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Abstract Number: 1265

Lipoprotein Subclass Particles and Small Vessel Elasticity As a Potential Marker for Early Atherosclerosis in Rheumatoid Arthritis:  a Prospective, Controlled Study

Marty T. Mertens1 and Elie Gertner2, 1Rheumatology, University of Minnesota, Minneapolis, MN, 2Section of Rheumatology, Regions Hospital and University of Minnesota Medical School, St. Paul, MN

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Cardiovascular disease, lipids and rheumatoid arthritis (RA)

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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) has increased rates of cardiovascular (CV) events.  However, standard CV risk factors, such as routine lipid profiles, are not different in RA patients.  It is still unclear how to best evaluate CV risk in RA.

Lipoprotein subclass determination differentiates lipoproteins by size and density.  Small, dense LDL particles have been associated with an increased risk of CV disease in a number of population studies.  Recently, small, dense HDL particles have been shown to be potentially anti-atherogenic.  In RA, lipoprotein subclasses have been evaluated in three studies with conflicting results. No studies have prospectively evaluated lipoprotein subclasses in RA.  Further, no studies have attempted to correlate these findings with a marker of endothelial function.

In this study, we evaluated lipoprotein subclasses and small arterial elasticity (SAE) in patients with RA over a 12 month period in comparison to healthy controls.  SAE is a marker for vascular function and reduction in SAE is predictive of development of atherosclerosis.

Methods:

Thirty-five seropositive RA and thirty-one control subjects without a history of coronary artery disease, diabetes mellitus, or active statin therapy were recruited.  DAS28-CRP was measured as a marker for disease activity.  Lipoprotein subclass concentrations were measured by nuclear magnetic resonance spectroscopy.  SAE was measured from pulse-wave analysis by radial artery tonometry.  After 12 months, the RA group underwent repeat DAS28-CRP, lipoprotein subclass determination, and SAE evaluations.

Results:

  1. There was no significant difference between the RA and control groups in small arterial elasticity. 
  2. The RA group had significantly lower total LDL and lower small LDL particle concentration as compared to the control group. 
  3. Average HDL size was significantly larger in the RA group compared to controls.
  4. Within the RA group, there was a statistically significant correlation of increased DAS28-CRP with a lesser number of small HDL particles (R = -0.07, p = 0.047).  No significant correlations were seen between changes in DAS28-CRP with small LDL particles or HDL size.   Changes in small LDL, small HDL particles, HDL size and DAS28-CRP did not correlate with changes in SAE.

 

Rheumatoid Arthritis  (SD)

N = 35

Controls (SD)

N = 31

p – value

Small Arterial Elasticity  (ml/mmHg x100)

5.90  (2.74)

6.48  (2.68)

0.42

 

 

 

 

Total LDL  (nmol/L)

1008  (317)

1210 (389)

0.028

Small LDL   (nmol/L)

504   (308)

753  (445)

0.012

LDL size  (nm)

21.4  (0.7)

21.1  (0.8)

0.085

Total HDL  (nmol/L)

32.5  (5.4)

33.3  (5.3)

0.57

Small HDL  (nmol/L)

18.5 (5.2)

19.6 (5.9)

0.38

HDL size  (nm)

9.3 (0.4)

9.1 (0.5)

0.039

Conclusion:

  1. In the RA group, there was lower total LDL and lower small LDL particle concentration as compared to controls.  HDL size was significantly larger in the RA group as compared to controls.
  2. Within the RA group, increased disease activity significantly correlated with a reduced number of small HDL particles.
  3. Small arterial elasticity did not differentiate RA from controls in assessing potential cardiovascular risk. SAE was not affected by changes in lipoprotein subclasses.

Alterations in LDL subclass populations may not account for the increased cardiovascular risk seen in RA.  However, reduction in the potentially anti-atherogenic small HDL particles may be a potential factor.


Disclosure:

M. T. Mertens,
None;

E. Gertner,
None.

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