Background/Purpose:

Women with SLE have increased rates of subclinical atherosclerosis and cardiovascular (CV) events.  We sought to determine which risk factors may be significant in the rate of subclinical atherosclerosis progression, as measured by coronary artery calcium score (CAC) in women with (cases) and without (controls) SLE.

Methods:

Baseline data were collected on cases and controls including demographics, self-reported and measured traditional CV risk factors.  SLE factors collected included modified SLICC/ACR-DI Damage Index (SDI) (excluding CV outcomes). CAC was measured by electron beam or multidimensional computed tomography at baseline and at 1 follow-up visit in the Study of Lupus Vascular and Bone Long-Term Endpoints (SOLVABLE).  A high risk CAC was defined as CAC>10 and progression in CAC at follow-up was defined as a CAC>10 and an increase of >10% compared to baseline.  Low risk CAC was defined as CAC<10.  Univariate regression models of CAC with risk factors were examined. These models were further adjusted for age.

Results:

At the baseline visit in 142 cases, the age was 43.3 ± 9.9 yrs, disease duration was 12.0 ± 8.4 yrs, SLEDAI was 3.8 ± 3.5, SDI was 1.5 ± 1.6 (mean ± SD). In 120 controls, the age was 46.7 ± 10.1 yrs (mean ± SD).  Follow-up time between imaging studies in 142 cases and 120 controls was 3.25 ± 0.35 yrs and 3.37 ± 0.41 yrs (mean ± SD), respectively. Follow-up time was longer in controls than in cases (p=0.02).  

In 142 cases, 103 (73%) had low risk CAC at baseline and at follow-up, 12 (8.5%) had low risk CAC at baseline with progression at follow-up, 2 (1.4%) with low risk CAC at baseline had regression to low risk at follow-up, and 21 (14.8%) with high risk CAC at baseline and progression at follow-up. Four (2.8%) had high risk CAC at baseline and follow-up without progression.

In 120 controls, 100 (83%) had low risk CAC at baseline and at follow-up, 7 (5.8%) had low risk CAC at baseline with progression at follow-up, 3 (2.5%) with high risk CAC at baseline had regression to low risk at follow-up, and 10 (8.3%) with high risk CAC at baseline and progression at follow-up.

In cases, progression in CAC was univariately associated with presence of diabetes, older age, and higher BMI. After adjustment for age, only SDI remained associated with CAC progression (Table 1). In controls, presence of hypertension and older age were univariately associated with CAC progression. After adjustment for age, no risk factors remained significant.

Conclusion:

In cases and controls, traditional CV risk factors are univariately associated with the progression of subclinical atherosclerosis as measured by CAC. In cases, SLE damage is significantly associated with progression. While aging mediates the effect of many traditional CV risk factors for CAC progression in women with and without SLE, increased risk due to SLE damage is independent of age. Further investigation with multivariate models is needed.