Myocardial Inflammation in Systemic Lupus Erythematosus

The over-arching goal of this work is to further the understanding of myocardial damage in
systemic lupus erythematosus (SLE) using state of the art CV imaging to investigate a novel
potential mechanism of CV injury in SLE, subclinical myocardial inflammation.

Aim 1: Investigate an alternative pathway for CV morbidity in SLE by measuring myocardial
edema at time of moderate to severe flare and compare values to post-flare studies and
historical healthy controls.

Hypothesis 1: Myocardial edema, measured quantitatively with T2 CMR mapping during moderate
to severe SLE flare will be significantly increased compared to 1) historical controls and
2) in SLE patients after resolution of flare.

Aim 2: Perform exploratory analyses investigating relationships between myocardial edema on
CMR and markers of SLE disease activity and CV risk factors.

Hypothesis 2: Markers of disease activity including inflammatory makers (ESR and high
sensitivity c-reactive protein), complement and autoantibody levels will predict the
presence of T2 CMR detected myocardial edema during flare.

Inclusion Criteria:

- • Diagnosis of SLE by American College of Rheumatology Classification Criteria [21]

- Active SLE Flare defined by Systemic Lupus Erythematosus Disease Activity Index
(SLEDAI)[22] > 6 or British Isles Lupus Assessment Group (BILAG) Index A or
B.[23]

Exclusion Criteria:

- Pregnant

- Allergy to gadolinium

- Severe claustrophobia

- Renal replacement therapy or glomerular filtration rate (GFR) < 30 mL/min/1.75m²

- Medically unstable for transportation to Ross MRI scanner. Stability will be defined
as: not on mechanical ventilation, HR < 120 BPM, MAP > 65 mmHg. The treating
providers' input on the patient's stability will also be considered in addition to
these criteria

- Weight > 500 pounds

- MR incompatible implanted devices such as neurostimulator pacemakers and implantable
defibrillators, presence of intracranial metal or any metal not compatible with CMR