{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T16:11:54Z","timestamp":1787242314314,"version":"build-2736575974"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2024,5,7]]},"abstract":"<jats:sec sec-type=\"background\" xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      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\u2009weeks. MFR &lt;2.5 in the absence of obstructive coronary artery disease was defined as coronary microvascular dysfunction. Blood samples at baseline and 24\u2009weeks were measured for inflammatory markers (eg, high\u2010sensitivity C\u2010reactive protein [hsCRP], interleukin\u20101b, and high\u2010sensitivity cardiac troponin T [hs\u2010cTnT]). The primary outcome was mean MFR before and after tumor necrosis factor inhibitor initiation, with \u0394hs\u2010cTnT as the secondary outcome. Secondary and exploratory analyses included the correlation between \u0394hsCRP and other inflammatory markers with MFR and hs\u2010cTnT. We studied 66 subjects, 82% of which were women, mean RA duration 7.4\u2009years. The median atherosclerotic cardiovascular disease risk was 2.5%; 47% had coronary microvascular dysfunction and 23% had detectable hs\u2010cTnT. We observed no change in mean MFR before (2.65) and after treatment (2.64,\n                      <jats:italic>P<\/jats:italic>\n                      =0.6) or hs\u2010cTnT. A correlation was observed between a reduction in hsCRP and interleukin\u20101b with a reduction in hs\u2010cTnT.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">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\u20101b and no other inflammatory pathways was correlated with a reduction in subclinical myocardial injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Registration<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.clinicaltrials.gov\">https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n                      ; Unique identifier: NCT02714881.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.123.030387","type":"journal-article","created":{"date-parts":[[2024,4,30]],"date-time":"2024-04-30T07:28:21Z","timestamp":1714462101000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":16,"title":["Interplay Between Systemic Inflammation, Myocardial Injury, and Coronary Microvascular Dysfunction in Rheumatoid Arthritis: Results From the LiiRA Study"],"prefix":"10.1161","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0177-2091","authenticated-orcid":false,"given":"Brittany","family":"Weber","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Medicine, Heart and Vascular Center Brigham and Women\u2019s Hospital, Harvard Medical School Boston MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7518-3871","authenticated-orcid":false,"given":"Dana","family":"Weisenfeld","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Inflammation, and Immunity Brigham and Women\u2019s Hospital, Harvard Medical School Boston MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Massarotti","sequence":"additional","affiliation":[{"name":"Division of 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