Discussion and review of literature:
The 2019 novel coronavirus disease is caused by the SARS-CoV-2. The
virus replicates in symptomatic and asymptomatic people and has resulted
in more than 323,000 deaths worldwide as of May 20th, 2020
(https://coronavirus.jhu.edu/map.html). Disease presentation
varies from nonspecific symptoms (fever, cough, sore throat, malaise,
abdominal pain, diarrhea, vomiting)1,7 to pneumonia
and acute respiratory distress syndrome (ARDS).2Cardiovascular involvement is increasingly recognized in critically ill
adult patients; the spectrum varies from myocarditis to acute heart
failure/cardiomyopathy, and may increase the risk of acute myocardial
infarction.4 In adults indirect cardiac injury related
to a hyperinflammatory process and cytokine storm has been
noted.8
On April 27th 2020, the Paediatric Intensive Care
Society released a statement describing a rise in critically ill
pediatric patients presenting with severe multisystem inflammatory
disease related to COVID-19 infection. A recently published
report,7 together with numerous anecdotal reports from
Spain, France, the United Kingdom and the Unites states have described
patients presenting with COVID-19 related hyperinflammatory shock
syndrome. These patients had a range of clinical presentations including
classic Kawasaki disease, atypical Kawasaki disease and toxic shock
syndrome, with and without cardiac dysfunction. The mechanism of the
cardiac injury is unclear but may be associated with a dramatic
inflammatory response and cytokine storm.7,8 The
clinical presentations reported are very similar to our patient, with
unrelenting fever, severe gastrointestinal symptoms, hypotension,
tachycardia, and minimal to no respiratory involvement. Elevated markers
of cardiac injury have also been commonly reported in these patients
pointing towards a more global cardiac involvement as part of the
hyperinflammatory shock syndrome.7 None of these
reports in children however describe concomitant focal myocarditis. Our
case presented with focal electrocardiographic abnormalities (T-wave
inversion in inferior leads) as well as regional wall motion
abnormalities on echocardiography prompting further investigation for
other potential mechanisms of cardiac involvement, such as inflammation.
Inflammation of cardiac muscle, or myocarditis, may be due to direct
virus-related injury to cardiomyocytes or as a consequence of indirect
injury from systemic inflammatory response syndrome or ARDS-induced
hypoxemia.9 Currently, CMRI is the non-invasive gold
standard to detect myocardial dysfunction, edema, and fibrosis, and to
diagnose myocarditis.10 Since its emergence in
December 2019, there have been few reported cases of COVID-19 related
myocarditis in adults6, but none in children. Due to
focal electrocardiographic abnormalities, regional dysfunction on
echocardiography, and reports of varying cardiovascular involvement in
adults with COVID-19, we obtained a CMRI to further delineate the
mechanism of cardiovascular involvement in our patient. CMRI confirmed a
diagnosis of focal myocarditis (suggested by T2 hyper-intensity and
mid-wall LGE) apart from a previously well-described phenomenon of
global cardiac dysfunction related to hyperinflammatory syndrome. In
addition, CMRI provided other useful information in terms of diagnosing
RV dysfunction (not well visualized by Lumify), and ruling out acute
coronary syndrome, reported in adult patients.6 In
contrast to coronary involvement in children with multisystem
inflammatory disease related to COVID-19 infection,7our patient had no coronary involvement, but rather cardiac dysfunction
and features consistent with focal myocarditis.