Systemic Inflammation May Induce Cardiac Injury in COVID-19 Patients Including Children and Adolescents Without Underlying Cardiovascular Diseases: A Systematic Review

https://doi.org/10.1016/j.carrev.2021.04.007Get rights and content
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Highlights

  • COVID-19 patients may develop different types of cardiac injury.

  • Comorbid CVD may increase the risk of developing cardiac injury in COVID-19 patients.

  • Cardiac injury was reported in both children and adults with COVID-19 without CVD.

  • Cardiac injury can be caused by viral attack of the cardiomyocytes or systemic inflammation.

  • In COVID-19, systemic inflammation is most likely the driving factor of cardiac injury.

Abstract

Coronavirus disease 2019(COVID-19) is an ongoing global pandemic with a daily increasing number of affected individuals and a relatively high mortality rate. COVID-19 patients that develop cardiac injury are at increased risk of a worse clinical course with higher rates of mortality. Increasing amounts of evidence suggest that a system-wide inflammatory response and a cytokine storm mediated type syndrome plays a crucial role in disease progression. This systematic review investigates the possible role of hyperinflammation in inducing cardiac injury as one of the severe complications of COVID-19. A systematic literature search was performed using PubMed, Embase and Scopus databases to identify relevant clinical studies that investigated cardiovascular injury manifestations and reported inflammatory and cardiac biomarkers in COVID-19 patients. Only 29 studies met our inclusion criteria and the majority of these studies demonstrated significantly elevated inflammatory and cardiac blood markers. It was evident that underlying cardiovascular diseases may increase the risk of developing cardiac injury. However, many COVID-19 patients included in this review, developed different types of cardiac injury without having any underlying cardiovascular diseases. Furthermore, many of these patients were either children or adolescents. Therefore, age and comorbidities may not always be the two main risk factors that dictate the severity and outcome of COVID-19. Further investigations are required to understand the underlying mechanisms of pathogenicity as an urgent requirement to develop the appropriate treatment and prevention strategies. These strategies may specifically target hyperinflammation as a suspected driving factor for some of the severe complications of COVID-19.

Abbreviations

ARDS
acute respiratory distress syndrome
BNP
brain natriuretic peptide
CI
cardiac injury
CKD
chronic kidney disease
CMR
cardiovascular magnetic resonance imaging
COPD
chronic obstructive pulmonary disease
COVID-19/SARS-COVID-19
severe acute respiratory syndrome coronavirus 2
CRP
C-reactive protein
CT
computed tomography
CVD
cardiovascular disease
DIC
disseminated intravascular coagulation
ECG
electrocardiogram
ECHO
echocardiogram
ECMO
extracorporeal membrane oxygenation
EF
ejection fraction
HCQ
hydroxychloroquine
HFOT
high flow oxygen therapy
HTN
hypertension
HFrEF
heart failure with reduced ejection fraction
IL-1
interleukin 1
IL-6
interleukin 6
IMV
invasive mechanical ventilation
IV fluids
intravenous fluids
IVIg
intravenous immunoglobulin
LA
left atrium
LV
left ventricle
MODS
multiple organ dysfunction syndrome
MRI
magnetic resonance imaging
NIV
non-invasive ventilation
NSAIDs
non-steroidal anti-inflammatory drugs
NT-proBNP
N-terminal (NT)-prohormone brain natriuretic peptide
PCT
procalcitonin
RV
right ventricle
TNF-alpha
tumour necrosis factor-alpha
TPA
tissue plasminogen activator
TTE
transthoracic echocardiography
US
ultrasound

Keywords

Coronavirus
COVID-19
Inflammation
Cardiac injury
Myocarditis

Cited by (0)

1

Equally contributed as first co-authors.

2

Equally contributed as second co-authors.