Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease (May 2024)

Interplay Between Systemic Inflammation, Myocardial Injury, and Coronary Microvascular Dysfunction in Rheumatoid Arthritis: Results From the LiiRA Study

  • Brittany Weber,
  • Dana Weisenfeld,
  • Elena Massarotti,
  • Thany Seyok,
  • Gabrielle Cremone,
  • Ethan Lam,
  • Charlotte Golnik,
  • Seth Brownmiller,
  • Feng Liu,
  • Sicong Huang,
  • Derrick J. Todd,
  • Jonathan S. Coblyn,
  • Michael E. Weinblatt,
  • Tianrun Cai,
  • Kumar Dahal,
  • Minna Kohler,
  • Janeth Yinh,
  • Leanne Barrett,
  • Daniel H. Solomon,
  • Jorge Plutzky,
  • Heinrich R. Schelbert,
  • Roxana Campisi,
  • Marcy B. Bolster,
  • Marcelo Di Carli,
  • Katherine P. Liao

DOI
https://doi.org/10.1161/JAHA.123.030387
Journal volume & issue
Vol. 13, no. 9

Abstract

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Background Coronary microvascular dysfunction as measured by myocardial flow reserve (MFR) is associated with increased cardiovascular risk in rheumatoid arthritis (RA). The objective of this study was to determine the association between reducing inflammation with MFR and other measures of cardiovascular risk. Methods and Results Patients with RA with active disease about to initiate a tumor necrosis factor inhibitor were enrolled (NCT02714881). All subjects underwent a cardiac perfusion positron emission tomography scan to quantify MFR at baseline before tumor necrosis factor inhibitor initiation, and after tumor necrosis factor inhibitor initiation at 24 weeks. MFR <2.5 in the absence of obstructive coronary artery disease was defined as coronary microvascular dysfunction. Blood samples at baseline and 24 weeks were measured for inflammatory markers (eg, high‐sensitivity C‐reactive protein [hsCRP], interleukin‐1b, and high‐sensitivity cardiac troponin T [hs‐cTnT]). The primary outcome was mean MFR before and after tumor necrosis factor inhibitor initiation, with Δhs‐cTnT as the secondary outcome. Secondary and exploratory analyses included the correlation between ΔhsCRP and other inflammatory markers with MFR and hs‐cTnT. We studied 66 subjects, 82% of which were women, mean RA duration 7.4 years. The median atherosclerotic cardiovascular disease risk was 2.5%; 47% had coronary microvascular dysfunction and 23% had detectable hs‐cTnT. We observed no change in mean MFR before (2.65) and after treatment (2.64, P=0.6) or hs‐cTnT. A correlation was observed between a reduction in hsCRP and interleukin‐1b with a reduction in hs‐cTnT. Conclusions In this RA cohort with low prevalence of cardiovascular risk factors, nearly 50% of subjects had coronary microvascular dysfunction at baseline. A reduction in inflammation was not associated with improved MFR. However, a modest reduction in interleukin‐1b and no other inflammatory pathways was correlated with a reduction in subclinical myocardial injury. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02714881.

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