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

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...

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Published inJournal of the American Heart Association Vol. 13; no. 9; p. e030387
Main Authors Weber, Brittany, Weisenfeld, Dana, Massarotti, Elena, Seyok, Thany, Cremone, Gabrielle, Lam, Ethan, Golnik, Charlotte, Brownmiller, Seth, Liu, Feng, Huang, Sicong, Todd, Derrick J., Coblyn, Jonathan S., Weinblatt, Michael E., Cai, Tianrun, Dahal, Kumar, Kohler, Minna, Yinh, Janeth, Barrett, Leanne, Solomon, Daniel H., Plutzky, Jorge, Schelbert, Heinrich R., Campisi, Roxana, Bolster, Marcy B., Di Carli, Marcelo, Liao, Katherine P.
Format Journal Article
LanguageEnglish
Published England John Wiley and Sons Inc 07.05.2024
Wiley
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ISSN2047-9980
2047-9980
DOI10.1161/JAHA.123.030387

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Summary: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. 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, =0.6) or hs-cTnT. A correlation was observed between a reduction in hsCRP and interleukin-1b with a reduction in hs-cTnT. 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. URL: https://www.clinicaltrials.gov; Unique identifier: NCT02714881.
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Results included in this work were presented at the American Heart Association Scientific Sessions, November 5 to 7, in Chicago, IL, and at the American College of Rheumatology Convergence, November 10 to 14, in Philadelphia, PA.
Supplemental Material is available at https://www.ahajournals.org/doi/suppl/10.1161/JAHA.123.030387
For Sources of Funding and Disclosures, see page 9.
This manuscript was sent to Katherine C. Wu, MD, Senior Associate Editor, for review by expert referees, editorial decision, and final disposition.
ISSN:2047-9980
2047-9980
DOI:10.1161/JAHA.123.030387