Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.

Superior Protection Against Vulnerable Coronary Plaque in Asymptomatic TNFi-Responders vs. DMARD Responders with Rheumatoid Arthritis (RA).

Karpouzas1,  George A., Ahmadi2,  Naser, Choi2,  Tae-Young, Hajsadeghi2,  Fereshteh, Munoz2,  Silvia, Budoff2,  Mathew

Harbor-UCLA, Long Beach, CA


A lower risk of myocardial infarction (MI) was recently reported in patients (pts) with RA exposed to Tumor necrosis factor-a inhibitors (TNFi). It is unclear, however, whether a good disease response is necessary for the observed benefit. Additionally, the mechanisms, as well as sequalae of disease response on coronary plaque quantity and composition are unknown. We prospectively evaluated the presence, total burden, and differences in the quality of coronary plaque in asymptomatic RA pts treated with TNFi vs. DMARDs alone.


We report on 74 RA pts recruited from a single center. Pt characteristics, including disease response, coronary risk factors and treatments are shown in table 1. Good EULAR response (DAS28<=3.2 and DAS28 change>1.2) distinguished responders (R) from non-responders (NR). Pts underwent 64+ slice cardiac Computed Tomography Angiography (CTA); this non-invasive modality includes an initial non-contrast phase assessing coronary calcium, followed by a contrast scan that detects plaque with equal accuracy to conventional angiography, and is superior in the assessment of non-calcified, lipid-rich, non-obstructive or "vulnerable" plaque. Individual coronary trees were evaluated for plaque volume and composition by standard methods (American Heart Association). Non-parametric tests were used for data analysis; regression models for plaque prevalence ratios (PR) and relative risk (RR) for plaque burden in TNFi R vs. NR and DMARD R vs NR, adjusted for conventional risk factors were constructed.


No differences in coronary risk factors were present in DMARD vs. TNFi treated pts. Both TNFi and DMARD responders (R) had significantly less plaque prevalence than NR of both categories (table). Both R groups had lower numbers of diseased coronary segments vs. NR (p=0.008 for DMARD and TNFi respectively), and less total plaque burden (p=0.04 for DMARD and p=0.005 for TNFi vs. NR respectively). More importantly, R groups had less NC/mixed plaque (p=0.001 for DMARD and p=0.0001 for TNFi vs. NR respectively). TNFi R had 61% lower risk of having "vulnerable" plaque, and 23% less burden of it compared to DMARD R, after adjustment for age, sex and traditional risk factors. Interestingly, TNFi NR also had 38% lower risk of NC/mixed plaque and 21% less burden, insinuating a superior protective effect of TNFi against plaque progression, independent of RA disease response.


Good EULAR response to TNFi affords superior protection against total, but more importantly, "vulnerable" coronary plaque progression compared to good response to DMARDs. TNFi seem to have an independent- to RA clinical response- protective effect against plaque as evidenced by significantly lower volume and vulnerable plaque features in the TNFi NR group.

Table 1. Patient Features

 DMARD-treated = 27TNFi-treated = 47p
Age (yrs)53 ± 1253 ± 100.9
Gender (% female)85910.5
Disease duration (yrs)7 ± 5.612 ± 7.60.0004
Time on TNFi (mon)–NA51.8 ± 25.9
 R = 16NR = 11pR = 28NR = 19p
DAS28-3v-ESR (M ± SD)2.2 ± 0.63.7 ± 0.2<0.00012.6 ± 0.54.3 ± 0.9<0.0001
ESR (mm/hr)16 ± 838 ± 210.00123 ± 1530 ± 170.009
CRP (mg/dl)0.6 ± 1.20.9 ± ± 1.91.4 ± 1.20.3
n (%) with plaque9 (56)8 (73)0.415 (53.5)14 (73)0.2
n (%) assessed segments64 (100)44 (100)112 (100)76 (100)
n (%) diseased segments16 (25)18 (40.9)0.00813 (11.6)20 (25.4)0.008
Non-calcified/mixed12 (18.8)15 (34.1)0.0018 (7.1)16 (21.1)0.0001
calcified4 (6.3)3 (5.9)0.35 (4.4)4 (4.3)0.8
Total plaque burden score3.5 ± 34.4 ± ± 2.53.4 ± 4.10.005
Non-calcified/mixed2.8 ± 3.24.4 ± ± 2.42.8 ± 3.80.01
calcified2.3 ± 3.82.1 ± 30.22.1 ± 2.64 ± 2.60.1
ModelDMARD- RespondersTNFi-Responders 
Prev Ratio-any plaque1 (ref)0.89 (CI = 0.38–2.78)0.61
non-calcified/1 (ref)0.39 (CI = 0.1–0.6)0.02
mixed calcified1 (ref)0.78 (CI = 0.2–1.3)0.25
RRisk-total burden score*1 (ref)0.78 (CI = 0.6–0.9)0.03
  non-calcified/1 (ref)0.77 (CI = 0.6–0.9)0.01
mixed calcified1 (ref)1.12 (CI = 0.9–1.3)0.3
ModelDMARD- Non RespondersTNFi-Non Responders 
Prev Ratio-any plaque1 (ref)0.99 (CI = 0.97–1.03)0.9
non-calcified/1 (ref)0.62 (CI = 0.1–0.7)0.02
mixed calcified1 (ref)0.74 (CI = 0.1–1.5)0.3
RRisk-total burden score*1 (ref)0.87 (CI = 0.6–0.9)0.09
Non-calcified/1 (ref)0.79 (CI = 0.6–0.98)0.04
mixed calcified1 (ref)1.75 (CI = 0.9–1.96)0.07

To cite this abstract, please use the following information:
Karpouzas, George A., Ahmadi, Naser, Choi, Tae-Young, Hajsadeghi, Fereshteh, Munoz, Silvia, Budoff, Mathew; Superior Protection Against Vulnerable Coronary Plaque in Asymptomatic TNFi-Responders vs. DMARD Responders with Rheumatoid Arthritis (RA). [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1443
DOI: 10.1002/art.29209

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