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Abstract Number: 207

Divergent Patterns of Cardiovascular Risk in Biomarkers of Lipids and Subclinical Myocardial Injury during Increased Inflammation in Rheumatoid Arthritis

Katherine P. Liao1, Jie Huang2, Gabrielle Cremone3, Ethan Lam3, Nicole Yang1, Martin Playford4, Christine K Iannaccone1, Jonathan Coblyn5, Elena Massarotti1, Michael E Weinblatt5, Nancy A. Shadick1, Nehal Mehta4 and Jorge Plutzky1, 1Brigham and Women's Hospital, Boston, MA, 2Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA, 3Rheumatology, Brigham and Women's Hospital, Boston, MA, 4NHLBI, Bethesda, MD, 5Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: Inflammation, Lipids, myocardial involvement and rheumatoid arthritis (RA)

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Session Information

Date: Sunday, October 21, 2018

Session Title: Epidemiology and Public Health Poster I: Rheumatoid Arthritis

Session Type: ACR Poster Session A

Session Time: 9:00AM-11:00AM

Background/Purpose: Inflammation is an independent risk factor for cardiovascular (CV) risk in rheumatoid arthritis (RA). Paradoxically, potentially cardioprotective decreases in inflammation is associated with increased low-density lipoprotein cholesterol (LDL-C). Few studies exist as to how increased inflammation modulates lipid parameters.  This study’s objective was to examine changes between lipids and markers of myocardial injury among RA patients demonstrating increased inflammation.

Methods: We studied a longitudinal, large academic medical center-based RA cohort, examining annually-collected clinical data, CRP and blood samples among patients with an increase in C-reactive protein (CRP) ≥10mg/L CRP between any two time points at least one year apart.  The first time point was defined as the baseline.  Subjects on statin therapy one year before baseline or during the one-year follow-up period were excluded.  For all subjects, we measured routine lipids: total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), LDL-C; advanced lipoprotein measures: apoA1, apoB, HDL cholesterol efflux capacity; myocardial injury markers: high sensitivity troponin T (hs-cTnT); myocardial strain: pro-BNP.  The paired t-test was used to determine significant differences between baseline and follow-up.

Results:

Among 1,443 unique RA patients we identified n=103 RA patients who experienced an ≥10mg/L CRP increase in two consecutive years. Baseline characteristics of this cohort were as follows: mean age 59 years, 80% female, 72% positive for RF and/or anti-CCP antibodies; baseline treatment MTX 50.5%, tumor necrosis factor inhibitor 49.5%; a mean CRP increase of 35.9 mg/dL was found.  On concurrent follow-up labs, TC, LDL-C, apoB and apoA1 were all significantly reduced (Table).  HDL cholesterol efflux capacity was not significantly altered.  Both biomarkers of myocardial strain and injury (pro-BNP, hs-cTnT) were significantly increased.

Conclusion:   Among 103 RA patients experiencing significant increases in inflammation, markers of subclinical myocardial injury and strain were increased despite concurrent decreases in routine lipid levels, including ones predictive of reduced CV risk.  These findings suggest that increases in inflammation in RA may promote subclinical cardiac damage and CV risk while other, accepted CV risk markers, i.e. LDL-C, may mislead clinicians in this setting.

 

Table.  Lipid and myocardial biomarkers at baseline and follow-up after RA patients experienced increase in inflammation.

Biomarker

Baseline

Follow-up

p-value

Routine lipids, mean (SD)

Total cholesterol (mg/dL)

192.1 (40.3)

177.0 (35.1)

<.0001

HDL-C (mg/dL)

59.1 (18.4)

57.0 (17.5)

0.2

LDL-C (mg/dL)

113.4 (32.4)

101.8 (29.2)

<.0001

Triglycerides (mg/dL)

112.1 (59.1)

101.1 (57.7)

0.003

Non-HDL (mg/dL)

133.0 (37.0)

120.0 (32.8)

<.0001

Total cholesterol/HDL-C

3.5 (1.1)

3.4 (1.7)

0.01

Advanced lipoprotein measures, mean (SD)

apoA1 (mg/dL)

162.0 (34.6)

152.5 (33.3)

<.0001

apoB (mg/dL)

94.0 (24.0)

90.4 (23.2)

0.02

apoB/apoA1

0.60 (0.20)

0.62 (0.22)

0.3

HDL cholesterol efflux capacity

1.3 (0.40)

1.2 (0.40)

0.1

Markers of myocardial injury or strain

Hs-cTnT (ng/mL)

8.3 (10.6)

9.8 (12.9)

0.0003

Pro-BNP (pg/mL)

197.4 (371.4)

298.9 (650.2)

0.001

Inflammatory markers and RA disease activity

hsCRP (mg/L)

8.7 (14.7)

44.6 (47.7)

<.0001

RA Clinical Disease Activity Index (CDAI)

14.8 (12.5)

19.5 (17.0)

0.02

CDAI: ≤10, remission/low disease activity; >10 and ≤22, moderate disease activity; >22 high disease activity

 


Disclosure: K. P. Liao, None; J. Huang, None; G. Cremone, None; E. Lam, None; N. Yang, None; M. Playford, None; C. K. Iannaccone, None; J. Coblyn, None; E. Massarotti, None; M. E. Weinblatt, Amgen, BMS, Crescendo Bioscience, Sanofi/Regeneron, 2,Abbvie, Amgen, BMS, Crescendo Bioscience, Corrono, GSK, Gilead, Eli Lilly and Company, Lycera, Merck, Novartis, Pfizer, Roche, Samsung, Set Point, UCB, 5,Lycero, Can-fite, Scipher, Vorso, Inmedix, 1; N. A. Shadick, Bristol-Myers Squibb, 5,Amgen Inc., 2,Mallinckrodt, 2,UCB, Inc., 2,Crescendo Biosciences, 2,Sanofi, 2,Bristol-Myers Squibb, 2,DxTerity, 2; N. Mehta, None; J. Plutzky, None.

To cite this abstract in AMA style:

Liao KP, Huang J, Cremone G, Lam E, Yang N, Playford M, Iannaccone CK, Coblyn J, Massarotti E, Weinblatt ME, Shadick NA, Mehta N, Plutzky J. Divergent Patterns of Cardiovascular Risk in Biomarkers of Lipids and Subclinical Myocardial Injury during Increased Inflammation in Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/divergent-patterns-of-cardiovascular-risk-in-biomarkers-of-lipids-and-subclinical-myocardial-injury-during-increased-inflammation-in-rheumatoid-arthritis/. Accessed March 7, 2021.
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