Sudden Cardiac Death in a Patient with Systemic Lupus
Erythematosus and Cytomegalovirus Myocarditis
Justin Chow, MD, FRCPC
, Umair Iftikhar, MD
, Victoria Weaver, MD, FRCPC
, Kwadwo Mponponsuo, MD
Amy Bromley, MD, FRCPC
Department of Medicine, University of Calgary, Calgary, AB, Canada;
Department of Medicine, Division of Cardiology, McMaster University, Hamilton, ON, Canada;
Department of Medicine, Division of Cardiology, McGill University, Montreal, QC, Canada;
Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, BC, Canada;
Department of Medicine, Division of Infectious Diseases, University of Calgary, Calgary, AB, Canada;
Department of Pathology and Laboratory Medicine, University of Calgary, Calgary, AB, Canada
Corresponding Author: Dr. Justin Chow:
Submitted: October10, 2019; Accepted: November 16, 2019; Published: 18 November, 2020.
Myocarditis is generally a self-limited illness with a benign course. Certain pathogens—such as
cytomegalovirus (CMV)—can cause severe/fulminant forms of myocarditis leading to congestive
heart failure or sudden cardiac death (SCD).
Case Presentation
A 54-year-old female was diagnosed with systemic lupus erythematosus (SLE) in hospital and
received inpatient immunosuppression due to significant multi-organ involvement. After a
prolonged admission, she later died of an in-hospital cardiac arrest. Autopsy revealed CMV
myocarditis involving the anterior wall of the left ventricle and cardiac conduction system. We
postulated that both CMV and complications of SLE caused the patient’s SCD.
Myocarditis can vary in its presentation, severity, and diagnostic workup. Immunocompromised
hosts are at risk of opportunistic infections such as CMV and are therefore prone to developing
more severe forms of myocarditis. When caring for this patient population, it becomes necessary
for clinicians to consider atypical manifestations of opportunistic pathogens in their diagnostic
La myocardite est généralement une maladie autolimitée dont l’évolution est bénigne. Certains
agents pathogènes, tels que le cytomégalovirus (CMV), peuvent provoquer des formes graves/
fulminantes de myocardite entraînant une insuffisance cardiaque congestive ou une mort
cardiaque subite (MCS).
Canadian Journal of General Internal Medicine
36 Volume 15, Issue 4, 2020
Nazaryan et al.
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Présentation de cas
Une femme de 54 ans a reçu un diagnostic de lupus érythémateux disséminé (LED) à l’hôpital et a
été hospitalisée pour une immunosuppression due à une importante atteinte de plusieurs organes.
Après une longue hospitalisation, elle est décédée d’un arrêt cardiaque à l’hôpital. Lautopsie a
révélé une myocardite à CMV impliquant la paroi antérieure du ventricule gauche et le système
de conduction cardiaque. Nous avons émis l’hypothèse que le CMV et les complications du LED
étaient tous deux à lorigine de l’arrêt cardiaque de la patiente.
La myocardite peut varier dans sa présentation, sa gravité et son diagnostic. Les hôtes
immunodéprimés sont exposés au risque d’infections opportunistes telles que le CMV et sont
donc susceptibles de développer des formes plus graves de myocardite. Lorsqu’ils soccupent de
cette population de patients, les cliniciens doivent tenir compte des manifestations atypiques
des agents pathogènes opportunistes dans leur approche diagnostique.
Keywords: cytomegalovirus; myocarditis; sudden cardiac death; systemic lupus erythematosus
Case Presentation
A 54-year-old female presented to the emergency department
with 4 weeks of fever, malaise, and anorexia. Her past medical
history included osteoporosis as well as a history of inflammatory
poly-arthralgia, not yet diagnosed—for which she was undergoing
outpatient workup by a rheumatologist. Family history was
significant for a sibling who had died in her forties from
complications related to systemic lupus erythematosus (SLE).
The patients only medications were alendronate and analgesics
(celecoxib and tramadol) as needed.
On examination, the patient’s temperature was 38.1°C, blood
pressure 85/58 mmHg with orthostatic changes, heart rate of 88
beats per minute, and respiratory rate of 18 breaths per minute.
Oxygen saturation was 74% on room air and increased to 92%
with 4 L of supplemental oxygen. Jugular venous pressure was flat
and oral mucosa was dry in keeping with intravascular volume
depletion. On auscultation, breath sounds were decreased with
bibasilar crackles. On examination, no other localizing signs of
infection were noted.
Admission investigations showed a white blood cell
(WBC) count of 1.7 (normal 2.0–9.0) × 10
, mild elevation
in high-sensitivity troponin T of 22 (normal 0–14) ng/L, and
mild liver function test abnormalities: alanine transaminase
(ALT) 89 (normal 1–40) U/L, alkaline phosphatase (ALP) 108
(normal 30–115) U/L, gamma-glutamyltransferase (GGT) 113
(normal 8–35) U/L, and lipase 204 (normal 0–80) U/L. Other
labs were normal. A 12-lead electrocardiogram showed normal
sinus rhythm. A portable anterior-posterior chest x-ray in the
emergency department revealed consolidation of the right lower
lobe (Figure 1). The patient was subsequently admitted to the
hospital with a diagnosis of sepsis due to community-acquired
The patient was started on intravenous (IV) fluids and
antibiotics (ceftriaxone and azithromycin). Given the mild
troponin elevation, a transthoracic echocardiogram was performed
to assess cardiac dysfunction; this study was normal. Despite
the initial clinical improvement, the patient developed severe
acute respiratory distress syndrome requiring intubation and
admission to the intensive care unit (ICU). Continuous renal
replacement therapy was initiated to manage acute renal failure.
An extensive infectious workup including bronchoalveolar lavage
and lumbar puncture failed to yield a microbiologic diagnosis.
Rheumatologic consultation was obtained given the patient’s
history of inflammatory polyarthralgia, family history of SLE,
and leukopenia. She was ultimately diagnosed with SLE based on
hypocomplementemia and a positive anti-ribosomal P antigen
(of note, the antinuclear antibody was positive at 1:80 and anti-
double-stranded DNA was negative). In addition to empiric
broad-spectrum antibiotics, the patient underwent combined
immunosuppressive therapy with IV steroids, immune globulin,
and cyclophosphamide. These measures again resulted in clinical
improvement and eventual transfer back to the ward.
Unfortunately, 10 days after leaving the ICU the patient suffered
a witnessed cardiac arrest while ambulating to the washroom
and a code blue was activated immediately. Her initial cardiac
rhythm was a pulseless electrical activity which later degenerated
to ventricular fibrillation. Despite exhaustive resuscitative efforts
and the eventual return of spontaneous circulation, the patient
developed refractory shock and multi-organ dysfunction. She
died several hours later in the ICU.
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Case Report
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