Miscellaneous
Relation of Carotid Intima-Media Thickness and Plaque With Incident Cardiovascular Events in Women With Systemic Lupus Erythematosus

https://doi.org/10.1016/j.amjcard.2013.05.040Get rights and content

Patients with systemic lupus erythematosus (SLE) are at increased risk for cardiovascular (CV) disease. The aim of this study was to investigate the association between subclinical CV disease as measured by carotid intima-media thickness (IMT) and plaque using B-mode carotid ultrasound and incident CV events in a combined cohort of female patients with SLE. This was a prospective, 2-center observational study of 392 adult women with SLE and no previous CV events with a mean 8 years of follow-up. Incident CV events confirmed by clinicians were defined as angina, myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass graft, fatal cardiac arrest, transient ischemic attack, and cerebrovascular accident. Incident hard CV events excluded angina and transient ischemic attack. The mean age was 43.5 years, and most patients were Caucasian (77.3%). During follow-up, 38 patients had incident CV events, and 17 had incident hard CV events. Patients with incident hard CV events had higher mean carotid IMT (0.80 vs 0.64 mm, p <0.01) and presence of carotid plaque (76.5% vs 30.4%, p <0.01) compared with those without incident hard CV events. Baseline carotid IMT and presence of plaque were predictive of any incident hard CV event (hazard ratio 1.35, 95% confidence interval 1.12 to 1.64, and hazard ratio 4.26, 95% confidence interval 1.23 to 14.83, respectively), independent of traditional CV risk factors and medication use. In conclusion, in women with SLE without previous CV events, carotid IMT and plaque are predictive of future CV events. This suggests that carotid ultrasound may provide an additional tool for CV risk stratification in patients with SLE.

Section snippets

Methods

A total of 392 women with SLE were enrolled in this study. We enrolled 289 women from the Pittsburgh Lupus Cardiovascular Study (1995 to 1998) as part of a longitudinal National Institutes of Health–funded study of CVD in patients with SLE. This cohort includes patients seen either at the University of Pittsburgh Medical Center inpatient and outpatient facilities or by rheumatologists in the Pittsburgh metropolitan area. Thus, the sample represents a community-based spectrum of mild to severe

Results

The 392 female subjects with SLE had a mean age of 43.5 years and were predominantly Caucasian (77.3%). The 2 study sites differed by ethnicity, level of education, and duration of follow-up (Table 1). The mean SLE disease duration was 10.7 years, and the mean Systemic Lupus International Collaborating Clinics damage score was 1.27 (Table 2). The overall mean duration of follow-up was 7.9 years. A total of 65 new CV events occurred during follow-up: 22 episodes of angina, 10 myocardial

Discussion

In this cohort of women with SLE who were free of CV events at study entry, carotid IMT and the presence of carotid plaque at baseline were significantly associated with incident hard CV events during a mean follow-up period of 7.9 years. The presence of carotid plaque at baseline was associated with a greater than fourfold increased risk for any hard CV events. Kaplan-Meier estimates indicated that the presence of plaque was related to a higher rate of any CV event compared with the absence of

Acknowledgment

We thank the study participants and the funding agencies. We thank Dr. William Pearce, Department of Vascular Surgery, Northwestern University Feinberg School of Medicine, and Dr. David D. McPherson, Division of Cardiovascular Medicine, University of Texas Houston, for providing oversight for the carotid ultrasound examinations for SOLVABLE. We also thank Michael Anderson for his editorial assistance.

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    This study was funded by the Arthritis Foundation, Lupus Foundation of America, Western Pennsylvania Chapter, grant-in-aid from the American Heart Association, grant R01 AR046588-01 and P60 AR030692 from the National Institutes of Health, M01-RR000056 and M01-RR000048 from the NIH/NCRR/GCRC, and P60 AR044811-01 from the NIH/MAC. Additional author support: AHK (ACR REF Physician Scientist Development Award; NIH K23 AR051044), AL (ACR REF/Amgen Rheumatology Fellowship Training Award; The Driskill Foundation), RR-G (NIH/NCATS UL 1 RR025741; NIH K24 AR002138), SM (NIH K24 AR002213-01).

    See page 1031 for disclosure information.

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