https://doi.org/10.53453/ms.2024.3.5
Janssen COVID-19 vaccine-related acute myocarditis
Gabriele Kybartaite
1
, Gabriele Rudokaite
2
, Jolanta Laukaitiene
2
1
Faculty of Medicine, Academy of Medicine, Lithuanian University of Health Sciences, Lithuania
2
Department of Cardiology, Hospital of Lithuanian University of Health Sciences Kaunas Clinics, Lithuania
Abstract
Introduction: according to reports, there is a link between the development of myocarditis and the use of coronavirus
vaccines.
Case presentation: we present two cases of male adolescents aged 19 and 49 who developed acute myocarditis within
a few days after receiving the second dose of the Janssen vaccine. They presented with acute chest pain, elevated
troponins, and ST elevations in the precordial leads without reciprocal changes. Although there is no formal evidence,
the presentation patterns and clinical course are associated with the COVID-19 vaccine. Myocarditis was confirmed
by cardiac magnetic resonance. During their hospitalization, both patients' hemodynamic status remained stable. There
was no evidence of an infectious or autoimmune etiology.
Conclusions: myocarditis is a rare complication following SARS-CoV-2 vaccination and benefits of vaccination
outweigh the risks and should not be avoided, especially for patients with underlying heart disease.
Keywords: acute myocarditis, COVID-19, Janssen vaccine
Journal of Medical Sciences. 11 Mar, 2024 - Volume 12 | Issue 2. Electronic - ISSN: 2345-0592
Medical Sciences 2024 Vol. 12 (2), p. 39-45, https://doi.org/10.53453/ms.2024.3.5
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1. Introduction
Myocarditis is characterized by progressive
inflammation of the middle layer of the heart, followed
by myocardium injury without ischemic events. Either
infectious or non-infectious agents can cause
myocarditis [1]. One of the causes of non-infectious
myocarditis is myocarditis as an adverse reaction to
the vaccine. It was primarily described for the
smallpox vaccine [2] and a few cases of myocarditis
following the seasonal influenza vaccine in otherwise
healthy adults, but the relationship is difficult to
establish, and the case reports could have been due to
chance [3]. COVID-19 vaccination began in Lithuania
in late December 2020 with mRNA vaccines from
Pfizer-BioNTech and Moderna; the Janssen vaccine
was introduced more recently in April 2021, and
people over the age of 18 may have been vaccinated.
Using mRNA-based vaccines, immunization against
COVID-19 and other viral pathogens is a new and
promising technology [4]. Systemic adverse reactions
after the second dose were reported more frequently in
clinical trials, primarily in younger males, with a
median onset time of one to two days [5].
2. Case presentation
2.1 Case nr. 1
A 19-year-old previously healthy male arrived at the
emergency department (ED) and presented with a
chief complaint of non-radiating chest pain of 3 days
duration. He reported pressure-like, dull pain, 8-9/10
intensity, not relieved by non-steroidal anti-
inflammatory drugs or paracetamol. He reported
receiving the second dose of the COVID-19 Janssen
vaccine four days before the symptoms. Soon after the
vaccination, he had a fever up to 39°C that lasted for
three days; the day after, chest pain occurred. He had
no previous history of viral illnesses and no known
COVID-19 exposure. ECG demonstrated sinus
rhythm, HR 80 bpm, ST elevation in the precordial
leads without reciprocal changes, as it is shown in
Figure 1. CRP was 43.78 mg/l (normal 0-5 mg/l),
troponin T 535.6 ng/l (normal 0-14 ng/l), leukocytes
10.07x10
9
/l (normal 3.6-10.2x10
9
/l) and BNP
74.2 ng/l (normal 0-26.5 ng/l) thus he was transferred
to University hospital for a cardiologist evaluation
(Table 1).
The laboratory testing showed high troponin I levels –
9.12 g/l (normal 0-0.04g/l); bedside echocardiography
revealed hypokinetic posterior and inferior walls of the
left ventricle. Coronary angiography showed no signs
of stenosis. The myocarditis was suspected, and the
patient was admitted to the Department of Cardiology.
The cardiac MRI revealed an increase in end-diastolic
volume (EDV), an increase of end-systolic volume
(ESV), decreased ejection fraction (EF) (40 %), areas
with elevated signal intensity in T2 sequence
indicating edema, late gadolinium accumulation and
signs of acute myocardial injury subepicardial, mostly
on basal segments of inferior and posterior walls, as
shown in Figure 2. No signs of significant arrhythmias
or conduction disturbances were registered. An
echocardiogram performed on the third post-
admission day revealed a dilated left ventricle (LV),
poor contraction of the inferior, posterior, and lateral
walls, and inferior part of the interventricular septum.
The patient received intravenous ketorolac 30 mg p.r.n
for pain. Troponin level decreased 50 % over the first
two 48 hours and almost reached a normal level
(0.06 g/l) on the day of discharge. He was discharged
from the hospital on day six due to improved
symptoms and a lower troponin level. At the time of
this submission, the patient had not yet returned for a
follow-up visit.
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Table 1. Summary of diagnostics in two patients with symptomatic myocarditis following the second dose of Janssen
COVID-19 vaccine.
Patient 1
Patient 2
Troponin I
8.18
9.75
Highest troponin
8.18
9.75
Lowest troponin (before
discharge)
0.06
0.04
BNP
74.2
97.1
CRP
57.1
5.0
COVID-19 PCR result
Negative
Negative on the day of admission,
positive before discharging
ECG
Sinus rhythm, T-wave abnormality, signs
of early repolarisation, ST elevation in
leads V7 – V9
Sinus rhythm, ST elevation in the
precordial leads without reciprocal
changes
Echocardiogram
Moderate dilation of LV, poor basal
segments of LV contraction
Poor LV contraction, decreased EF,
higher pericardium intensity
Cardiac MRI
LGE (subepicardial) involving inferior
and posterior LV basal segments;
myocardial edema of anterior LV wall,
apex, and all basal segments; decreased
EF.
LGE (subepicardial and midventricular)
involving lateral LV wall and apex;
myocardial edema of apical segments.
* Except for the lowest troponin recorded before discharge, laboratory test values were chosen on the day of
admission. LGE – late gadolinium enhancement; LV – left ventricle; EF – ejection fraction;
Figure 1. ECG showing ST elevation in the precordial leads without reciprocal changes
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Figure 2. Cardiac MRI showing signs of late
gadolinium enhancement
2.2 Case nr. 2
A 49-year-old male presented to the emergency
department with a chief complaint of acute chest pain
that radiates to the shoulders and left arm and is
evaluated 10/10 in intensity. The patient stated that he
was suffering from chest pain for the second time. He
claimed that he had received the second dose of the
COVID-19 Janssen vaccine two days prior to the onset
of the symptoms. He had no prior history of viral
illnesses and had never been exposed to COVID-19.
The primary evaluation consisted of ECG, which
showed sinus rhythm, HR 102 bpm, ST elevation in
the precordial leads without reciprocal changes, as
shown in Figure 3; laboratory testing, which revealed
an elevated troponin I 3496 (normal up to 100),
echocardiography showed signs of the hypokinetic
interventricular septum and anterior wall of the left
ventricle (Table 1). He was prescribed dual antiplatelet
therapy and transferred to the university hospital's
emergency department. He received anticoagulant
therapy and was admitted to the cardiac intensive care
unit (CICU) for further differentiation between acute
coronary syndrome (ACS) and myopericarditis.
Urgent cardiac catheterization revealed less than 50 %
lumen stenoses, and ACS diagnosis was rejected. He
was transferred to the Department of Cardiology for
further investigations and treatment. X-ray showed no
signs of pericardial effusion. Premature ventricular
complex (PVC) triplets were detected using Holter
monitoring. For the confirmation of the diagnosis,
MRI was done and revealed normal EF (69 %),
increased EDV, higher signal intensity in T2 sequence
indicating edema in apical regions, late gadolinium
accumulation, all primarily in the subepicardial and
midventricular apical and lateral LV free wall, also in
the interventricular septum, as shown in Figure 4.The
patient received ibuprofen 600 mg orally three times a
day. When the treatment began, myocardial damage
markers were significantly reduced. On day nine, he
was discharged from the hospital due to improved
symptoms and a lower troponin level. The day before
discharge, a positive COVID-19 PCR result was
found. His outpatient follow-up appointment is in 30
days. At the time of this submission, he had not yet
returned for a follow-up visit.
Figure 4. Cardiac MRI showing higher signal
intensity in T2 and late gadolinium enhancement.
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Figure 3. ECG with ST elevation in the precordial leads without reciprocal changes.
3. Discussion
3.1 COVID-19 vaccines and myocarditis
The coronavirus disease-2019 (COVID-19) outbreak
was declared a pandemic by the World Health
Organisation (WHO) on 11 March 2020, and the
development of an effective COVID-19 vaccine
rapidly became a global priority. Indeed, vaccination
is a settled component of preventive medicine but is
not without risk. COVID-19 vaccines mostly lead to
minor side effects, such as pain, redness, or swelling
on the injection site, and systemic symptoms, such as
fatigue, headache, or fever [6]. Viral infection is one
of the most common causes of myocarditis, mainly
associated with influenza and parvovirus B19
infection. Vaccines can also cause myocarditis, and
the most robust associations have been reported with
the smallpox vaccine [7], but it is considered an
unusual adverse event after vaccination [8]. The
Janssen COVID-19 vaccine has been granted an
Emergency Use Authorization (EUA) for individuals
18 years old and older. Like our patients, most
reported cases describe young male patients with no
past cardiac medical history, presenting with chest
pain within a few days after their second vaccine dose
of COVID-19 vaccine and finally diagnosed with
myocarditis. Li et al. [9] noted the incidence rate and
risk for myocarditis and pericarditis following
COVID-19 vaccination in the US according to age and
type of vaccine. The incidence rate of myocar-
ditis/pericarditis was 5.64/1 million doses after recei-
ving the Janssen vaccine, 4.98/1 million doses after
receiving the Moderna vaccine, and 6.70/1 million
doses after receiving the Pfizer-BioNTech vaccine.
Janssen was not associated with a higher incidence
rate of myocarditis/pericarditis in comparison to other
vaccines (odds ratio 1.39; 95 % Cl, 0.99-1.97).
Distribution according to gender was 34.6 % female
and 65.4 % male [9]. Although age (mainly <30 years)
and sex (mainly male) may modify general conside-
rations of the small risk for myocarditis after COVID-
19 vaccination, a discussion should consider an
individual personal risk based on their health status
[10]. Another study of individuals was conducted by
Takuva et al. [11], where they reported data about the
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frequency and incidence rate of myocarditis in South
African individuals who were vaccinated with the
Janssen vaccine. It was found that the median age of
the total population was 42 year, and the majority was
women. The incidence of myocarditis was 1.06 per
100 000 participants [11]. Analysis of Vaccine
Adverse Effects Reporting System (VAERS) for
episodes of myocarditis following COVID-19 vacci-
nation was significant for an increased prevalence of
myocarditis in males, consistent with prior findings.
Individuals below 40 years old, who accounted for
32 % of the total full vaccination, resulted in 81 % of
the myocarditis case in VAERS. As there is wide-
spread vaccine distribution, increasing cases of myo-
carditis have been detected with the mRNA vaccines.
Since the Janssen vaccine has a similar end product as
the mRNA vaccines, further cases of myocarditis with
the Janssen vaccine may be expected [12, 13].
3.2 Diagnosis of vaccine caused myocarditis
Centers for Disease Control and Prevention (CDC)
recommends ECG, troponin level, and inflammatory
markers such as C-reactive protein and erythrocyte
sedimentation rate for initial evaluation of COVID-19
vaccines caused myocarditis. Myocarditis is unlikely
in the setting of normal ECG, troponin, and
inflammatory markers [14]. A recent systematic
review revealed that myocarditis mainly progresses
with marked elevation in cardiac troponins, CK-MB,
BNP, and CRP in COVID-19 vaccine patients with
myocarditis [15]. ECG is considered a second-order
investigation due to the insufficient specificity of the
findings. However, most ECGs have one of the
following: ST elevation, PR depression, new-onset of
bundle branch block, QT prolongation, pseudo-infarct
patterns, PVC, bradyarrhythmia with an advanced
atrioventricular nodal block [16]. American Heart
Association (AHA) recommends that patients with
clinical and biochemical abnormalities of myocarditis
require to be tested with further imaging modalities,
such as echocardiogram and cardiovascular magnetic
resonance (CMR) [17]. Echocardiography helps
determine potential complications and evaluate
possible abnormalities, such as higher wall thickness,
chamber dilation, pericardial effusion, global or
regional hypokinesia, and systolic dysfunction. CMR
helps to determine myocardial edema and injury and
pericardial effusion. It also includes T1/T2-weighted
imaging criteria for myocardial inflammation [17]. It
is essential to rule out other possible causes of the
presentation, specifically acute coronary syndromes
and other cardiovascular or extra-cardiac non-
inflammatory diseases that could explain the clinical
presentation. In our cases, cardiac catheterization has
been performed, and acute coronary syndromes were
ruled out.
4. Conclusion
Myocarditis is a rare complication following SARS-
CoV-2 vaccination. Although the actual incidence of
myocarditis following mRNA COVID-19 vaccines is
unknown, this raises concerns about the potential for
adverse cardiovascular effects, particularly in young
patients. Based on current knowledge, the benefits of
vaccination outweigh the risks and should not be
avoided, especially for patients with underlying heart
disease.
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