The mechanisms underlying myocardial injury in those with COVID-19 infection are not fully understood, however in keeping with other severe respiratory illnesses, direct ("non-coronary") myocardial damage is almost certainly the most common cause.

Given the presence of abundant distribution of ACE2 – the binding site for the SARS-CoV-2 in cardiomyocytes – some have postulated that myocarditis might be a common cause.

Support for this comes from reports of COVID-19-related acute left ventricular failure. Other possibilities include acute MI – either Type 1 MI based on plaque rupture triggered by the infection or Type 2 MI based on supply-demand inequity.

Importantly, a rise and/or fall of troponin is insufficient to secure the diagnosis of acute MI; rather, it should be based on clinical judgment, symptoms and signs, and ECG changes.

Given the frequency and nonpecific nature of abnormal troponin results among patients with COVID-19 infection, clinicians are advised to only measure troponin if the diagnosis of acute MI is being considered on clinical grounds.

In addition, an abnormal troponin should not be considered evidence for an acute MI without corroborating evidence.

Use of echocardiography or coronary angiography for COVID-19 patients with myocardial injury or elevated troponin should be restricted to those in whom additional diagnostics would meaningfully affect clinical outcomes.

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Patients with COVID-19 infection often demonstrate significant elevation of BNP or NT-proBNP levels. The significance of this finding is uncertain and should not trigger an evaluation or treatment for heart failure unless there is clear clinical evidence for the diagnosis.

Use of echocardiography or coronary angiography for COVID-19 patients with myocardial injury or elevated natriuretic peptides should be restricted to those in whom additional diagnostics would meaningfully affect clinical outcomes.

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• The renin-angiotensin-aldosterone system (RAAS) plays a key role in the pathophysiology of hypertension, heart failure and kidney disease.
• SARS-CoV-2, the virus that causes COVID-19, appears to infect human cells via the ACE-2 (angiotensin converting enzyme 2) receptor.
• ACE-2 plays a key role in the regulation of the RAAS and mediates the breakdown of angiotensin I and II to inactivated proteins (angiotensin 1-9 and angiotensin 1-7, respectively).
• Pharmacologic RAAS inhibition with ACE inhibitors or angiotensin receptor blockers (ARBs) may increase ACE-2 levels and thus raise theoretical safety concerns in treated COVID-19 patients, available here.
• No studies to date have prospectively evaluated the impact of RAAS inhibition in COVID-19 patients.
• While there is inconsistent data on clinical outcomes with RAAS inhibition among hospitalized COVID-19 patients, some recent studies suggest a protective effect with lower morbidity and mortality rates, available here.
• Several clinical trials are underway to evaluate the effect of RAAS modulation (recombinant ACE-2 and losartan) on outcomes in COVID-19 patients.
• Until more data are available, RAAS inhibitors should be continued in clinically stable COVID-19 patients and follow recommendations published by the American College of Cardiology, American Heart Association, and the Heart Failure Society of America and the European Society of Cardiology Council on Hypertension.

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One randomized trial suggested possible beneficial effects of initiating oral statin therapy for intubated pneumonia cases; another trial did not find benefit.

Nonetheless, these findings have been used to hypothesize a potentially beneficial effect of statins for patients with MERS-COV (and other beta coronaviruses like SARS-CoV-2). Currently no randomized or observational evidence to supports these conjectures.

Importantly, however, statins do not appear to be harmful in this setting.

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• Point-of-care ultrasound (POCUS) may be advisable for COVID+ patients because it allows in-room patient evaluation while minimizing staff exposure.
  
  When possible, pre-plan procedures, including the use of ultrasound enhancing agent (UEA), to rapidly acquire the most relevant sequence of images. UEA have been proved safe and effective in ICU patients.
  
  Archiving and transmitting images to experienced echocardiographers may obviate the need for additional echoes and/or accurately guide the clinical need for advanced imaging (e.g., wall motion, quantitative valvular assessment, etc.).
• Contrast enhanced computed tomography and MR should be considered as alternatives to aerosol-inducing TEE for exclusion of left atrial appendage thrombus prior to cardioversion.
• Consider deferring stress echoes or utilizing an alternative modality given the additional transmission risk associated with deep breathing and potential cough.
• As with all procedures, special attention should be given to matching PPE with risk and rigorously cleaning and disinfecting equipment between patients.

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Telephone visits should be maintained and will be reimbursed if patients cannot or do not wish to use video technology.

Encounters with noninfected older adults during the pandemic should focus on disease prevention and COVID-19 preparation.

1. Safeguarding measures should be reiterated at every opportunity, and clinicians should utilize the teach-back method to ensure understanding.
2. Direct encounters with high-risk older adults should be proactively avoided by clinicians if they have recent significant COVID exposure despite lack of symptoms.
3. All relevant guideline-directed medication therapy should be continued in the absence of contraindications; it is reasonable to consider initiating statin therapy according to ACC guidelines.
4. The importance of maintaining nutrition, hydration and daily exercise despite social isolation measures should be emphasized.
5. Older adults should be instructed to identify a healthy, low risk, trusted point-of-contact with whom physicians can maintain communication.
6. All older adults should be strongly encouraged to prepare advance directives and clarify religious preferences prior to potential SARS-CoV-2 infection in order to make treatment decisions at the time of potential illness concordant with their goals.

COVID-19 disease management in older adults should be individualized as older adults are heterogeneous with respect to health status and resiliency; chronologic age alone should not determine management strategy.

1. Pharmacologic management for eligible older adults should follow guidelines outlined by the CDC. In particular, the efficacy of hydroxychloroquine and chloroquine remain unproven and optimally should be administered within clinical research protocols and monitored carefully given the increased QT prolongation risk.
2. Patients should be informed that hospitalization and recovery will be challenging given isolation requirements.
3. Patients should be instructed to identify a caregiver to assist in recovery if sent home, and prepare means to maintain social connections (e.g., FaceTime, family chat rooms, etc.) to help ease the emotionally challenging experience of isolated recovery in a skilled nursing facility.
4. Finally, older adults should be encouraged to participate in clinical trials pertaining to COVID-19 management if feasible.

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However, chloroquine, hydroxychloroquine and azithromycin all prolong the QT interval, raising concerns about the risk of arrhythmic death from individual or concurrent use of these medications.

We strongly encourage enrollment of patients in clinical research protocols, whenever available.

All clinical use that occurs outside of a research setting should incorporate anticipated benefits balanced against risks. As additional research results become available, recommendations for QT monitoring may escalate or de-escalate.

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These include minimizing face-to-face contact between employees, assigning work tasks that allow the patient to maintain six-foot distance from other workers, customers and visitors, or to telework if possible.

For patients who work in health care settings, avoidance of direct COVID-19 patient exposure should be attempted.

In addition, they should be assured of adequate personal protective equipment appropriate to their work environment. Please refer to the CDC recommendations regarding workplace accommodations, found here.

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High D-dimer levels appear to predict a poor prognosis in COVID-19 patients, although the relationship between elevated D-dimer levels and mortality has been shown in previous cohorts of critically ill patients.

Therapeutic anticoagulation is not mandatory for all patients based only on an elevated D-dimer test and there is no evidence supporting use of D-dimer values to guide intensity of anticoagulation.

However, D-dimer values may be helpful for clinical monitoring, characterizing the coagulopathy, and conducting clinical trials to rigorously test management strategies.

Use of higher-intensity, non-standard VTE prophylaxis can be considered for patients with COVID-19, but ideally should be done within the context of a clinical trial given current lack of efficacy evidence.

Assessment for VTE should incorporate multiple elements of the patient condition, including interval history, physical exam and vital signs, currently administered treatments, and laboratory studies.

The decision to order imaging for VTE should not be based on an elevated D-dimer alone. Targeted imaging to confirm suspected VTE and guide therapeutic anticoagulation is preferred if it can be performed with acceptable exposure risk.

Post-hospital VTE prophylaxis should be considered in patients with COVID-19 given the long duration of the illness and the increased likelihood of immobility and superinfection.

Experience from several studies suggests that in select patients without COVID-19, post-discharge thromboprophylaxis (particularly with a DOAC) may be beneficial if bleeding risk can be minimized.

Use of a validated risk score (e.g., IMPROVE or IMPROVEDD score with D-dimer) may be particularly helpful in guiding decision-making.

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Nonetheless, most AMI cases in the U.S. remain COVID- and should be managed for expedient revascularization according to standard PCI protocols.

Fibrinolysis-based reperfusion strategy may be appropriate in non-PCI capable hospitals, especially when timely transfer is not practical, or when otherwise clinically indicated.

• AMI standard-of-care during COVID-19: All efforts should be made to maintain the current AMI standard-of-care. Door-to-balloon times remain important and should continue to be measured, however additional time may be required for careful clinical differentiation of both COVID status and precise MI etiology to minimize exposure risk and ensure the appropriate therapeutic intervention.
  
  AMI management protocols in the context of pandemic COVID-19 should be developed in advance, and include EMS, the ED, and the cardiac catheterization laboratory. Dedicated COVID-19 CCLs and PPE should be available in geographies with widespread community transmission.
• Definite STEMI: Primary PCI within 90 minutes remains the standard-of-care in PCI capable hospitals regardless of COVID status. Additional exposure precautions are mandatory in probable and confirmed COVID-19 patients, but may be considered for all cases given asymptomatic presentation and the potential for false-negative COVID test results.
• Possible STEMI: For patients who have an unclear, or equivocal, diagnosis of STEMI due to atypical symptoms, diffuse ST-segment elevation or atypical ECG findings, or a delayed presentation, additional noninvasive evaluation in the ED is recommended.
  
  The focus of this evaluation is further risk stratification for COVID-19 status and further evaluation of the potential for coronary thrombotic occlusion versus other pathologies.
• Futile prognosis: Not all COVID-19 patients with ST elevation with/without an acute coronary occlusion will benefit from any reperfusion strategy or advanced mechanical support.
  
  In COVID-19 confirmed patients with severe pulmonary decompensation (adult respiratory distress syndrome) or pneumonia who are intubated in the ICU and felt to have an excessively high mortality, consideration for compassionate medical care may be appropriate.
• Non-STEMI capable referral hospitals: Primary PCI remains the standard of care for patients transferred rapidly from non-PCI centers (within 120 minutes of first medical contact at Referral Hospital).
  
  For patients in whom rapid reperfusion with primary PCI is not feasible, a pharmacoinvasive approach is recommended with initial fibrinolysis followed by consideration of transfer to a PCI center.
  
  The COVID status of the individual patient, along with the COVID burden at both the referring and receiving hospital may require modifications to this standard.
• Cardiogenic shock and/or out-of-hospital cardiac arrest: Patients with resuscitated out-of-hospital cardiac arrest (OHCA) and/or cardiogenic shock will continue to be the highest risk subgroup of AMI patients.
  
  These patients will also be the highest risk for droplet-based spread of COVID-19. Patients with resuscitated OHCA should be selectively considered for CCL activation in the presence of persistent ST-elevation on their electrocardiogram, and a concomitant wall motion abnormality on echocardiographic evaluation.
• Non-ST elevation AMI: Standard of care to both COVID positive and negative patients. COVID-19 positive or probable patients with an NSTEMI presentation should be managed medically and only taken for urgent coronary angiography and possible PCI in the presence of high-risk clinical features (Global Registry of Acute Coronary Events [GRACE] score >140) or hemodynamic instability.

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In severe COVID-19 cases, cardiomyopathy may result from SARS-CoV-2-induced myocarditis, profound systemic inflammation, and/or microvascular dysfunction.

There is currently very little data to guide the optimal management of patients with COVID-19 disease who develop cardiomyopathy or mixed/cardiogenic shock.

Cardiac imaging may be useful, but only when testing is likely to result in differential management and exposure risk can be adequately mitigated.

• In patients hospitalized with COVID-19 cardiac biomarkers should be checked on admission and in follow-up approximately 24-48 hours later.
• Myocarditis or inflammatory cardiac dysfunction should be considered in patients with COVID-19 who have elevated cardiac biomarkers and worsening hemodynamics or arrhythmias.
• ECG should be employed to screen for evidence of ST-T wave changes.
• Maintain a low threshold for POCUS in patients with the above clinical features.
• If evidence of cardiac dysfunction, consider select view for transthoracic echocardiography (TTE) to define LV/RV size and function, wall motion abnormalities, and/or pericardial effusion.
• Stable patients with suspected cardiovascular involvement should continue on guideline-directed medical therapy for heart failure.
• In patients with refractory shock, consider pulmonary artery catheters to help guide the use of inotropes, vasopressors or mechanical support.
• Endomyocardial biopsy may have a role in select patients being considered for clinical trials of anti-inflammatory therapy.

The mainstay of managing patients with severe COVID-19 disease who have cardiac involvement is supportive care.

There is currently no evidence to direct the management of these patients differently than any other inflammatory or "mixed" shock state.

Experimental strategies including antiviral, anti-inflammatory, convalescent sera are being considered as part of research protocols or compassionate use for COVID-19 infection with or without cardiac involvement.

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• In case series, patients with hypertension and COVID-19 infection have higher rates of morbidity and mortality.
• Many hospitalized COVID-19 patients are older with multiple comorbidities; there is no clear evidence of a causal link between hypertension and COVID-19-related morbidity and mortality.
• Hypertension remains the greatest modifiable risk factor for atherosclerotic cardiovascular disease.
• Clinicians should continue to follow the 2017 ACC/AHA blood pressure management guidelines to reduce long-term cardiovascular risk associated with hypertension, available here.

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• Home-based cardiac rehabilitation (HBCR) may serve as a viable alternative during the COVID-19 pandemic; studies demonstrate HBCR to be beneficial in terms of exercise capacity and modifiable cardiovascular risk factor improvement, including blood pressure and LDL-C control.
• A recent AACVPR/AHA/ACC Scientific Statement on HBCR concluded that HBCR may be a reasonable option for clinically stable, low-to-moderate risk patients unable to attend conventional cardiac rehab, available here.
• The AACVPR has identified a number of viable options for HBCR, ranging from standalone apps to device-integrated programs that can monitor blood pressure, ECG and other physiological data, available here.
• For those at higher risk, a hybrid model which leverages the complementary aspects of both clinic-based CR and HBCR may be most desirable.
• Limited reimbursement represents an ongoing challenge; at present, HBCR is not a covered service under expanded Centers for Medicare and Medicaid Services telehealth rules.

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• An increasing number of mobile health (mHealth) options exist to assist patients in achieving healthful behaviors and lifestyle, both in primary and secondary prevention of heart disease, available here.
• Formal telehealth, however, should not be forgotten. Codes are currently available for medical nutrition therapy (97802, 97903, 97804), behavioral counseling for obesity (G0447 [HCPCS code]), intensive behavior therapy for cardiovascular disease (G0446 [HCPCS code]), and smoking and tobacco cessation counseling (99406, 99407).
• Referral to psychiatric services should be considered for patients with a potential mental health crisis or mental health diagnosis.

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• While most cardiovascular clinicians are use to remote monitoring for patients with cardiovascular implantable electronic devices (e.g., pacemakers, ICDs), different RPM codes are likely to be helpful in cardiovascular prevention (99453, 99454, 99457 and 99458).
• 99453—Remote monitoring of physiologic parameters, such as weight, blood pressure, etc. This is the code for initial set-up and patient education related to the monitoring equipment.
• 99454—Device supply with daily recording or programmed alert transmission every 30 days. This is the code for collection, transmission and report/summary to the clinician managing the patient.
• 99457—Remote physiologic monitoring with >20 minutes of clinical staff/physician/other qualified health care professional time spent in interactive communication with the patient/caregiver during the month. This is the code for interpretation of the received data and interaction with the patient to arrive at a treatment plan.
• 99458—Additional 20 minutes of add-on time to 99457.
• Importantly, these codes require that 1) patient consent be obtained in advance of the service with documentation of this in the patient's record and 2) billing is limited to one time in a 30-day period.

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2. Does treatment for COVID-19 affect the use of antiarrhythmic medications for AFib?
   Drugs like chloroquine, hydroxychloroquine, azithromycin, lopinavir and ritonavir used in the management of COVID-19 can prolong the QT interval, available here. The effect of remdesivir on the QT interval is unknown. AFib patients on antiarrhythmic agents like dofetilide, sotalol, amiodarone and dronedarone need careful monitoring of the QT interval. When there is significant QT prolongation and COVID treatment is warranted, stopping antiarrhythmic medication is reasonable if clinical circumstances allow. Lopinavir-ritonavir combination increases serum amiodarone (U.S. Food and Drug Administration labeling recommends caution and monitoring of serum amiodarone levels), digoxin and flecainide levels. Similarly, chloroquine and hydroxychloroquine can increase serum amiodarone, digoxin and flecainide levels to a lesser extent. Sotalol and dofetilide may need dosing adjustments in COVID-19 patients with acute kidney injury, available here.
3. Does treatment for COVID-19 affect anticoagulation for AFib?
   Lopinavir-ritonavir combination (combined P-glycoprotein/strong CYP3A4 inhibitor) can potentially reduce warfarin levels and increase apixaban, rivaroxaban and edoxaban levels. FDA labelling suggests reducing apixaban dose to 2.5 mg twice daily if used concomitantly with lopinavir-ritonavir combination. Consider switching to alternate agents (preferably heparin or enoxaparin). Chloroquine and hydroxychloroquine can increase serum apixaban, dabigatran, rivaroxaban and edoxaban levels. Close clinical monitoring is required. Apixaban, dabigatran, edoxaban and rivaroxaban may need dosing adjustment in COVID-19 patients with acute kidney injury, available here.
4. How do you treat AFib in COVID-19 positive patients?
   Where possible, a rate control strategy is preferable, especially in critically ill patients who can tolerate these medications. When anticoagulation is indicated, use of heparin or enoxaparin is preferable in patients where chloroquine, hydroxychloroquine, lopinavir/ritonavir use is anticipated. Antiarrhythmic drugs should be used with caution due to the risk of QT prolongation and drug-drug interactions with the above-mentioned agents.
5. Should my treatment approach for AFib change with the COVID-19 crisis?
   The treatment approach for AFib should be tailored to the individual patient based on a multitude of factors including severity of symptoms, underlying comorbidities and prevalence of COVID-19 in the community. It would be best to avoid elective procedures for AFib if the procedure can be safely deferred to a later date. A recent guidance document published outlines triaging of these procedures in various clinical scenarios, available here.
6. What strategies can be used to manage patients with AFib who are unable to undergo cardioversion or ablation due to the COVID-19 crisis?
   Rate control strategy should be maximized first, where possible. In patients with significant symptoms where no contraindications exist, antiarrhythmic agents such as flecainide and amiodarone can be instituted on an outpatient basis.

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