Sicong Huang1,2,3,4, Tianrun Cai1,2,4, Brittany N Weber1,5, Zeling He1,2, Kumar P Dahal1,2,4, Chuan Hong4,6,7, Jue Hou4,7, Thany Seyok1,2, Andrew Cagan1,8, Marcelo F DiCarli1,5, Jacob Joseph1,4,5, Seoyoung C Kim1,2,9, Daniel H Solomon1,2, Tianxi Cai4,6,7, Katherine P Liao1,2,3,4,6. 1. Brigham and Women's Hospital, Harvard Medical School. 2. Division of Rheumatology, Inflammation, and Immunity. 3. Section of Rheumatology. 4. Veterans Administration Boston Healthcare System. 5. Cardiovascular Division. 6. Department of Biomedical Informatics, Harvard Medical School. 7. Harvard T.H. Chan School of Public Health, Biostatistics. 8. Research Information Science and Computing, Mass General Brigham. 9. Division of Pharmacoepidemiology and Pharmacoeconomics.
Abstract
OBJECTIVES: In RA, there are limited data on risk factors for clinical heart failure (HF) subtypes, HF with reduced ejection fraction (HFrEF) and preserved EF (HFpEF). This study examined the association between inflammation and incident HF subtypes in RA. Since inflammation changes over time with disease activity, we hypothesized that the effect of inflammation may be stronger at five-year follow-up compared to the standard ten-year from general population studies of cardiovascular risk. METHODS: We studied an electronic health record (EHR)-based RA cohort with data pre-/post-RA incidence. We applied a validated approach to identify HF, and extract EF to classify HFrEF and HFpEF. Follow-up started from the RA incidence date (index-date) to the earliest occurrence of incident HF, death, last EHR encounter, or ten-years. Baseline inflammation was assessed using erythrocyte sedimentation rate or C-reactive protein values. Covariates included demographics, established HF risk factors, and RA-related factors. We tested the association between baseline inflammation with incident HF and its subtypes using Cox proportional hazards models. RESULTS: We studied 9087 RA patients; 8.2% developed HF during ten years of follow-up. Elevated inflammation was associated with increased risk for HF at both five- and ten-year follow-up (HR=1.66 [1.12-2.46] and 1.46 [1.13-1.90], respectively), which is also seen for HFpEF at five years (HR=1.72 [1.09-2.70]) and ten years (HR=1.45 [1.07-1.94]). HFrEF was not associated with inflammation for either follow-up time. CONCLUSION: Elevated inflammation early in RA diagnosis was associated HF; this association was driven by HFpEF and not HFrEF, suggesting a window of opportunity for prevention of HFpEF in RA. This article is protected by copyright. All rights reserved.
OBJECTIVES: In RA, there are limited data on risk factors for clinical heart failure (HF) subtypes, HF with reduced ejection fraction (HFrEF) and preserved EF (HFpEF). This study examined the association between inflammation and incident HF subtypes in RA. Since inflammation changes over time with disease activity, we hypothesized that the effect of inflammation may be stronger at five-year follow-up compared to the standard ten-year from general population studies of cardiovascular risk. METHODS: We studied an electronic health record (EHR)-based RA cohort with data pre-/post-RA incidence. We applied a validated approach to identify HF, and extract EF to classify HFrEF and HFpEF. Follow-up started from the RA incidence date (index-date) to the earliest occurrence of incident HF, death, last EHR encounter, or ten-years. Baseline inflammation was assessed using erythrocyte sedimentation rate or C-reactive protein values. Covariates included demographics, established HF risk factors, and RA-related factors. We tested the association between baseline inflammation with incident HF and its subtypes using Cox proportional hazards models. RESULTS: We studied 9087 RA patients; 8.2% developed HF during ten years of follow-up. Elevated inflammation was associated with increased risk for HF at both five- and ten-year follow-up (HR=1.66 [1.12-2.46] and 1.46 [1.13-1.90], respectively), which is also seen for HFpEF at five years (HR=1.72 [1.09-2.70]) and ten years (HR=1.45 [1.07-1.94]). HFrEF was not associated with inflammation for either follow-up time. CONCLUSION: Elevated inflammation early in RA diagnosis was associated HF; this association was driven by HFpEF and not HFrEF, suggesting a window of opportunity for prevention of HFpEF in RA. This article is protected by copyright. All rights reserved.
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