Session Information
Title: Rheumatoid Arthritis - Clinical Aspects II: Clinical Features & Comorbidity/Cardiovascular Disease
Session Type: Abstract Submissions (ACR)
Background/Purpose:
Rheumatoid arthritis (RA) increases the risk for coronary heart disease and ischemic events like myocardial infarction (MI). The association between traditional cardiovascular risk factors in this population remains unknown. Objective: To determine the association between myocardial infarction (MI), low density lipoprotein (LDL), seropositive RA and inflammation as determined by C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) among patients with RA.
Methods:
Retrospective data from the national Veterans Health Administration (VHA) from 1998-2011 was used for this study. Identification of the RA population and incident hospitalized MI was done using a validated algorithm using ICD-9 codes for RA from outpatient rheumatology visits and MI primary diagnosis code on hospitalization. Patients eligible for this analysis included RA patients with no previous MI. Baseline characteristics were determined during the first 12 months of observation in the VHA system, after which follow-up time for this analysis began. Laboratory data was examined in a time-varying fashion and updated on a daily basis and assessed at each event time. Seropositivitiy was characterized by having either positive rheumatoid factor (RF) or anti-cyclic citrullinated peptide (CCP) antibody. Cox proportional hazard models were used to determine the hazard ratios (HR) between first hospitalized MI and LDL (in quartiles and using ATP III cutpoints); CRP, ESR in quartiles (to avoid assumptions of linearity) and seropositivity using age as the time axis.
Results:
A total of 38,694 VHA patients with RA were identified. They were 90.3% male; mean ± SD age was 63.5 (± 12.1) years. Mean CRP, ESR and LDL levels at baseline were 10.4 mg/L (± 20.5), 30.1 mm/h (SD ± 24.9) and 100 mg/dL (SD ± 31.7) respectively; 85% of the RA cohort was seropositive. The baseline prevalence of diabetes was 12.5% and hypertension 33.9%.
The number of usable MI events varied according conditional on the availability of laboratory results. The crude rates of MI by each exposure variable are listed (table). A strong relationship was seen with increasing ESR. Trends in MI rates associated with increasing CRP were observed only for the 4thquartile. Higher HDL appeared protective, and patients in the lowest LDL quartile had the highest rates of MI.
After controlling for age, the HR for ESR (comparing the highest to lowest quartile) was 2.4 (p < 0.001), and the HR for CRP (highest to lowest quartile) was 1.6 (p = 0.08). The HR for sepositive RA was 1.7 (p < 0.001). HR for LDL ≥160 mg/dL compared to LDL < 100 was 1.2 (p= 0.30).
Conclusion: In this U.S., predominantly male RA cohort, ESR and seropositivity were significantly associated with a risk for MI and trends suggested CRP was as well. Higher LDL was not associated with a significantly increased risk for MI.
Table: Myocardial Infarction Incident rates by ESR, CRP, LDL, High Density Lipoprotein (HDL) and Serologic Status by Quartiles
|
ESR (mm/hour) Quartile |
MI Events |
Person Years |
Iincident Rate per 1,000 Person year |
|
1st (<11) |
80 |
2406 |
3.3 |
|
2nd (≥11 and <23) |
87 |
21131 |
4.1 |
|
3rd (≥23 and <42) |
133 |
20247 |
6.6 |
|
4th (>42) |
171 |
18896 |
9.0 |
|
CRP (mg/L) Quartile |
|
||
|
1st ( < 0.89 ) |
26 |
4975 |
5.2 |
|
2nd ( ≥ 0.89 and <3.1) |
17 |
4302 |
4.0 |
|
3rd (≥3.1 and <9.5) |
20 |
3941 |
5.1 |
|
4th (>9.5) |
30 |
3483 |
8.6 |
|
LDL 9mg/dL) Quartile |
|
|
|
|
1st (< 77.4) |
245 |
31437 |
7.8 |
|
2nd (≥ 77.4 and ≤ 97.2) |
184 |
32797 |
5.6 |
|
3rd (≥ 97.2 and ≤ 121) |
143 |
31965 |
4.5 |
|
4th (>121) |
162 |
30392 |
5.3 |
|
HDL (mg/dL) Quartile |
|
|
|
|
1st (< 34.4) |
220 |
27241 |
8.1 |
|
2nd (≥ 34.4 and ≤ 41.0) |
190 |
30203 |
6.3 |
|
3rd (≥ 41.0 and ≤ 50.4) |
180 |
35294 |
5.1 |
|
4th (>50.4) |
153 |
34345 |
4.5 |
|
Serologic status (RF/CCP) |
|
|
|
|
Seronegative |
43 |
14588 |
2.9 |
|
Seropositive |
443 |
84193 |
5.3 |
Disclosure:
I. Navarro-Millan,
None;
S. Yang,
None;
S. L. DuVall,
Anolinx LLC,
2,
Genentech Inc.,
2,
F. Hoffmann-La Roche Ltd,
2,
Amgen Inc,
2,
Shire PLC,
2,
Mylan Specialty PLC,
2;
L. Chen,
None;
J. Baddley,
Merck Pharmaceuticals,
5;
G. W. Cannon,
None;
E. S. Delzell,
Amgen,
2;
J. Zhang,
None;
M. M. Safford,
None;
N. M. Patkar,
None;
T. R. Mikuls,
Amgen; Genentech ,
2;
J. A. Singh,
research and travel grants from Takeda, Savient, Wyeth and Amgen,
2,
speaker honoraria from Abbott,
,
Consultant fees from URL pharmaceuticals, Savient, Takeda, Ardea, Allergan and Novartis.,
5;
J. R. Curtis,
Roche/Genetech, UCB< Centocor, Corrona,Amgen, Pfizer, BMS, Crescendo, Abbott, 2, Roche/Genetech,UCB, Centocor, CORRONA, Amgen, Pfizer, BMS, Crescendo, Abbott, 5.
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