Key clinical message
Although it is rare presentation, suspicious of COVID-19 infection in
patient with acute pericarditis is crucial in setting of pandemic
irrespective of absent of typical clinical feature of COVID-19.
Introduction:
Since the first case of coronavirus disease (COVID-19) in Wuhan, China
in late December 2019 and up to now with emerging of mutated virus
variants such as Delta and Omicron Variant’s; Sever Acute Respiratory
Syndrome Coronavirus-2 (SARS-CoV-2) remains the most common
presentation, which frequently presents with respiratory symptoms that
can progress to pneumonia, and in severe cases, acute respiratory
distress syndrome (ARDS) and shock (1). However, there are increasing
concerns of cardiovascular manifestations and complications that can
occur due to the virus, which may occur either isolated or concomitant
with a pulmonary disease. The commonest cardiac complications include:
acute myocardial injury, arrhythmias, acute myocarditis and severe left
ventricular dysfunction (2). Conversely, some cases of pericarditis and
pericardial effusion have been reported within recent months, which
necessitate this case report to review and improve understanding of
uncommon presentations and complications that may occur with COVID-19
(3). Hereby, we report a 50 years old male who presented with acute
chest pain diagnosed as acute pericarditis complicated with pericardial
effusion due to COVID-19 after exclusion of other possible causes.
Case presentation:
A previously healthy 50-years old Sudanese man with clear medical
background presented to Medani Teaching Hospital in Wad Medani, Sudan,
complaining of chest pain; stabbing in nature, increased in severity in
supine position and improved by leaning forward. He denied any history
of cough or shortness of breath.
During physical examination, the patient noticed that he preferred
sitting leaning forward, but not dyspneic. His BP was 160/80, pulse rate
96 regular, temperature 38.1 and oxygen saturation 96 % on room air.
The JVP was not raised. Pericardial friction rub was not heard.
Cardiovascular and chest examination was unremarkable.
Initial laboratory investigations revealed the following: WBCs 11.0 ×
109/L (4.0 -11.0 × 109/L), lymphopenia 5%, ESR 50mm / hour, the liver
and kidney function were within normal values. D-dimer was 350 ng/ml.
Serum quantitative troponin was 0.5 ng/ml (normal lab value 0-0.6
ng/ml). ECG Showed widespread ST-segment elevation and the baseline
trans-thoracic echocardiography was normal; hence, the patient was
diagnosed as acute pericarditis according to European Society of
Cardiology Diagnostic Criteria (Typical pericardial chest pain and new
widespread ST-segment elevation) in addition to raised inflammatory
markers. At first, the patient received I.V fluids, ibuprofen tabs 600
mg TDS and was advised to restrict exercise. But the presence of
lymphopenia necessitated exclusion of COVID-19 – as an emerging
pandemic - so nasopharyngeal swap had been taken for (PCR), which came
back later positive. The patient was admitted to the isolation center of
COVID-19. According to local guidelines of COVID-19 management, the
patient was started on paracetamol infusion, low molecular weight
heparin (LMWH) 75 IU / kg, dexamethasone 6 mg QID, and vitamins
supplement and Ibuprofen tabs were replaced with paracetamol.
On the fifth day of admission, the patient developed mild shortness of
breath and dry cough. Physical examination revealed a dyspneic,
tachypneic patient without raised JVP, BP was 140 / 80; further
assessment showed that the apex beat was difficult to locate with
muffled first and second heart sound, also there were no added sounds or
murmurs. The ECG showed low voltage QRS complexes in all leads (Figure
1). The chest radiograph revealed an enlarged cardiac silhouette with
absence of pulmonary infiltrates, and no pleural effusion was detected
(Figure 2). Subsequently, a transthoracic echocardiogram was performed
which showed a moderate pericardial effusion not consisting with
tamponade, with no regional wall motion abnormalities. Left ventricular
ejection fraction was 55%. Laboratory investigations showed an elevated
C- reactive protein (CRP) level 150 mg / L (0-10 mg / L).
Pericardiocentesis was not performed considering the absence of cardiac
tamponade features, moderate pericardial effusion, and that there was no
suspicion of bacterial or neoplastic etiology. The patient was continued
on LMWH 75 IU / kg, dexamethasone 6 mg QID, and vitamins supplements;
follow-up 8 days later showed clinical and laboratory improvement, and
subsequent resolution of effusion on echocardiogram only to confirm
COVID-19 clearance with a negative PCR, which made discharge a suitable
decision, and for the patient to be seen one month later on refer
clinic.
Discussion:
The coronavirus infection 2019 (COVID-19), which is caused by
SARS-CoV-2, causes mainly respiratory tract symptoms. While much of the
focus has been on pulmonary complications, emergency clinicians need to
be aware of the cardiovascular complications as well, which can be a
significant contributor to the deaths associated with this disease.
Cardiovascular complications that are associated with COVID-19 include:
arrhythmias, acute myocardial infarction, myocarditis, heart failure,
and thromboembolic events (4).These complications could be explained by
many mechanisms such as: plaque rupture and coronary thrombosis,
exaggerated immune response, direct myocardial injury, systemic
inflammation, altered myocardial demand-supply ratio, electrolyte
imbalances or adverse effects of therapies (5).
Acute pericarditis, which is an inflammation of the sac surrounding the
heart, is a rare extra pulmonary complication of COVID-19. Generally,
the etiology of pericarditis could be classified into infectious and
non-infectious (6). Both depend on the clinical context and
epidemiological framework; in developing countries, infectious
etiologies represent the most common causes, whereas Idiopathic or
post-viral infection are the major causes of this illness in developed
countries. Tuberculosis is the commonest cause globally (7). Generally,
it is postulated that viruses can cause pericardial inflammation via
direct cytotoxic effects or immune-mediated mechanisms (8). COVID-19 has
been stated to trigger an exaggerated systemic inflammatory response in
certain patients (9). Likewise in other viral infections, this
inflammatory response could lead to pericarditis and the consequent
pericardial effusion; however, the exact mechanism is unknown. According
to European Society of Cardiology (ESC) guidelines, the diagnosis of
acute pericarditis depends on the presence of at least two out of four
criteria: pericarditis chest pain, pericardial rub, new widespread
ST-segment elevation or PR depression, and new or worsening pericardial
effusion. Additional finding that can support the diagnosis of acute
pericarditis include: Elevation of inflammatory markers (white blood
cell count, C-reactive protein and erythrocyte sedimentation rate),
evidence of pericardial inflammation on computed tomography (CT) and
cardiac magnetic resonance (CMR).
However, in our patients, we did not perform pericardiocentesis due to
the nonexistence of cardiac tamponade features, the moderate pericardial
effusion, and absence of suspicion regarding bacterial or neoplastic
etiology. Moreover, the molecular diagnosis of other viral causes of
pericarditis is unavailable in our center. Therefore, the diagnosis of
pericarditis due to COVID-19 in this patient is presumptive.
The mainstay treatment of acute pericarditis is a high-dose aspirin and
NSAIDs, other options include colchicine (8). A patient who has
contraindications or failed to respond to first-line therapy may get
benefit from corticosteroids. In our patient, we considered
administering colchicine - as it remains a more suitable drug than
steroids - but it was unavailable in the center. Using corticosteroids
and NSAIDs could worsen the general condition of COVID-19 patients; and
this has emerged us a management dilemma due to safety concerns
regarding our patient (8). To date, no evidence prohibits the use of
high-dose aspirin in Covid-19 patients (5). The matters were mainly
regarding the use of ibuprofen, and there is no compelling evidence
available connecting “worsening of COVID-19 patients’ status” with
“aspirin or other NSAIDs”. To navigate this uncertainty, the use of
NSAIDs when clinically indicated was supported by the Centre for Disease
Control and Prevention (CDC) and the US Food and Drug Administration
(FDA).
The most frequent anticoagulant for COVID-19 patients is LMWH, which is
correlated with survival when administered at a prophylactic dose (10).
Regarding use of LMWH in our patient, we continued its administration
until the patient showed improvement and clearance of COVID-19 hence
discharge.
Predictors of poor prognosis in acute pericarditis include the
following: fever more than 38, large pericardial effusion, sub-acute
onset, cardiac tamponade and lack of response to NSAID or aspirin after
at least one week of therapy (11). Our patient presented with a fever of
38.1 C, which resembled a poor prognostic feature, hence required
additional monitoring; but due to the preparedness of the team and the
careful evaluation, we were fortunate to tackle this case successfully.
Therefore, in order to achieve the best outcome for patients, we
emphasize on the importance of prior knowledge of prognostic factors,
careful evaluation and immediate optimal responses.
Conclusion:
Acute pericarditis and pericardial effusion are rare extra-pulmonary
presentations of COVID-19, especially without concomitant pulmonary
disease or myocardial injury. A high index of suspicion is necessary to
assure early diagnosis and treatment. Studies are needed to determine
the exact mechanism of acute pericarditis and pericardial effusion in
COVID-19 patients and the optimal therapeutic strategies.