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Abstract Number: 1253

Identifying Vulnerable Plaque in Rheumatoid Arthritis:  A Pilot Study Using Novel Microbubble-Contrast Enhanced Carotid Ultrasonography

Kimberly P. Liang1, Douglas P. Landsittel2, Suresh R. Mulukutla3, Steven E. Reis4, Marc C. Levesque1, Flordeliza S. Villanueva3, Hunter C. Champion5 and Larry W. Moreland1, 1Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, 2Medicine, Biostatistics and Clinical and Translational Science, University of Pittsburgh, Center for Health Care Research Data Center, Pittsburgh, PA, 3Division of Cardiology, University of Pittsburgh, Pittsburgh, PA, 4Division of Cardiology and Department of Clinical and Translational Science, University of Pittsburgh, Pittsburgh, PA, 5Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Arteriosclerosis, Atherosclerosis, Cardiovascular disease, rheumatoid arthritis (RA) and ultrasound

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Session Information

Title: Rheumatoid Arthritis - Clinical Aspects II: Clinical Features & Comorbidity/Cardiovascular Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Rheumatoid arthritis (RA) is independently associated with a higher risk of cardiovascular disease (CVD). Markers of systemic inflammation, as seen in RA, are associated with plaque vulnerability. Recently, increased vasa vasorum neovascularization has been identified as a common feature of inflammation and plaque vulnerability, and independently predicts future CV events in the non-RA general population. Excess CVD risk in RA may be caused by disease-related factors leading to vulnerable plaque characterized by increased vasa vasorum neovascularization, which is not assessed by traditional imaging modalities. Microbubble contrast-enhanced carotid ultrasound (CU) is a novel imaging technique that has been validated in detecting measures of vulnerable plaque, namely increased adventitial vasa vasorum density (aVVD), in non-RA subjects.

Our objective was to establish feasibility of measuring aVVD in RA patients; to determine whether RA patients have higher aVVD compared to non-RA controls, and whether disease-related RA measures correlate with increased aVVD, using CU.

Methods: We performed a preliminary cross-sectional study of 23 RA cases and 28 non-RA controls; this project is ongoing.  All 51 subjects underwent CU with measurement of intima-media thickness (IMT, using maximum of both sides) and the mean common carotid artery adventitial to lumen videointensity ratio (using maximum of both sides) to quantify aVVD. Demographic and CV risk factor data were collected on all subjects, and tested for differences between cases and controls, using the Wilcoxon rank-sum test for continuous data and Fisher’s exact test for categorical data. RA disease activity measures (CDAI and DAS28), erythrocyte sedimentation rate, high sensitivity C-reactive protein (CRP), rheumatoid factor (RF), and anti-cyclic citrullinated peptide (CCP), were collected systematically on RA subjects. Spearman correlations were assessed between disease activity measures and aVVD and IMT within RA cases.

Results: Demographic and CV risk factors between RA and controls were similar, except for mean age (58.0 years in RA, 66.1 years in controls; p<0.01); systolic blood pressure (138 in RA, 120 in controls; p<0.01); and race (91.3% white in RA, 64.3% white in controls; p=0.02). We successfully measured aVVD, which was higher in RA (mean=0.634; SD=0.097) versus controls (mean=0.595; SD=0.112), although so far non-significantly (p=0.31). IMT was also higher, although again non-significantly so far (p=0.65), in RA (mean = 0.85; SD=0.28) versus controls (mean=0.80; SD=0.18). After adjusting for age and personal history of CVD, results did not qualitatively change. As expected, CRP, RF and CCP were all significantly higher in RA than controls (p<0.001). No correlations between disease activity measures with aVVD and IMT were significant.

Conclusion: Measurement of aVVD to quantify plaque vulnerability in RA patients is feasible utilizing the novel CU technique. In this pilot study, the aVVD was slightly higher in RA than control subjects, though not significantly. Our study is ongoing, with plans for targeted enrollment of larger numbers of subjects and further adjustment for differences in demographic and CV risk factors.


Disclosure:

K. P. Liang,
None;

D. P. Landsittel,
None;

S. R. Mulukutla,
None;

S. E. Reis,
None;

M. C. Levesque,

Genentech and Biogen IDEC Inc.,

2,

UCB,

5,

Crescendo,

5;

F. S. Villanueva,
None;

H. C. Champion,
None;

L. W. Moreland,
None.

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