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Cardiology Department, Sunshine Coast University Hospital, Sunshine Coast, Qld, AustraliaSchool of Medicine, Griffith University, Sunshine Coast, Qld, AustraliaSchool of Human Movement and Nutrition Sciences, The University of Queensland, Brisbane, Australia
School of Medicine, The University of Queensland, Brisbane, Qld, AustraliaInfectious Diseases Service, Sunshine Coast University Hospital, Sunshine Coast, Qld, Australia
Cardiology Department, Sunshine Coast University Hospital, Sunshine Coast, Qld, AustraliaSchool of Medicine, Griffith University, Sunshine Coast, Qld, AustraliaSchool of Health and Sport Sciences, University of the Sunshine Coast, Sunshine Coast, Qld, Australia
Coronavirus disease 2019 (COVID-19) caused by the SARS-CoV-2 virus is likely to remain endemic globally despite widespread vaccination. There is increasing concern for myocardial involvement and ensuing cardiac complications due to COVID-19, however, the available evidence suggests these risks are low. Pandemic publishing has resulted in rapid manuscript availability though pre-print servers. Subsequent article retractions, a lack of standardised definitions, over-reliance on isolated troponin elevation and the heterogeneity of studied patient groups (i.e. severe vs. symptomatic vs all infections) resulted in early concern for high rates of myocarditis in patients with and recovering from COVID-19. The estimated incidence of myocarditis in COVID-19 infection is 11 cases per 100,000 infections compared with an estimated 2.7 cases per 100,000 persons following mRNA vaccination. For substantiated cases, the clinical course of myocarditis related to COVID-19 or mRNA vaccination appears mild and self-limiting, with reports of severe/fulminant myocarditis being rare. There is limited data available on the management of myocarditis in these settings.
Clinical guidance for appropriate use of cardiac investigations and monitoring in COVID-19 is needed for effective risk stratification and efficient use of cardiac resources in Australia. An amalgamation of national and international position statements and guidelines is helpful for guiding clinical practice. This paper reviews the current available evidence and guidelines and provides a summary of the risks and potential use of cardiac investigations and monitoring for patients with COVID-19.
The severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) is approaching worldwide endemic status. The clinical manifestations of Coronavirus disease (COVID-19), particularly the potential cardiac complications such as myocarditis, heart failure and cardiovascular death, are feared, particularly in the context of media reports of sudden death. However, the true incidence of these outcomes has been difficult to quantify, as estimates of global case numbers are limited by testing protocols and reporting activity [
]. Although potentially serious, clinically significant cardiac complications are relatively infrequent. While cardiac complications appear more common following COVID-19 infection rather than following vaccination [
], the incidence of vaccine-induced complications such as myocarditis can be expected to rise as messenger ribonucleic acid (mRNA) based inoculation becomes omnipresent.
Studies in patients with COVID-19 initially raised concern for high rates of clinically suspected myocarditis based on elevated biomarkers, particularly high-sensitivity cardiac troponin [
]. The availability of non-peer-reviewed manuscripts on pre-print servers and the rapid rate of publication acceptance during the pandemic, the prevalence of troponin elevation of questionable clinical significance, and non-specific cardiac magnetic resonance (CMR) findings, have contributed to an initially overinflated estimation of the incidence and risk of myocarditis. Current data suggests that myocarditis is an uncommon complication of COVID-19 [
The Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1—epidemiology, pathophysiology, and diagnosis.
Less than 2 years after identification of the virus, global COVID-19 experience remains relatively immature. At the onset of the COVID-19 pandemic, several national and international guidelines and position statements were developed to guide the investigation, monitoring and management of patients with suspected cardiac complications. However, established guidelines have been principally based on expert opinion and observational or case series data. The accumulation of prospective global data and increasing local experience affords the opportunity to re-evaluate the true incidence of cardiac complications of COVID-19 and mRNA vaccination to guide clinical practice. This review was conducted to evaluate the incidence of substantiated cardiac complications of COVID-19 infection and mRNA vaccination in adult patients to provide evidence to inform and risk stratify allocations of community and hospital-based cardiology resources and services. Evidence on the epidemiology, investigations and management of myocarditis are summarised and recommendations for cardiac investigations are provided and have been drawn from robust original studies, available meta-analyses and position statements from international cardiology societies [
The Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1—epidemiology, pathophysiology, and diagnosis.
Position Statement on the Management of Cardiac Electrophysiology and Cardiac Implantable Electronic Devices in Australia During the COVID-19 Pandemic: A Living Document.
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
The Task Force for the management of COVID-19 of the European Society of Cardiology ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 2—care pathways, treatment, and follow-up.
We conducted a pragmatic narrative review of the literature using PubMed with the generic terms "coronavirus", "SARS-CoV-2", "COVID-19" and "cardiology". Specific search terms included "troponin", "biomarker", "electrocardiography", "telemetry", "imaging", "echocardiography", "cardiac magnetic resonance", "arrhythmia", "myocarditis", "heart failure", "hospitalisation" and "mortality". Reference lists of papers of interest and position statements were also reviewed. The Cardiac Society of Australia and New Zealand (CSANZ) position statements, guidance from The Australian Technical Advisory Group on Immunisation (ATAGI), European Society of Cardiology (ESC) guidelines, and statements and recommendations endorsed by the American College of Cardiology (ACC) and American Heart Association (AHA) were reviewed.
Spectrum of Cardiac Complications of COVID-19
The angiotensin converting enzyme 2 receptor, thought to be the viral entry point of SARS-CoV-2, is highly distributed in pulmonary epithelium in addition to systemic organs including the myocardium [
]. Following infection, it is theorised that myocardial injury characterised by elevated biomarkers (i.e., troponin) may result from direct viral damage. However, it is more likely that systemic inflammation or stress related to COVID-19 infection drives myocardial injury [
], however, interpretation within clinical context is required. Though strongly associated with outcome, particularly in patients with cardiovascular disease and risk factors [
], elevated troponin is more likely a marker of disease severity and the end-organ effects of systemic illness in the majority of cases. Myocardial involvement may range from minor asymptomatic troponin elevation to fulminant myocarditis and heart failure, as described in case reports [
]. There appears to be a marginal increase in the risk of arrhythmia, stress cardiomyopathy and myocardial infarction due to plaque instability or supply-demand mismatch (i.e. type 2 myocardial infarction) [
Most reports of myocarditis due to COVID-19 are clinically suspected, based principally on elevated biomarkers, and are not well validated. Where elevated troponin alone is used as a definition, myocardial injury in the context of COVID-19 is common, with an estimated prevalence up to 40% [
]. Biomarkers are central to the diagnosis of myocarditis and myocardial injury, however, elevated troponin detected by high-sensitivity assays does not substantiate the diagnosis of myocarditis without supportingclinical or imaging evidence. In most published studies on COVID-19 there is little corroborating data using multi-modality imaging, biomarkers and endomyocardial biopsy results. Available data suggests that the pattern of myocardial inflammation is often highly variable [
], though the criteria for the diagnosis of myocarditis have not been consistently stated. Similarly, there is little data on the rates of myocarditis specifically associated with newer viral variants, such as the Delta and Omicron strains.
Early imaging reports raised concern over the high prevalence of radiological myocarditis on CMR imaging in recovered COVID-19 survivors, present weeks after initial infection [
]. Subsequent CMR studies in health care workers recovered after mild infection have been more reassuring, with similar rates of cardiovascular abnormalities in seropositive compared with seronegative cases [
]. A major limitation to the validity of CMR-based studies has been the lack of concordance with accepted revised Lake Louise CMR criteria for myocarditis, where the presence of late gadolinium enhancement, T1 and T2 criteria on CMR imaging confirms the diagnosis of myocarditis in the appropriate clinical setting [
]. Radiological findings may not specifically represent myocardial involvement of COVID-19 given the lack of baseline imaging prior to infection, limited imaging during the acute infectious period and limited correlation to positive biopsies. Also, co-infection with other viruses (e.g. Influenza A and Respiratory Syncytial Virus) may occur in one fifth of COVID-19 cases [
], and may not have been excluded as the underlying cause of myocardial inflammation. While CMR proven myocardial oedema may be common during the acute phase of illness [
]. Furthermore, the short-term clinical significance and long-term outcomes related to these CMR findings has not been established. Endomyocardial biopsies are often unrevealing with non-specific inflammatory changes, whilst autopsy studies suggest that the true prevalence of myocarditis, particularly that of clinical significance [
], is far lower than what is suspected from imaging studies.
The 2013 European Society of Cardiology (ESC) position statement on myocarditis presents diagnostic criteria for clinically suspected myocarditis where endomyocardial biopsy has not been performed [
Current State of Knowledge on Aetiology, Diagnosis, Management, and Therapy of Myocarditis: A Position Statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases.
]. In the absence of angiographically detectable coronary disease, known pre-existing cardiovascular disease or significant extra-cardiac causes, the diagnostic criteria use both clinical features and objective evidence such as raised cardiac biomarkers, changes on ECG or abnormal cardiac imaging [
Current State of Knowledge on Aetiology, Diagnosis, Management, and Therapy of Myocarditis: A Position Statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases.
]. In the setting of COVID-19 infection without a significant history of cardiac disease, there should be a high index of suspicion for myocarditis in patients presenting with acute severe cardiac failure or cardiogenic shock. Recommended investigations in suspected cases of COVID-19 myocarditis are discussed below and presented in Table 1.
Table 1Summary of clinical investigations recommended in suspected/positive COVID-19 cases.
The Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1—epidemiology, pathophysiology, and diagnosis.
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
The Task Force for the management of COVID-19 of the European Society of Cardiology ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 2—care pathways, treatment, and follow-up.
Position Statement on the Management of Cardiac Electrophysiology and Cardiac Implantable Electronic Devices in Australia During the COVID-19 Pandemic: A Living Document.
Position Statement on the Management of Cardiac Electrophysiology and Cardiac Implantable Electronic Devices in Australia During the COVID-19 Pandemic: A Living Document.
Significantly elevated troponin (>5 x ULN) and not consistent with MI, acute HF/shock, significantly elevated BNP, malignant ventricular arrhythmia. Targeted study using POCUS where appropriate.
ASE Statement on Protection of Patients and Echocardiography Service Providers During the 2019 Novel Coronavirus Outbreak: Endorsed by the American College of Cardiology.
Indicated in suspected HF or myocarditis, significant arrhythmias or ECG changes, more than mild pericardial effusion on chest CT, haemodynamic instability or previous heart disease with shock. Consider POCUS as first-line imaging modality.
Suspected acute myocarditis with clinical signs or symptoms not explained by other diagnostic tools.
Consider in myocarditis or stress cardiomyopathy in new LV dysfunction with non-dilated LV and a non-coronary distribution of wall motion abnormalities, with no known cardiomyopathy. Useful for MINOCA [
Avoid in COVID-19. Reasonable to confirm myocarditis associated with mRNA vaccination in those with significantly elevated troponin elevation or ECG changes. LGE may inform risk of arrhythmia.
Interventional Procedures
Angiography (including CT coronary angiography)
STEMI when angiography determines outcome. Consider fibrinolysis where appropriate. Delay in stable NSTEACS, consider angiography for very high-risk or unstable cases. CT coronary angiography can be considered for select patients [
STEMI indication. Consider in cardiogenic shock. Angiography <24 hrs in very high-risk NSTEACS. Await two negative swab results within 48 hrs and no clinical suspicion of COVID-19 for other cases. Consider as may expedite risk stratification and facilitate early discharge. Use COVID-19 dedicated laboratory.
Primary PCI should remain standard of care for STEMI or very high-risk NSTEACS in PCI-capable centres [
Management of Acute Myocardial Infarction During the COVID-19 Pandemic: A Position Statement from the Society for Cardiovascular Angiography and Interventions (SCAI), the American College of Cardiology (ACC), and the American College of Emergency Physicians (ACEP).
Management of Acute Myocardial Infarction During the COVID-19 Pandemic: A Position Statement from the Society for Cardiovascular Angiography and Interventions (SCAI), the American College of Cardiology (ACC), and the American College of Emergency Physicians (ACEP).
Management of Acute Myocardial Infarction During the COVID-19 Pandemic: A Position Statement from the Society for Cardiovascular Angiography and Interventions (SCAI), the American College of Cardiology (ACC), and the American College of Emergency Physicians (ACEP).
Perform in STEMI where angiography will significantly alter outcome. Consider fibrinolysis in appropriately selected patients. Defer in NSTEACS if no high-risk features.
Pericardiocentesis
No formal recommendation.
No formal indications. Consider bedside procedure where possible.
No formal recommendation.
Indicated for treatment of tamponade where appropriate, where expectant management is likely to result in preventable poor outcome.
Position Statement on the Management of Cardiac Electrophysiology and Cardiac Implantable Electronic Devices in Australia During the COVID-19 Pandemic: A Living Document.
Management of Acute Myocardial Infarction During the COVID-19 Pandemic: A Position Statement from the Society for Cardiovascular Angiography and Interventions (SCAI), the American College of Cardiology (ACC), and the American College of Emergency Physicians (ACEP).
Deferral of elective procedures as per local policy.
Abbreviations: CSANZ, Cardiac Society of Australia and New Zealand; ESC, European Society of Cardiology; AHA, American Heart Association; ACC, American College of Cardiology; ASE, American Society of Echocardiography; SCAI, Society for Cardiovascular Angiography and Interventions; MI, myocardial infarction; LV, left ventricular; HF, heart failure; ECG, electrocardiogram; POCUS, point-of-care ultrasound; BNP, brain natriuretic peptide; CT, computed tomography; MINOCA, myocardial infarction with non-obstructive coronary arteries; LGE, late gadolinium enhancement; STEMI, ST-elevation myocardial infarction; NSTEACs, non-ST elevation acute coronary syndromes; PCI, percutaneous coronary intervention.
Current State of Knowledge on Aetiology, Diagnosis, Management, and Therapy of Myocarditis: A Position Statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases.
The Task Force for the management of COVID-19 of the European Society of Cardiology ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 2—care pathways, treatment, and follow-up.
]. Guideline-directed heart failure therapy is recommended in cases of ventricular dysfunction. Advanced heart failure and mechanical therapies (i.e., extracorporeal membrane oxygenation) are reasonable strategies for unstable patients as a bridge to recovery or cardiac transplant [
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
]. There is insufficient evidence to recommend antiviral or immunomodulatory therapy (steroids and intravenous immunoglobulin), except when accompanied by significant respiratory involvement where corticosteroids may be of benefit [
The Task Force for the management of COVID-19 of the European Society of Cardiology ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 2—care pathways, treatment, and follow-up.
]. Following a diagnosis of myocarditis, restriction of physical activity is recommended, and is based on expert opinion. For myocarditis associated with COVID-19 and other aetiologies, the ESC recommend at least 6 months exercise restriction and pre-participation screening prior to return to competitive sport, and make similar suggestions for non-athletes [
The Task Force for the management of COVID-19 of the European Society of Cardiology ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 2—care pathways, treatment, and follow-up.
Current State of Knowledge on Aetiology, Diagnosis, Management, and Therapy of Myocarditis: A Position Statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases.
]. The ACC/AHA guidelines consider return to sport following 3–6 months exercise restriction and normal pre-participation testing, but do not make recommendations specific to myocarditis associated with COVID-19 [
Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 3: hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and other cardiomyopathies, and myocarditis.
]. Clinical follow-up is at the treating clinician’s discretion, but may be guided by severity of myocarditis and other organ involvement, the presence of pre-existing cardiovascular disease, ongoing active issues (i.e. LV dysfunction, arrhythmia) or high-risk features (i.e. high burden of scar/late gadolinium enhancement on CMR).
Myocarditis Due to mRNA Vaccination
The risk of mRNA vaccine induced myocarditis is approximately 2.7 excess cases per 100,000 persons [
], but may occur after a second exposure in those receiving a first vaccine dose after previous viral infection. There are differences in the rate of reported myocarditis with variations of mRNA-based vaccines [
]. Non-mRNA vaccines have not been associated with an increased risk of myocarditis/pericarditis.
The diagnosis of vaccine induced myocarditis should be established clinically with an appropriate temporal relationship to vaccination and supportive investigations. A 12-lead ECG, chest X-ray and high-sensitivity troponin should be obtained. Whilst ECG and chest X-ray findings may be non-specific, a modest elevation of troponin is expected in myocarditis [
]. Pericarditis has also been reported, and without the overlap syndrome of myopericarditis, may present with normal troponin and exhibit classic ECG findings of PR segment depression and diffuse ST segment elevation. Non-invasive imaging with transthoracic echocardiography is reasonable to evaluate cardiac function and exclude complications such as pericardial effusion, where supported by bedside investigations. Left ventricular function is often preserved or only mildly impaired [
]. Vaccine associated myocarditis is reportable to the Therapeutic Goods Administration (TGA), and unlike cases of myocarditis suspected to be due to COVID-19, there is no infection risk and advanced imaging with CMR may be helpful to establish the diagnosis. Hospitalisation for confirmed cases is recommended until symptom resolution and identification of peak biomarkers [
]. Figure 1 demonstrates typical findings in a case of acute mRNA vaccine induced myopericarditis.
Figure 1Electrocardiogram and cardiac resonance imaging in an example case of myocarditis following mRNA vaccine. A 16-year-old male presented with typical central chest pain with onset 2 days post second dose of mRNA vaccination. The ECG was consistent with myopericarditis with supporting peak troponin I of 19,322 ng/L. Non-sustained ventricular tachycardia was recorded on telemetry. Echocardiography demonstrated normal LV size with mildly reduced systolic function (ejection fraction 51%) with mid-septal regional wall motion abnormalities. Global longitudinal strain was 18.2%. Inpatient CMR identified a small pericardial effusion and myocardial oedema with mid-wall LGE confirming acute myocarditis. Though there were no preceding viral symptoms, a viral screen for other causes was performed and was negative.
a)
12-lead ECG demonstrating myopericarditis with diffuse ST segment elevation and PR depression.
b)
Short axis CMR imaging at the mid left ventricular level demonstrating pericardial effusion (arrows).
c)
Native T1 mapping showing elevated values in the lateral segments consistent with myocardial inflammation. Normal T1 values were identified in the remote myocardium.
d)
T2 mapping showing elevated T2 values in the lateral segments consistent with myocardial oedema. Normal T2 values were identified in the remote myocardium.
e)
Late gadolinium enhancement images at basal and mid ventricular levels showing a sub-epicardial to mid-wall pattern of regional fibrosis, as typically seen in myocarditis (arrows).
The guidance statement published by the Australian Technical Advisory Group on Immunisation (ATAGI) is endorsed by the CSANZ and several other governing medical bodies, and recommends that the mRNA vaccine can be received with precautions for most patients regardless of the history of pre-existing cardiovascular disease [
]. In cases of myocarditis following mRNA vaccination, further doses of the mRNA vaccine are not recommended, with alternate non-mRNA formulations being preferred. Myocarditis due to other causes is not a contraindication to mRNA vaccination following recovery. Post-vaccination pericarditis is not a preclusion to further doses, depending on normal investigation results and a recovery period of at least 6 weeks. Management of patients with confirmed myocarditis in the setting of a preceding mRNA vaccination is largely supportive. Cases should be treated as for myocarditis from other causes, with guideline directed heart failure therapies if indicated, exercise restriction (as aforementioned) and cardiology follow-up.
Cardiac Biomarker Testing in COVID-19
Cardiac biomarkers are elevated in up to half of patients admitted with COVID-19 [
], however, most cases of infection do not require inpatient admission. Any magnitude of troponin elevation is associated with increased risk of adverse outcome [
], with higher levels seen in patients with pre-existing cardiovascular disease or risk factors. There are several mechanisms of troponin elevation, which most commonly reflects overall disease severity and secondary myocardial injury. The rise in troponin often mirrors other acute phase reactants and markers of end organ dysfunction such as lactate dehydrogenase, ferritin, interleukin-6 and D-dimer [
Troponin elevation may reflect direct myocardial injury or represent sequelae of systemic inflammation and critical illness. Although it is a specific marker of myocyte injury, it is not specific for myocarditis or myocardial infarction in the absence of a supporting clinical syndrome. Small elevations in troponin are expected, particularly in older patients or those with pre-existing cardiovascular disease. Routine troponin measurement is not supported by either the ESC [
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
], where it is reserved for those patients where acute type 1 myocardial infarction is suspected, or in cases of likely myocarditis or acute heart failure. The CSANZ do recommend a routine screening troponin on admission for all patients with COVID-19 to screen for cardiomyopathy or myocarditis [
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
]. Exclusion of acutely decompensated heart failure and prognostication in pulmonary embolism are the strongest indications for measurement. However, an elevated BNP represents the acute haemodynamic stress of COVID-19 and right heart strain in the setting of pneumonia or pulmonary embolism. Although BNP does risk stratify patients with COVID-19 [
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
]. Continuous cardiac monitoring is reasonable in patients with COVID-19 who are critically unwell or those at risk of deterioration, such as those with significant pre-existing cardiovascular disease [
An admission 12-lead ECG is recommended for patients hospitalised with symptomatic infection. Any abnormality on 12-lead ECG is predictive of outcome in symptomatic patients admitted with COVID-19 [
Position Statement on the Management of Cardiac Electrophysiology and Cardiac Implantable Electronic Devices in Australia During the COVID-19 Pandemic: A Living Document.
Echocardiography: Non-invasive cardiac imaging is useful in evaluating patients with COVID-19 who have clinical or biochemical suggestion of cardiac involvement and may assist in establishing the diagnosis of myocardial complications such as ventricular dysfunction and myocarditis. In a global prospective survey of echocardiography in patients with presumed or confirmed COVID-19, an abnormal study was common in those with a clinical indication for echocardiography, despite lacking pre-existing cardiovascular disease (46%) [
]. However, these were cases for which imaging was clinically indicated and likely overestimates the true community prevalence. The strongest predictors of LV dysfunction are abnormal biomarkers (troponin and BNP), whereas right ventricular function is more closely related to illness severity. In unselected patients, the detection of clinically relevant findings on echocardiography appears to be around 24%, and is less frequent in those without known cardiovascular disease (14%) and elevated biomarkers [
]. In hospitalised patients, the absence of biomarker elevation is reassuring, with no urgent echocardiogram findings in 95.1% of ward-based patients and 91.3% of those admitted to intensive care [
Whilst echocardiography provides incremental prognostic information, exposure risks (staff and equipment) must be weighed against the utility of the test, as routine echocardiography in unselected patients may have limited clinical utility. Despite the prevalence of abnormal findings, the echocardiogram may only change management (disease-specific therapy, level of care and haemodynamic support) in a select number of cases [
]. The absence of positive biomarkers is reassuring and may serve as an appropriate gatekeeper, supporting the deferral of non-urgent imaging until infection transmission risk subsides [
ASE Statement on Protection of Patients and Echocardiography Service Providers During the 2019 Novel Coronavirus Outbreak: Endorsed by the American College of Cardiology.
]. However, formal transthoracic echocardiography remains preferable in patients with clinical heart failure, haemodynamic instability, concerning ECG changes (including frequent ectopy or non-sustained ventricular tachycardia), and with cardiac biomarkers suggestive of myocarditis [
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
]. Transoesophageal echocardiography is a potential aerosol-generating procedure and should be performed only when the benefits strongly outweigh the risks [
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
ASE Statement on Protection of Patients and Echocardiography Service Providers During the 2019 Novel Coronavirus Outbreak: Endorsed by the American College of Cardiology.
Whilst principally utilised for pulmonary pathology, computed tomography (CT) may provide incremental information on COVID-19 cardiac complications such as intracardiac thrombus, right heart strain, pericardial and pleural effusions. Although chest CT or pulmonary angiography studies are rarely gated for coronary assessment, prognostically significant coronary artery pathology may be detectable [
] and may help defer formal coronary assessment where clinically appropriate.
Cardiac Magnetic Resonance Imaging
Although not routinely recommended in COVID-19, CMR provides the highest resolution assessment of myocardial structure and function and is the optimal modality in the assessment of acute and chronic myocarditis. Abnormalities in tissue characterisation are common in cases of COVID-19 [
], however, these findings are not specific for acute myocarditis in COVID-19. Studies of CMR are also limited by adherence to defined criteria for myocardial inflammation and parametric mapping protocols [
], is central to the diagnosis of acute myocarditis, and is particularly useful in suspected acute cases following mRNA vaccination. Reporting of late gadolinium enhancement (LGE) patterns has been heterogenous with highly variable degrees of scar and fibrosis [
Cardiac magnetic resonance imaging in Coronavirus disease 2019 (COVID-19): a systematic review of cardiac magnetic resonance imaging findings in 199 patients.
] and many cases of suspected myocarditis may be presumed based on biomarker elevation, rather than diagnostic criteria or histological results. The ESC suggest that CMR has limited utility in this context but may be necessary in selected cases [
Task Force for the management of COVID-19 of the European Society of Cardiology European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
]. CSANZ recommends that inpatient CMR be avoided, given the substantial exposure risks associated with lengthy scan times and equipment contamination [
]. In patients with mRNA vaccination induced myocarditis, CMR may prove a valuable imaging modality to temporally confirm the diagnosis in the absence of endomyocardial biopsy. In practice, CMR should probably be reserved for those with significant biomarker elevation, myocardial dysfunction on echocardiography, or for diagnostic clarity.
Interventional Cardiology Procedures in COVID-19
Detailed recommendations for the utilisation of interventional cardiology facilities for acute coronary syndrome are available [
]. In brief, high-risk patients with ST-elevation myocardial infarction (STEMI) should not proceed to angiography unless urgent catheterisation is deemed likely to significantly alter outcome. To limit exposure, fibrinolysis may be the preferred reperfusion option, even in centres with cardiac catheterisation facilities. Primary intervention using appropriate personal protective equipment (PPE) is appropriate in patients with STEMI and low risk of exposure. For non-ST elevation acute coronary syndromes (NSTEACs), invasive intervention can be reasonably deferred in most cases as there is no strong evidence for reduced mortality or non-fatal myocardial infarction with early invasive angiography [
]. Similarly, invasive angiography should be deferred in all but the highest-risk cases of type 2 myocardial infarction. Management strategies for unstable patients (haemodynamic instability, ongoing ischaemia or arrhythmias) require individual appraisal. Patients with stable coronary artery disease can be appropriately managed with medical therapy [
Electrophysiology procedures, including implantation of permanent pacemakers, should be based on clinical assessment as established in national guidelines, and remote device monitoring employed where appropriate [
Position Statement on the Management of Cardiac Electrophysiology and Cardiac Implantable Electronic Devices in Australia During the COVID-19 Pandemic: A Living Document.
Endomyocardial biopsy is the gold standard for the diagnosis of myocarditis, however, there is limited data regarding the role of biopsy in COVID-19 related disease. Autopsy data suggests the true incidence of clinically significant myocarditis due to COVID-19 is low [
], and biopsy is therefore not routinely recommended. Similarly, pericardiocentesis should only be considered as an urgent therapeutic option in high-risk patients where patient prognosis will be significantly improved.
Discussion
The COVID-19 knowledge base is rapidly expanding. With the increasing emergence of prospective data, the true incidence of myocarditis and serious cardiac complications are more clearly delineated. Early research raised concern for the potentially serious complications associated with myocardial involvement in COVID-19, based principally on elevated troponin levels and non-specific or potentially temporally unrelated findings on CMR tissue characterisation. With more robust evidence emerging, the initial concern over biomarker elevation and the potential relationship with myocarditis and significant myocardial injury has been tempered, with acceptance that myocardial injury or low-level inflammation is common but of minimal clinical significance. The incidence rate of myocarditis in those with COVID-19 is approximately 11 per 100,000 cases, compared with approximately 2.7 per 100,000 cases in those who have received the mRNA vaccination [
], vaccination is uniformly recommended. Cases in whom significant myocardial involvement occurs are likely to present with more severe illness, and cardiac biomarkers are likely to be more substantially elevated. As such, the presence of normal biomarkers is very reassuring, and in such patients, few major abnormalities are found on echocardiography. Cardiac biomarkers, therefore, serve as an appropriate gatekeeper for cardiac imaging. Where abnormalities are found on highly sensitive imaging techniques such as CMR, there appears to be little long-term consequence.
Overall recommendations considering the evidence and available clinical guidelines are presented in Table 1 and are clinically based, utilising a staged approach to the evaluation of patients with COVID-19. Bedside and advanced imaging techniques appear to be unnecessary for most cases, where clinical reasoning should guide the use of these tests based on the likelihood the results will change management. This approach aims to minimise exposure risk to staff and patients, whilst continually balancing the equation of benefits and risks. Finally, although Australian data exists [
]. Australia is well-suited to “Big Data” initiatives, and given the demand on public resources, equipment, PPE and hospital beds, the allocation of research funding should arguably be determined by the likelihood that studies will be additive to the established worldwide experience. Finally, a mature and cognisant approach to managing patients with COVID-19 is required, whereby appropriate testing procedures should be based on robust evidence and the likelihood of altering the overall management strategy.
Conflict of Interest
None declared.
Funding
None declared.
Acknowledgements
None declared.
References
Whittaker C.
Walker P.G.T.
Alhaffar M.
Hamlet A.
Djaafara B.A.
Ghani A.
et al.
Under-reporting of deaths limits our understanding of true burden of covid-19.
The Task Force for the management of COVID-19 of the European Society of Cardiology
European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1—epidemiology, pathophysiology, and diagnosis.
Position Statement on the Management of Cardiac Electrophysiology and Cardiac Implantable Electronic Devices in Australia During the COVID-19 Pandemic: A Living Document.
Task Force for the management of COVID-19 of the European Society of Cardiology
European Society of Cardiology guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 1-epidemiology, pathophysiology, and diagnosis.
Current State of Knowledge on Aetiology, Diagnosis, Management, and Therapy of Myocarditis: A Position Statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases.
Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 3: hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and other cardiomyopathies, and myocarditis.
ASE Statement on Protection of Patients and Echocardiography Service Providers During the 2019 Novel Coronavirus Outbreak: Endorsed by the American College of Cardiology.
Cardiac magnetic resonance imaging in Coronavirus disease 2019 (COVID-19): a systematic review of cardiac magnetic resonance imaging findings in 199 patients.
Management of Acute Myocardial Infarction During the COVID-19 Pandemic: A Position Statement from the Society for Cardiovascular Angiography and Interventions (SCAI), the American College of Cardiology (ACC), and the American College of Emergency Physicians (ACEP).
We read with interest the article by Holland and colleagues who provide an extensive review and summary of the literature relating to COVID-19 and mRNA vaccine associated myocarditis [1], conditions for which clinical guidance has been lacking. The authors discuss in their article that there is insufficient evidence to recommend antiviral or immunomodulatory therapy (with the exception of significant respiratory involvement for which steroids may be beneficial); however, discussion surrounding the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in COVID-19 and/or mRNA vaccine associated myocarditis is absent.
We thank Lampejo and Durkin for their interest in our recent publication, Myocarditis and Cardiac Complications Associated With COVID-19 and mRNA Vaccination: A Pragmatic Narrative Review to Guide Clinical Practice [1], and for their letter regarding the use of non-steroidal anti-inflammatory drugs (NSAIDs) in these clinical settings.
Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has propelled the world into a global pandemic. In addition to causing death and disability, COVID-19 has contributed to significant individual, economic, social, and political disruption [1]. The current co-occurring global geopolitical instability is fuelled by nationalism, populism, and disrupted global supply chains [2]. Throughout history, we look for critical junctures to help us make sense of changing and evolving circumstances.
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