Acute cardiac injury, variably defined as increased circulating troponin levels and/or new abnormalities on ECG or echocardiography, were noted in 7-22% of hospitalized patients in early reports from Wuhan (Ruan et al; Wang et al; Chen et al; Shi et al; Guo et al, Zhou et al). When present, these findings were associated with increased risk of ICU admission and death.
- Direct SARS-CoV-2 infection of cardiac myocytes (myocarditis)
- Demand ischemia, with either large or small vessel thrombosis
- Stress (Takotsubo) cardiomyopathy
- Pathological myocardial response to inflammation or cytokine storm
Specific cardiac pathologies include myocarditis, arrhythmia, and precipitation of an acute coronary syndrome. Hypercoagulability in COVID-19, including its impact on the heart, are discussed in Hematology.
Fulminant SARS-CoV-2 myocarditis was clinically suspected in some early case reports (Ruan et al; Zeng et al; Hu et al; Inciardi et al), based on pre-existing clinical criteria and, in some cases, suggestive findings on cardiac MRI (Inciardi et al, Kim et al). Subsequent examination of myocardial tissue in autopsy series (Fox et al; Elsoukkary et al; Basso et al) found direct evidence for viral myocarditis (e.g., lymphocytic infiltrates) were relatively rare (0-14%).
The clinical significance of direct SARS-CoV-2 myocarditis remains unclear. If a patient has elevated troponins with no evidence of obstructive coronary artery disease, it may be on the differential diagnosis but is unlikely to alter management.
- Provide supportive care for heart failure (Zhang et al.) or Cardiogenic Shock
- Where possible, discuss with cardiology and/or infectious disease consultants to see if the patient might benefit from antivirals or steroids (benefit is unknown)
- Endomyocardial biopsy is unlikely to be informative.
- See Advanced CV Imaging below regarding uses of cardiac MRI.
Cardiac arrhythmias can occur in COVID-19. An early case series of 138 patients in Wuhan, China, (Wang et al) found evidence of some arrhythmias in 17% of hospitalized patients with COVID-19, rising to 44% in those transferred to the ICU. Another early study of 189 hospitalized patients noted nearly 6% of inpatients had an episode of ventricular fibrillation or sustained ventricular tachycardia (Guo et al).
- Atrial Fibrillation/Atrial Flutter
- Consider beta-blockers, if no evidence of heart failure or shock.
- If acute heart failure or concern for hypotension, use amiodarone if not otherwise contraindicated.
- If unstable (with a pulse), synchronized DC cardioversion with 200 joules (biphasic).
- Ventricular Tachycardia
- If unstable or without palpable pulses: initiate local advanced life support protocol (e.g., ACLS).
- If stable:
- Involve a cardiologist. If cardiologist is not available, involve a senior clinician.Consider a single IV dose of amiodarone 150mg or lidocaine 100mg
Myocardial infarction in COVID-19 may be triggered by a combination of hypercoagulability, cardiac expression of SARS-CoV-2 entry receptor ACE2, possible direct viral myocardial injury, increased myocardial demand, or toxicity from inflammation. Cardiac markers and ECG changes alone may not be able to determine whether an underlying obstructive lesion exists as evidenced by the fact that up to 45% of hospitalized COVID patients have elevated cardiac markers (Lombardi et al).
The diagnosis of an acute coronary syndrome depends on:
- Symptoms (if able to communicate): worsening shortness of breath, chest pain, or other anginal equivalents
- Regional changes in the ECG or wall motion abnormalities on echocardiography
- Rate of change of troponin changes (rapid rise or fall suggests an acute event)
Tool: Life in the Fast Lane Acute Coronary Syndromes
When the diagnosis is not clear, a cardiologist should be consulted.
If a patient is diagnosed with ACS, management should be coordinated with a cardiologist if at all possible. Medical management typically includes:
- Treatment with full dose aspirin, clopidogrel (if not bleeding), heparin, oxygen (if hypoxemic), high-dose statin, nitrates (if hypertensive), and opioids as needed for symptom control. Beta blockers should be used with caution, given the risk of concomitant myocarditis or decompensated heart failure
- If cardiac catheterization is available, there are no fundamental contraindications for patients with COVID-19 as long as strict infection control precautions are followed.
- If cardiac catheterization is not available or if constrained resources unacceptably prolong door-to-balloon time, thrombolytic medications may be considered in lieu of PCI.
Laboratory markers of cardiac injury (troponins, CK-MB, BNP) and electrocardiography are appropriate for most COVID-19 patients admitted to the hospital. Depending on availability and expertise, point-of-care ultrasound can also be considered, particularly in patients with concerning symptoms, lab values or ECG.
The indications for more advanced cardiac diagnostics are similar to patients without COVID-19, but with additional consideration for infection control. Testing should be limited to cases where the results will alter management to avoid unnecessary risk to providers and other patients.
- Transthoracic echocardiography
- Do not obtain routinely.
- When possible, a bedside provider should assess cardiac function with point-of-care ultrasound for the following indications:
- Marked elevation in troponin or NTproBNP, or decline in ScvO2/MvO2
- New heart failure
- New persistent arrhythmia
- Significant ECG changes
- If abnormalities are identified on point-of-care ultrasound (such as a new decrease in LV ejection fraction to below < 50%) and the patient is stable, a formal echocardiogram should be obtained if possible.
- Evaluate both left and right ventricular function.
- The differential diagnosis for right ventricular dysfunction includes myocarditis, hypoxic vasoconstriction, pulmonary embolus, and cytokine mediated dysfunction.
- The differential diagnosis for left ventricular dysfunction includes myocarditis, acute coronary syndrome, and stress-induced cardiomyopathy.
- Regional wall motion abnormalities with elevated troponins suggest an acute coronary syndrome, though direct myocardial injury by the virus can also result in focal wall motion abnormalities.
- Stress Testing:
- Should not be commonly required in patients with active COVID. If needed (and if available), consider pharmacologic nuclear stress testing or coronary CT angiography rather than exercise stress test.
- Transesophageal Echocardiogram (TEE)
- Only request if absolutely necessary. Although unclear whether this generates aerosolized virus, it likely does represent increased risk to the patient and provider.
- Consider alternative noninvasive imaging modalities (such as cardiac CT or PET/CT) if they are available and appropriate for the question being asked.
- Cardiac CT
- Can consider for selected patients with elevated cardiac biomarkers when there is a need to distinguish myocardial injury from acute coronary syndrome. The decision to use CT in this context should be discussed with a cardiologist.
- Consider in selected patients as a substitute for TEE to rule out left atrial appendage clot or to evaluate for endocarditis.
- In appropriate cases, multiphase data acquisition may be used to evaluate both left and right ventricular function while concurrently evaluating the lung parenchyma or pulmonary artery.
- Cardiac MRI
- Consider for selected patients with elevated cardiac biomarkers and concern for myocarditis, if this information will impact patient management.
- In the acute and subacute periods, T1 and T2 mapping as well as assessment of extracellular volume fraction (ECV) may improve sensitivity for myocarditis. However, the prognostic significance of such abnormalities (especially in the presence of normal ventricular function or when late enhancement abnormalities are absent) remains unclear.
- In selected patients who have recovered from COVID, cardiac MRI using late gadolinium enhancement may be useful for evaluating for residual scar tissue.
- Nuclear Imaging
- In COVID-19 patients who require stress testing, vasodilator stress testing is preferred over exercise testing.
- In selected patients who have recovered from COVID-19, PET MPI using a quantitative assessment of myocardial blood flow may be useful for evaluating microvascular dysfunction.
Preexisting cardiovascular disease and metabolic disorders (including diabetes and hyperlipidemia) worsen prognosis in acute COVID-19 (Izcovich et al).
See Anticoagulation in the Hematology section below.
Patients with pre-existing heart failure have a nearly two-fold increased mortality and over three-fold greater risk of mechanical ventilation when they develop COVID-19 (Alvarez-Garcia et al).
There are currently no specific medication changes recommended for patients with prior heart failure who develop COVID-19, though all medications should be titrated based on other clinical context (e.g., in a patient with fevers and decreased oral intake, home diuretic doses may need adjustment).
Patients with rheumatic heart disease or other conditions requiring surgical intervention should continue to be considered as a potential priority case during the COVID-19 pandemic.
Literature Review: Gallery View,