Session Information
Date: Monday, November 9, 2015
Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment Poster Session II
Session Type: ACR Poster Session B
Session Time: 9:00AM-11:00AM
Background/Purpose: Accelerated atherosclerosis leading to premature coronary artery disease remains the major cause of late death in SLE. Coronary artery calcium (CAC) is a late phase of atherosclerosis. Noncalcified coronary plaque (NCP) represents an early inflammatory plaque more likely to rupture.
Methods: To determine rates of CAC and NCP progression and identify risk factors for progression, CT angiography was performed at baseline and after several years of follow-up in 38 SLE patients; 36 scans allowed repeat assessment of NCP and 35 for CAC. Duration between assessments was 2-3 years (13%), 3-4 years (53%), 4-7 years (21%) and >7 years (13%). Of the patients, 37% were below 45 years; 76% female; 74% Caucasian and 18% African-American. CAC was quantified by the Agatston score and classified as none, low (1-99) or high (100+). NCP was quantified based on a score that we have previously described and classified as none, low (<0.5) or high (0.5+). SLE disease activity was quantified using the SELENA-SLEDAI and Physician Global Assessment (PGA) indices. To assess the association between quantitative clinical variables and changes in NCP adjusting for time we fit linear regression models.
Results: Tables 1 and 2 show the follow-up classifications for CAC and NCP, respectively, by baseline classification.
Table 1: Number (%) with CAC at follow-up by baseline level |
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|
|
Follow-up |
||
Baseline |
|
None |
Low |
High |
None |
23 (96%) |
1 ( 4%) |
0 ( 0%) |
|
Low |
1 (20%) |
3 (60%) |
1 ( 20%) |
|
High |
0 ( 0%) |
0 ( 0%) |
6 (100%) |
Table 2: Number (%) with NCP at follow-up by baseline level |
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|
|
Follow-up |
||
Baseline |
|
Low |
Medium |
High |
Low |
4 (33%) |
3 (25%) |
5 (42%) |
|
Medium |
1 ( 6%) |
13 (72%) |
4 (22%) |
|
HIgh |
0 ( 0%) |
4 (67%) |
2 (18%) |
For CAC, the pre-post scores agreed qualitatively for 32/35 (91%), while for NCP, the pre-post scores agree qualitatively for 19/36 (53%). Twelve (33%) had an increase in NCP while 5 had a decrease. Change in NCP was positively associated with time between assessments (estimated mean change score of 0.09 per year, p=0.038). Table 3 shows the association between various exposures experienced between the assessments and mean change in NCP score.
Table 3. Mean change in NCP score by various clinical variables, adjusted for time between assessments. |
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Clinical Variable |
Mean Change* |
P-value |
SLEDAI at the time of follow-up assessment |
0.01 (per 1 unit change) |
0.82 |
PGA at the time of follow-up assessment |
-0.16 (per 1 unit change) |
0.28 |
Mean SLEDAI |
-0.02 (per 1 unit change) |
0.63 |
Mean PGA |
-0.19 (per 1 unit change) |
0.20 |
Mean Systolic Blood Pressure |
-0.08 (per 10 mmHg change) |
0.19 |
Mean Total Serum Cholesterol |
-0.08 (per 25 mm/dl change |
0.26 |
History of Smoking |
-0.12 |
0.49 |
Current Smoking |
-0.33 |
0.17 |
Mean Lupus Anticoagulant (dRVVT) |
0.01 (per second) |
0.61 |
Proportion of time with Low C3 |
0.06 (per 0.5 difference) |
0.66 |
Proportion of time with Low C4 |
-0.01 (per 0.5 difference) |
0.95 |
Proportion of time with positive anti-dsDNA |
0.11 (per 0.5 difference |
0.33 |
Mean Daily Prednisone Dose |
-0.19 (per 10 mg/d difference) |
0.38 |
Proportion of time on Plaquenil |
-0.07 (per 0.5 difference) |
0.71 |
*Means and proportions calculated over the interval between the two plaque assessments. |
Conclusion: Calcified coronary plaque levels were relatively stable over a period of 2-7 years. Noncalcified coronary plaque levels were more variable and more likely to increase over time. Those with longer duration of follow-up tended to have increases in noncalcified plaque. Traditional cardiovascular risk factors and SLE-related measures did not predict increases in noncalcified coronary plaque. Noncalcified coronary plaque, the plaque most likely to rupture and lead to a cardiovascular event, is likely to increase over time regardless of traditional cardiovascular risk factors and SLE clinical and serologic activity.
To cite this abstract in AMA style:
Petri M, Zadeh A, Kiani A, Magder LS. Progression of Noncalcified and Calcified Coronary Plaque (by CT Angiography) in SLE [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/progression-of-noncalcified-and-calcified-coronary-plaque-by-ct-angiography-in-sle/. Accessed .« Back to 2015 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/progression-of-noncalcified-and-calcified-coronary-plaque-by-ct-angiography-in-sle/