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COVID-19: Evaluation and management of cardiac disease in adults

COVID-19: Evaluation and management of cardiac disease in adults
Author:
Alida LP Caforio, MD, PhD, FESC
Section Editor:
Donna Mancini, MD
Deputy Editor:
Todd F Dardas, MD, MS
Literature review current through: Nov 2022. | This topic last updated: Dec 02, 2020.

INTRODUCTION — The coronavirus disease of 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; previously referred to as 2019-nCoV). Patients with COVID-19 typically present with symptoms and signs of respiratory tract infection, but cardiac manifestations, including signs of myocardial injury, are common. This topic will discuss evaluation and management of cardiac disease in adults with COVID-19.

Cardiac manifestations in adults with COVID-19 are discussed separately. (See "COVID-19: Cardiac manifestations in adults".)

Some specific cardiac issues in adults with COVID-19 are discussed separately:

(See "COVID-19: Myocardial infarction and other coronary artery disease issues".)

(See "COVID-19: Arrhythmias and conduction system disease".)

Other clinical aspects of COVID-19 are discussed separately, including these and other topics:

(See "COVID-19: Clinical features".)

(See "COVID-19: Diagnosis".)

(See "COVID-19: Epidemiology, virology, and prevention".)

(See "COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension".)

(See "COVID-19: Management in hospitalized adults".)

(See "COVID-19: Management of the intubated adult".)

(See "COVID-19: Hypercoagulability".)

(See "COVID-19: Evaluation of adults with acute illness in the outpatient setting" and "COVID-19: Management of adults with acute illness in the outpatient setting".)

(See "COVID-19: Clinical manifestations and diagnosis in children".)

(See "COVID-19: Infection prevention for persons with SARS-CoV-2 infection".)

(See "COVID-19: Questions and answers".)

ROUTINE EVALUATION — The general routine evaluation of patients with COVID-19 or suspected COVID-19 includes cardiovascular elements.

Outpatient evaluation — Outpatient evaluation includes assessment of symptoms that may be caused by respiratory or cardiac disease, such as dyspnea, symptoms suggestive of hypoxia (eg, mental confusion), and known risk factors for more severe COVID-19, which include known cardiovascular disease (coronary artery disease, heart failure [HF], or cardiomyopathy), type 2 diabetes mellitus, and smoking, and possible risk factors for more severe COVID-19 including hypertension and type I diabetes mellitus. This evaluation is discussed separately. (See "COVID-19: Evaluation of adults with acute illness in the outpatient setting".)

Inpatient evaluation — The evaluation of patients hospitalized with COVID-19 includes elements of a cardiovascular evaluation, including assessment of known cardiovascular disease and risk factors for cardiovascular disease, assessment of symptoms that may be caused by respiratory or cardiac disease, laboratory testing (including a complete blood count and complete metabolic panel), chest radiograph, electrocardiogram (ECG), and troponin testing (which is followed if elevated). (See "COVID-19: Management in hospitalized adults", section on 'Evaluation'.)

Troponin — Troponin testing is commonly performed in hospitalized patients with COVID-19, as it may have prognostic value and may serve as a useful baseline for comparison in patients who develop manifestations of possible myocardial injury (such as HF or arrhythmia). Some experts also perform troponin testing in selected outpatients with uncertain level of risk. As mentioned above, among patients with COVID-19, troponin levels are most prevalent and most elevated with more severe disease [1,2]. (See "COVID-19: Cardiac manifestations in adults", section on 'Troponin'.)

An elevated troponin level is likely not indicative of an acute coronary syndrome in the absence of suggestive symptoms, signs, or ECG findings. Although peak troponin elevation is typically higher in patients with myocardial infarction (MI) than in patients with noncoronary myocardial injury, troponin levels in these clinical settings are overlapping [3]. The evaluation of COVID-19 patients for acute coronary syndrome is discussed separately. (See "COVID-19: Myocardial infarction and other coronary artery disease issues", section on 'Acute coronary syndrome patients'.)

ECG — A baseline ECG is generally performed in patients presenting for acute care with suspected symptomatic COVID-19. This enables documentation of baseline QRS-T morphology should the patient develop symptoms or signs of a type of myocardial injury such as an acute coronary syndrome or stress cardiomyopathy. Additionally, the baseline ECG allows for documentation of the QT (and corrected QTc) interval. Importantly, QTc will need to be monitored if QT-prolonging therapies are initiated (eg, azithromycin, chloroquine) to reduce the risk of acquired long QT syndrome. (See "COVID-19: Arrhythmias and conduction system disease", section on 'ECG' and "COVID-19: Arrhythmias and conduction system disease", section on 'Patients receiving therapies that prolong the QT interval' and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)

ECG abnormalities that have been reported in patients with COVID-19 and troponin elevation include T-wave depression and inversion, ST-segment elevation or depression, and Q waves [3-6]. When ST-segment elevation is present, diagnostic evaluation is required to distinguish MI from other causes of myocardial injury [3,5,6]. In a case series of 18 patients with COVID-19 with ST-segment elevation, MI was clinically diagnosed in eight (of which six underwent coronary angiography that confirmed obstructive coronary disease), with the remaining 10 diagnosed with noncoronary myocardial injury [3]. Four of the patients with MI and nine of the patients with noncoronary myocardial injury died in hospital. (See "COVID-19: Cardiac manifestations in adults", section on 'Electrocardiogram' and "COVID-19: Myocardial infarction and other coronary artery disease issues", section on 'ST-elevation myocardial infarction'.)

The most common arrhythmia in patients with COVID-19 is sinus tachycardia, but atrial fibrillation, atrial flutter, or ventricular tachycardia may occur. (See "COVID-19: Arrhythmias and conduction system disease".)

TARGETED CARDIAC EVALUATION

Indications — Targeted cardiac evaluation is indicated in selected patients with COVID-19 with one or more of the following: new-onset HF (including left HF and acute cor pulmonale), unexplained cardiac arrhythmias, or ECG changes (particularly ST elevation). The approach to cardiac evaluation in patients with known or suspected COVID-19 may differ from the standard approach to evaluation, as it is based upon weighing the following considerations [2]:

The likelihood that evaluation will change management and guide prognosis. Thus, it is important to identify a treatable cause of myocardial injury that requires timely intervention, such as acute MI. (See "COVID-19: Myocardial infarction and other coronary artery disease issues".)

Considerations of nosocomial infection control to limit the spread of disease.

Optimal management of limited available medical staff and resources to provide for the health care needs of the community.

Diagnostic approach — The diagnostic evaluation includes the following components (see "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Approach to diagnosis of myocarditis'):

Clinical evaluation includes history, physical examination, ECG, serum cardiac troponin levels, and initial laboratory tests to assess for symptoms and signs of HF and possible causes (including conditions unrelated to SARS-CoV-2 infection). (See 'Routine evaluation' above.)

Natriuretic peptide (B-type natriuretic peptide [BNP] or N-terminal pro-BNP) measurement is indicated if the diagnosis of HF is suspected. As described separately, natriuretic peptide levels are commonly elevated in hospitalized patients with COVID-19, particularly in patients with elevated cardiac troponin levels. (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Natriuretic peptide'.)

Decisions regarding the need for further evaluation are based upon whether test results will alter clinical management and guide prognosis.

If the clinical presentation is suggestive of acute coronary syndrome (ACS; including MI or unstable angina) based upon the presence of chest pain, other anginal symptoms, new HF, sudden cardiac arrest, and/or new ischemic ECG changes, timely evaluation is required to determine if urgent coronary angiography and intervention are indicated and to institute appropriate therapies. There is an elevated risk of ACS among patients with COVID-19 given the high prevalence of comorbidities in this patient population. Evaluation of coronary disease in patients with COVID-19 is discussed separately. (See "COVID-19: Myocardial infarction and other coronary artery disease issues" and "Diagnosis of acute myocardial infarction", section on 'When to suspect acute MI'.)

For patients with COVID-19 without suspected ACS, further cardiac testing is generally limited since specific diagnostic tests and treatments are not available for most of the noncoronary causes of myocardial injury in COVID-19 patients:

-Most patients with mild troponin elevation without symptoms and signs of acute HF can be clinically monitored without cardiac imaging.

-For patients who develop new-onset HF, an echocardiogram may be performed to evaluate regional and global ventricular and valvular function if this is requested by a consulting cardiologist and is expected to have a significant impact on management or is likely to change the patient's prognosis. Echocardiographic findings in patients with COVID-19 are discussed separately. (See "COVID-19: Cardiac manifestations in adults", section on 'Echocardiogram'.)

For patients with a ventricular motion abnormality, elevated troponin, and no ACS, possible diagnoses include stress cardiomyopathy, clinically suspected myocarditis, and acute cor pulmonale (along with multiple other causes of myocardial injury described separately). (See "COVID-19: Cardiac manifestations in adults", section on 'Myocardial injury' and "COVID-19: Cardiac manifestations in adults", section on 'Possible causes'.)

Stress cardiomyopathy commonly presents with features similar to those of ACS, so a diagnosis of stress cardiomyopathy generally requires coronary angiography to exclude ACS. In the setting of the COVID-19 pandemic, the likelihood of ACS requiring urgent intervention and availability of cardiac catheterization laboratory resources are considered in determining whether to proceed with coronary angiography. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Diagnosis' and "COVID-19: Myocardial infarction and other coronary artery disease issues", section on 'Acute coronary syndrome patients'.)

A diagnosis of stress cardiomyopathy is based on presence of all of the following four features:

-Transient left ventricular (LV) systolic dysfunction (typically not in a single coronary distribution; patterns include apical, midventricular, and basal).

-Absence of angiographic evidence of obstructive coronary disease or acute plaque rupture (or if coronary artery disease is present, the wall motion abnormalities are not in the territory of the affected coronary artery).

-New ECG abnormalities (ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin.

-Absence of pheochromocytoma or myocarditis.

Although patients with stress cardiomyopathy are at risk for the development of acute HF and cardiogenic shock, those who survive the acute episode typically recover ventricular function within one to four weeks. Thus, a clinical diagnosis of stress cardiomyopathy may aid in evaluating prognosis. The diagnosis, prognosis, and management of stress cardiomyopathy are discussed separately. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy" and "Management and prognosis of stress (takotsubo) cardiomyopathy".)

During the COVID-19 pandemic, stress cardiomyopathy has been diagnosed in patients with and without COVID-19. (See "COVID-19: Cardiac manifestations in adults", section on 'Stress cardiomyopathy'.)

In patients with COVID-19 with suspected myocarditis, the decision on whether to proceed with further evaluation for myocarditis (with cardiovascular magnetic resonance imaging [CMR] and possible endomyocardial biopsy) is based on the likelihood of a diagnosis that would alter therapy. Care must be taken to balance the risk of potential nosocomial spread of the disease and benefit of this additional information to modifying treatment. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Diagnosis'.)

-Since there is no established therapy for clinically suspected myocarditis, we do not recommend routine evaluation for myocarditis in patients with COVID-19. Although case reports have described empiric immunotherapy in a few patients with COVID-19 with clinically suspected myocarditis (with or without CMR confirmation), the safety and efficacy of such therapy are uncertain.

-CMR features of myocarditis are nonspecific and have variable sensitivity. CMR findings in patients with COVID-19 are discussed separately (see "COVID-19: Cardiac manifestations in adults" and "COVID-19: Cardiac manifestations in adults", section on 'Cardiovascular magnetic resonance'). Endomyocardial biopsy is required for a definitive diagnosis of myocarditis, if clinically indicated.

-Evaluation for myocarditis by endomyocardial biopsy (with or without prior CMR, depending on the patient's condition and available resources) may be appropriate in selected cases when a treatable type of myocarditis is suspected (eg, giant cell myocarditis) or in the presence of severe unexplained biventricular dysfunction, unexplained cardiogenic shock, or unexplained life-threatening arrhythmia with normal coronary arteries (with or without troponin increase) to confirm a definitive diagnosis of myocarditis and identify its cause to enable possible etiology-directed therapy [7]. Since biopsy-proven myocarditis is highly prevalent in young patients and very rare in older adults, the clinical suspicion of myocarditis should be higher, and the threshold to perform an endomyocardial biopsy should be lower, in young patients without cardiovascular comorbidities. Criteria for diagnosis of myocarditis are discussed separately. (See "COVID-19: Cardiac manifestations in adults", section on 'Myocardial histology and viral genome analysis' and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Approach to diagnosis of myocarditis' and "Treatment and prognosis of myocarditis in adults", section on 'Management of specific disorders'.)

Acute cor pulmonale may be caused by acute pulmonary embolism or adult respiratory distress syndrome, given the risk of these conditions in patients with COVID-19. (See "COVID-19: Cardiac manifestations in adults", section on 'Right heart failure' and "COVID-19: Hypercoagulability", section on 'VTE' and "COVID-19: Epidemiology, clinical features, and prognosis of the critically ill adult", section on 'Clinical features in critically ill patients'.)

DIFFERENTIAL DIAGNOSIS — Evaluation of the possible acute coronary and noncoronary causes of myocardial injury in patients with COVID-19 is described above. (See 'Diagnostic approach' above and "COVID-19: Cardiac manifestations in adults", section on 'Possible causes'.)

The differential diagnosis of acute myocardial injury includes chronic troponin elevation, which at low levels may not reflect risk of cardiac disease. With the use of high-sensitivity cardiac troponin assays, most healthy individuals have small but detectable levels of troponins in their blood. Therefore, myocardial injury is identified as a troponin elevation above the sex-specific 99th percentile upper reference limit, but this threshold varies among different patient populations. Troponin elevations have been identified in patients with high cardiovascular risk without an identified cardiovascular event, and troponin elevations are commonly persistent in patients with kidney disease. (See "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".)

Troponin elevations are infrequently analytic false-positive results. (See "Troponin testing: Analytical considerations", section on 'Assay false positives and false negatives'.)

MANAGEMENT

General approach

Supportive cardiac care — The optimal management for myocardial injury associated with COVID-19 has not been determined. Thus, the management of patients with myocardial injury, including clinically suspected myocarditis, involves supportive care (including management of HF, therapy for arrhythmias, and avoidance of cardiotoxins), as discussed separately. (See "COVID-19: Management in hospitalized adults" and "COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension" and "COVID-19: Management of the intubated adult" and "COVID-19: Arrhythmias and conduction system disease", section on 'Management' and "Treatment and prognosis of myocarditis in adults", section on 'General management' and "Treatment of acute decompensated heart failure: General considerations" and "Treatment of acute decompensated heart failure: Specific therapies" and "Overview of the management of heart failure with reduced ejection fraction in adults" and "Treatment and prognosis of heart failure with preserved ejection fraction" and "Treatment and prognosis of heart failure with mid-range ejection fraction".)

Patients with COVID-19 and HF or asymptomatic LV systolic dysfunction should receive standard therapy for these conditions including pharmacologic therapy, careful management of fluid balance, and advanced therapies as needed. (See "Treatment of acute decompensated heart failure: General considerations" and "Treatment of acute decompensated heart failure: Specific therapies" and "Overview of the management of heart failure with reduced ejection fraction in adults" and "Treatment and prognosis of heart failure with preserved ejection fraction" and "Management of refractory heart failure with reduced ejection fraction" and "Management and prognosis of asymptomatic left ventricular systolic dysfunction".)

ACE inhibitors and ARBs — Of note, standard indications for an angiotensin receptor-neprilysin inhibitor, angiotensin converting enzyme (ACE) inhibitor, or angiotensin receptor blocker (ARB) in treatment of HF with reduced ejection fraction (and for the latter two drugs in treatment of hypertension) apply to patients with COVID-19. Although there has been speculation that elevated ACE2 levels caused by renin-angiotensin-aldosterone system inhibitors might impact susceptibility to SARS-CoV-2 because ACE2 is a receptor for this virus, there is no evidence that treatment with these drugs worsens the clinical course of SARS-CoV-2 infection. (See "COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension", section on 'Renin angiotensin system inhibitors'.)

General management including thromboprophylaxis — General management of COVID-19 and critical care issues are discussed separately. (See "COVID-19: Management in hospitalized adults" and "COVID-19: Management of the intubated adult".)

Hypercoagulability and the role of thromboprophylaxis in patients with COVID-19 are discussed separately. (See "COVID-19: Hypercoagulability".)

Investigational agents — While laboratory evidence of a marked inflammatory response similar to cytokine release syndrome is associated with critical and fatal illness in patients with COVID-19, no treatment has been identified for this syndrome. Investigational protocols using the interleukin-6 inhibitors tocilizumab and sarilumab are ongoing. (See "Treatment and prognosis of myocarditis in adults", section on 'Management of specific disorders' and "COVID-19: Management in hospitalized adults", section on 'IL-6 pathway inhibitors (eg, tocilizumab)'.)

Mechanical circulatory support — As suggested by International Society for Heart and Lung Transplantation (ISHLT) guidance, ventricular assist device (VAD) implantation may be limited to INTERMACS status 1 to 3 patients based upon on local resource considerations during the COVID-19 pandemic [8].

Patients with COVID-19 supported by LV assist devices (LVADs) may present with low-flow alarms due to vasodilation coupled with diarrhea and dehydration, which can occur with COVID-19. However, vigorous fluid resuscitation can result in right HF in these LVAD patients. (See "Management of long-term mechanical circulatory support devices", section on 'Right heart failure' and "Right heart failure: Causes and management".)

VAD recipients may safely be placed in a prone position if indicated, with special attention paid to the driveline to avoid tugging [8].

Use of extracorporeal membrane oxygenation (ECMO) in patients with COVID-19 is discussed separately. (See "COVID-19: Extracorporeal membrane oxygenation (ECMO)".)

Cardiac transplantation — In accordance with ISHLT guidance, cardiac transplantation candidates with active SARS-CoV-2 infection are made inactive on the waitlist [8]. For cardiac transplantation candidates who recover from COVID-19, criteria for heart transplantation include waiting at least 14 days after initial COVID-19 diagnosis and documenting two successive negative polymerase chain reaction-based tests at least 48 hours apart.

Management of cardiac transplantation recipients who develop COVID-19 is based upon the severity of illness [8]:

Heart transplantation recipients with mild COVID-19 (no shortness of breath or hypoxia) are generally managed by quarantine at home for two weeks and continuation of baseline maintenance immunosuppression with frequent follow-up to monitor for worsening symptoms.

Heart transplantation recipients with moderate disease (shortness of breath or hypoxia requiring supplemental oxygen via nasal cannula) or severe disease (respiratory failure requiring intensive care unit admission and/or ventilator support, acute respiratory distress syndrome, circulatory collapse, acute kidney failure, cardiomyopathy, and/or clinical syndrome compatible with cytokine storm) are treated with in-hospital supportive care. Many heart transplantation centers reduce (or hold) antiproliferative agents (eg, mycophenolate mofetil or azathioprine) in heart transplantation recipients hospitalized with COVID-19 with close monitoring for rejection [1,8,9]; generally, calcineurin inhibitors and prednisone doses have been maintained in this setting. (See "Heart transplantation in adults: Induction and maintenance of immunosuppressive therapy".)

Whether maintenance immunosuppression for cardiac transplantation recipients should be altered and whether these patients have more or less severe COVID-19 is unknown [8]. There has been some suggestion that the late stage of COVID-19 associated with acute respiratory distress syndrome may be alleviated by the presence of immunosuppression, as it may reduce the cytokine response.

Other issues related to COVID-19 and solid organ transplantation are discussed separately. (See "COVID-19: Issues related to solid organ transplantation".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: COVID-19 – Index of guideline topics".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: COVID-19 overview (The Basics)" and "Patient education: COVID-19 vaccines (The Basics)")

SUMMARY AND RECOMMENDATIONS

Patients with COVID-19 typically present with symptoms and signs of respiratory tract infection, but cardiac manifestations, including signs of myocardial injury, are common. Troponin testing is commonly performed in hospitalized patients with COVID-19, as it may have prognostic value and may serve as a useful baseline for comparison in patients who develop manifestations of possible myocardial injury (such as heart failure [HF] or arrhythmia). (See 'Routine evaluation' above and "COVID-19: Cardiac manifestations in adults", section on 'Troponin'.)

Targeted cardiac evaluation is indicated in selected patients with COVID-19 with one or more of the following: new-onset HF, unexplained cardiac arrhythmias, or ECG changes (particularly ST elevation). The approach to cardiac evaluation may differ from the standard approach to evaluation, as it is based upon weighing the likelihood that evaluation will change management and guide prognosis, nosocomial infection control considerations, and optimal management of limited available medical staff and resources. (See 'Indications' above.)

If the clinical presentation is suggestive of acute coronary syndrome (ACS), timely evaluation is required to determine if urgent intervention is indicated. Evaluation of coronary disease in patients with COVID-19 is discussed separately. (See 'Routine evaluation' above and "COVID-19: Myocardial infarction and other coronary artery disease issues".)

Most patients with COVID-19 without suspected ACS, with mild troponin elevation, and without acute HF can be clinically monitored without cardiac imaging. (See 'Diagnostic approach' above.)

For patients who develop new-onset HF, an echocardiogram may be performed to evaluate regional and global ventricular and valvular function if this is requested by a consulting cardiologist and is expected to have a significant impact on management or is likely to change the patient's prognosis. (See 'Diagnostic approach' above.)

Since there is no established therapy for clinically suspected myocarditis, we do not recommend routine evaluation for myocarditis in patients with COVID-19. Evaluation for myocarditis by endomyocardial biopsy (with or without prior cardiac magnetic resonance imaging, depending on the patient's condition and available resources) may be appropriate in selected cases when a treatable type of myocarditis is suspected (eg, giant cell myocarditis) or in the presence of severe unexplained biventricular dysfunction, unexplained cardiogenic shock, or unexplained life-threatening arrhythmia with normal coronary arteries (with or without troponin increase) to confirm a definitive diagnosis of myocarditis and identify its cause to enable possible etiology-directed therapy. (See 'Routine evaluation' above and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Diagnosis'.)

The optimal management for myocardial injury associated with COVID-19 has not been determined. Thus, the management of patients with myocardial injury, including clinically suspected myocarditis, involves supportive care (including management of HF, therapy for arrhythmias, and avoidance of cardiotoxins). (See 'Management' above and "COVID-19: Arrhythmias and conduction system disease", section on 'Management' and "Treatment and prognosis of myocarditis in adults", section on 'General management' and "COVID-19: Arrhythmias and conduction system disease".)

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