Background/Purpose:   Cardiovascular (CV) disease is an important cause of morbidity in systemic lupus erythematosus (SLE) .  Myocarditis is considered an uncommon complication of SLE but autopsy studies suggest prevalence of up to 40%.  With this study we used cardiac magenetic resonance (CMR) quantitative T2 mapping to assess for subclinical myocardial involvement during SLE flare.  

Methods:   Consecutive patients with active SLE (defined by SLEDAI > 5 and clinician’s intention to change therapy due to disease activity) without bias to CV symptoms were enrolled at a single academic center.  Clinical, demographic and laboratory data were collected. CMR was performed on 1.5 Tesla scanner and included cine imaging, T2 mapping in long and short axes. Late gadolinium enhancement was assessed after contrast administration if GFR > 30.  Left ventricular (LV) end diastolic volumes, end systolic mass and peak circumferential strain were measured.  All images were scored by an experienced, blinded reader.  To reduce artifactual findings, T2 mapping was limited to the 6 mid cardiac segments, and involvement of ≥2 mid-segments was considered abnormal. Based upon myocarditis literature, T2 scores > 59 ms were considered abnormal. Descriptive statistics were performed; means were compared using Student’s t-test and correlation assessed with Pearsons’ coefficient.

Results:   27 patients underwent CMR: mean age 32.4 years, 82% female, 44% black, mean SLEDAI-2K 10.4, mean SLICC DI 0.52 (see Table 1).  12/27 (44%) of patients had ≥ 2 mid cardiac segments with elevated T2 signal (Table 2). The mean T2 signal for mid cardiac segments was elevated compared to 40 historical healthy controls (57.0 ms ± 5 vs. 54.5 ms ± 2.2; p= 0.010)   The mean LV circumferential strain was -15.2% ± 5.4 which is lower than accepted normal values (-20%).  SLEDAI-2K scores positively correlated with mean mid cardiac T2 signal (r = 0.57); and mid cardiac maximum T2 signal (r = 0.65). Only 2/27 (7%) patients had positive LGE.

Conclusion: In this cohort of active SLE patients, CMR with quantitative T2 mapping identified a high prevalence (44%) of patients with abnormal T2 signal in ≥2 mid cardiac segments, suggesting subclinical myocardial inflammation may be common in SLE flare. Both mean and max mid segment T2 showed correlation with SLE disease activity measured by SLEDAI scores.  Mean LV circumferential strain was lower than normal, suggesting impaired LV function.  Very few CMR showed evidence of myocardial fibrosis as measured by LGE enhancement. Further study is needed to determine if abnormal quantitative T2 mapping during SLE flare foreshadows longer term CV complications.  

Table 1:  Patient Characteristics
Age, mean ± SD years	32.4 ± 9.7
Female, no. (%)	22 (82%)
Black/White/Other, no. (%)	12 (44%), 11 (41%), 4 (15%)
Hispanic, no. (%)	2 (7%)
History of hypertension, no. (%)	9 (33%)
History of hyperlipidemia, no. (%)	6 (22%)
History of myocardial infarction, no. (%)	0
History of ischemic stroke, no. (%)	3 (11%)
History of congestive heart failure, no. (%)	0
Current/former smoker, no. (%)	9 (33%)
Anti-phospholipid antibody positive, no. (%)	6 (22%)
Anti-phospholipid antibody syndrome, no. (%)	1 (4%)
SLEDAI-2K score, mean ± SD	10.4 ± 6.3
SLICC Damage Index, mean ± SD	0.5 ± 0.77
Troponin I, mean ±, ng/mL	0.057 ± 0.009
CK, mean ± SD, U/L	146.8 ±500.6
C-reactive protein ± mg/L	25.6 ±16.1

 

Table 2: CMR Findings in Patients with Active SLE
≥ 2 mid segments with T2 >59 ms, no. (%)	12 (44%)
Mean mid segment T2, mean ± ms	57.2 ± 5.0
Peak mid segment  T2, mean ± ms	63.0 ± 7.7
Heart rate, mean ±SD	78.4 ± 16.0
LV end diastolic volume, mean ±SD	147.9 ± 35.5
LV end systolic volume, mean ±SD	61.9 ± 30.7
LV ejection fraction, mean  ± SD, %	0.60 ± 0.10
LV mass, mean ± SD	86.5 ±29.6

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