Sandbox:Mitra

Template:COVID-19 associated Heart Failure For patient information, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]

Synonyms and keywords:

Pathophysiology

• Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
• Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
• Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:
  • Acute exacerbation of chronic heart failure
  • Acute myocardial injury (which in turn can be caused by several mechanisms)
  • Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
  • Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
  • Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)

Diagnosis

Diagnostic study of choice History and Symptoms

Symptoms and signs

• Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
• Lower limb edema
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Confusion and altered mentation
• Cool extremities
• Cyanosis
• Syncope
• Fatigue
• Hemoptysis
• Palpitations
• Weakness
• Wheezing or cardiac asthma
• Distended jugular veins
• Crackles on auscultation

| Physical Examination | Laboratory Findings | Electrocardiogram

Electrocardiography (ECG)

• There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
• The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
• These ECG findings may include:
  • Low QRS Voltage
  • Left ventricular hypertrophy
  • Left atrial enlargement
  • Left bundle branch block
  • Poor R progression
  • ST-T changes

| X-Ray Findings

Chest x-ray (CXR)

• The Chest x-ray may show evidence of:
  • Cardiomegaly
  • Pulmonary congestion
  • Increased pulmonary vascular markings.
• Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

| Echocardiography and Ultrasound

Echocardiography

• A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.
• To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
• In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
  • Cardiac point-of-care ultrasound (POCUS)
  • Focused cardiac ultrasound study (FoCUS)
  • Critical care echocardiography
• Cardiac ultrasound can help in assessing the following parameters:
  • Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
  • Left ventricular diastolic function
  • Left ventricular structural abnormalities, including LV size and LV wall thickness
  • Left atrial size
  • Right ventricular size and function
  • Detection and quantification of valvular abnormalities
  • Measurement of systolic pulmonary artery pressure
  • Detection and quantification of pericardial effusion
  • Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia

| CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

Cardiac biomarkers

• Cardiac Troponins:
  • Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
  • Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.
• Natriuretic Peptides:
  • Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.
  • Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
  • Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
  • Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.
  • However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.
  • Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

Treatment

Medical Therapy

• Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists.
• Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
  • Fluid restriction
  • Diuretic therapy
  • Vasopressors and/or inotropes
  • Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
• Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.
• Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.

| Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case #1