COVID-19-associated heart failure

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]Mandana Chitsazan, M.D. [3]

Synonyms and keywords: coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

Overview

• Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
• Patients with chronic heart failure may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.

Classification

• Heart Failure ((HF) in COVID-19 may be classified similarly to heart failure from other causes.
• In general, heart failure can be classified based on:
  • The pathophysiology of heart failure:
    • systolic HF vs diastolic HF
    • left-sided HF vs right-sided HF
  • The duration of symptoms:
    • acute HF (AHF) vs chronic HF (CHF)
  • The underlying physiology based on left ventricular ejection fraction (LVEF):
    • Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF)
  • The severity of heart failure (i.e., the New York Heart Association Class I-IV)
  • The stage of congestive heart failure (i.e., AHA Class A, B, C, D)

• Acute heart failure has two forms:
  • Newly-arisen (“de novo”) acute heart failure
  • Acutely decompensated chronic heart failure (ADCHF)

Pathophysiology

• Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:

• • Acute exacerbation of chronic heart failure caused by precipitating factors
  • 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)

Causes

• Acute myocardial injury
• Acute coronary syndromes
• Myocarditis
• Hypertensive crisis
• Arrhythmias: Tachycardia or severe bradycardia
• Stress-induced cardiomyopathy
• Circulatory failure:
  • Acute pulmonary embolism
  • Pericardial tamponade
• Iatrogenic

Differentiating ((COVID-19 associated heart failure)) from other Diseases

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea. The differentials include the following:

• Pneumonia
• ARDS
• Myocarditis/pericarditis
• Acute pulmonary embolism

Epidemiology and Demographics

• Data on incidence on acute heart failure in COVID-19 patients is limited.
• In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
• In a retrospective study on 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

Screening

• There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
• Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

Natural History, Complications, and Prognosis

• COVID-19 patients with chronic heart failure are more likely to develop severe forms of the disease.
• COVID-19 patients who develop acute heart failure (either de novo AHF or ADHF) have worse outcomes.
• Acute heart failure in COVID-19 may progress to cardiogenic shock.

Diagnosis

History and Symptoms

• The most common symptoms of acute heart failure in COVID-19 patients are:
  • New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
  • Peripheral edema
  • Confusion and altered mentation
  • Orthopnea
  • Palpitations
• Less common symptoms include:
  • Paroxysmal nocturnal dyspnea
  • Cool extremities
  • Cyanosis
• *Dizziness
  • Syncope
  • Fatigue
  • Hemoptysis

Physical Examination

• Physical examination of patients with acute heart failure is usually remarkable for:
  • Crackles on auscultation
  • Distended jugular veins
  • Lower extremity edema

Laboratory Findings

• 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 heart failure.

• 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 heart failure based on clinical grounds.

Electrocardiogram

• There is no specific electrocardiographic finding 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

• A Chest x-ray may be helpful in the diagnosis of heart failure. Findings on chest X-ray suggestive of heart failure include:
  • Cardiomegaly
  • Pulmonary congestion
  • Increased pulmonary vascular markings.

• However, signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

Echocardiography or Ultrasound

• A complete standard transthoracicechocardiography (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 (left ventricular ejection fraction, LVEF) to distinguish systolic dysfunction with a reduced ejection fraction (LVEF<40%) from diastolic dysfunction with a preserved ejection fraction (LVEF>40%)
  • Left ventricular diastolic function
  • Left ventricular structural abnormalities, including left ventricular size and left ventricular 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 underlying ischemia.

Treatment

Medical Therapy

• 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.
• Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACE inhibitors or Angiotensin II receptor blockers, and mineralocorticoid receptor antagonists.

References

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