structures, and expand the infrastructure for home nursing, palliative care, and hospice services.

The COVID-19 pandemic has significantly impacted our patients with advanced HF, including the LVAD/HT population, and our care delivery systems. Over the coming months, anticipated and unforeseen challenges will arise as we manage the ramifications of this pandemic for our patients and the HF community. Potential contributing factors and mechanisms of worsening heart failure in patients with COVID-19 include increased oxygen demand, myocarditis, stress cardiomyopathy, ischemia or infarction, cytokine release syndrome, elevated pulmonary pressures, and venous thromboembolism.

The spike proteins of the SARS-CoV-2 virus bind to the ACE2 receptor, leading to viral entry, replication, and SARS-CoV-2 infection. ADAM17 facilitates shedding of ACE2 from the membrane leading to the release of the soluble form of ACE2. Soluble ACE2 may bind the virus and prevent binding to the membrane-anchored ACE2 on cells, preventing cell entry.

Reorganization of care delivery has resulted in increased access to telemedicine, adaptations to physical exam and laboratory data, and changes in procedural volume. BP = blood pressure; CRT = cardiac resynchronization therapy; GDMT = guideline-directed medical therapy; HIPAA = Health Insurance Portability and Accountability Act; JVD = jugular venous distension

Considerations for patients with COVID-19 who develop acute heart failure as well as patients with pre-existing heart failure are depicted. Presented with typical symptoms, did not require ICU admission, discharged on hospital day 12, repeat PCR testing negative *Heart-kidney recipient ARDS = acute respiratory distress syndrome; HCQ = hydroxychloroquine, ICU = intensive care unit; MMF = mycophenolate mofetil, PCR = polymerase chain reaction 

Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

Coronavirus Disease 2019 (COVID-19) and Cardiovascular Disease

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

Elevated Troponin in Patients With Coronavirus Disease 2019: Possible Mechanisms

Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the Coronavirus Disease

COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-up

Pulmonary Embolism in COVID-19 Patients: Awareness of an Increased Prevalence

Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection

Myocardial localization of coronavirus in COVID-19 cardiogenic shock

Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin

Characteristics and Outcomes of 21 Critically Ill Patients With COVID-19 in Washington State

Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study

The Role of Data Registries in the Time of COVID-19

Seeking Cardiac Tissue Samples from Myocarditis Patients for Assessing SARS-CoV2 and

Initial ELSO Guidance Document: ECMO for COVID-19 Patients with Severe Cardiopulmonary Failure

SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor

Cardiovascular Disease, Drug Therapy, and Mortality in Covid-19

Renin-Angiotensin-Aldosterone System Inhibitors and Risk of Covid-19

HFSA/ACC/AHA Statement Addresses Concerns Re: Using RAAS Antagonists in COVID-19

A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury

Neprilysin inhibitorangiotensin II receptor blocker combination (sacubitril/valsartan): rationale for adoption in SARS-CoV-2 patients

Receptor Blocker Combination Therapy (Sacubitril/valsartan) Suppresses Atherosclerotic Plaque Formation and Inhibits Inflammation in Apolipoprotein E-Deficient Mice

Venous Thromboembolism in Heart Failure Patients: Pathophysiology, Predictability, Prevention

Incident Heart Failure and Long-Term Risk for Venous Thromboembolism

Venous thromboembolism and women's health

ISTH interim guidance on recognition and management of coagulopathy in COVID 19

Diagnostic and Therapeutic Gaps in Patients With Heart Failure and Chronic Obstructive Pulmonary Disease

Pulmonary Hypertension Due to Left Heart Diseases

Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome

Hemodynamic Response to Exercise in Patients Supported by Continuous Flow Left Ventricular Assist Devices

Prognostic significance and measurement of exercisederived hemodynamic variables in patients with heart failure

Observational Study of Hydroxychloroquine in Hospitalized Patients with Covid-19

Hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19: a multinational registry analysis. The Lancet

Inpatient Use of Ambulatory Telemetry Monitors for COVID-19 Patients Treated with Hydroxychloroquine and/or Azithromycin

Risk of QT Interval Prolongation Associated With Use of Hydroxychloroquine With or Without Concomitant Azithromycin Among Hospitalized Patients Testing Positive for Coronavirus Disease 2019 (COVID-19)

Evaluation of Toxicity for Heart Failure Therapeutics: Studying Effects on the QT Interval

Prolonged QTc interval and high B-type natriuretic peptide levels together predict mortality in patients with advanced heart failure

Considerations for Drug Interactions on QTc in Exploratory COVID-19 (Coronavirus Disease 2019) Treatment

Development and validation of a risk score to predict QT interval prolongation in hospitalized patients

Inflammation in Heart Failure

The Inflammatory Response to

Markers of inflammation in recipients of continuous-flow left ventricular assist devices

Improving Communication in Heart Failure Patient Care

Cellular immunity impaired among patients on left ventricular assist device for 6 months

Activation-induced T-cell death and immune dysfunction after implantation of left-ventricular assist device

The Imperfect Cytokine Storm

Novel Coronavirus Disease 2019 in a Patient on Durable Left Ventricular Assist Device Support

Guidance from the International Society of Heart and Lung Transplantation regarding the SARS CoV-2 pandemic. International Society of Heart and Lung Transplantation

Novel Coronavirus-19 (COVID-19) in the immunocompromised transplant recipient: #Flatteningthecurve

Immunosuppression drug related and clinical manifestation of Coronavirus disease 2019: A therapeutical hypothesis

Impact of mycophenolic acid and tacrolimus on Th17-related immune response

Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in

mTOR inhibitors lower an intrinsic barrier to virus infection mediated by IFITM3

COVID-19 in solid organ transplant recipients: a single-center case series from Spain

First Cases of COVID-19 in Heart Transplantation From China

Characteristics and Outcomes of Recipients of Heart Transplant With Coronavirus Disease

Challenges in Heart Transplantation in the Era of COVID-19

Clinical features and short-term outcomes of 221 patients with COVID-19 in Wuhan

Virtual Visits for Care of Patients with Heart Failure in the Era of COVID-19: A Statement from the Heart Failure Society of America

ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

Secondary Impact of the COVID-19 Pandemic on Patients With Heart Failure

COVID-19)

Guidance for Cardiac Electrophysiology During the Coronavirus (COVID-19) Pandemic from the Heart Rhythm Society COVID-19 Task Force; Electrophysiology Section of the American College of Cardiology; and the Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology

COVID-19: A Global Transplant Perspective on Successfully Navigating a Pandemic

COVID-19 and solid organ transplant

COVID 19 in a High Risk Dual Heart and Kidney Transplant Recipient

Early Experience of COVID 19 in Two Heart Transplant Recipients: Case Reports and Review of Treatment Options

A Case of SARS CoV 2 pneumonia with successful antiviral therapy in a 77 year old male with heart transplant