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Background Rheumatoid arthritis (RA) is associated with excess cardiovascular risk, but within-patient changes in complete blood count (CBC)-derived inflammatory indices at the onset of acute coronary syndrome (ACS) are not well described. We compared pre-event and acute-phase values in the same patients and contextualized pre-event values against a healthy cohort. Methods This retrospective, single-center, within-patient paired study reviewed hospital records from July 1, 2018, to December 30, 2025 (approximately 90 months). Among 3,960 hospitalized patients with RA, 89 had clinician-confirmed ACS and qualifying paired CBC measurements. Acute-phase CBCs were obtained within 24 hours after symptom onset, and pre-event CBCs were the most recent routine measurements obtained more than 14 days before the event. The neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI) were calculated and natural log-transformed. Pre-event values were also compared with a healthy cohort (n = 110), with age- and sex-adjusted analyses used because residual demographic imbalance was present. Results Pre-event log(NLR), log(SII), and log(SIRI) were higher in the RA cohort than in healthy controls and remained higher after adjustment for age and sex (all P< 0.001). Within-patient analyses showed increases during ACS, with mean Δlog values of 0.466 for NLR, 0.508 for SII, and 0.381 for SIRI (all Benjamini–Hochberg-adjusted q< 0.001). Neutrophilia increased from 11.2% before the event to 41.6% during ACS (McNemar P< 0.001). Exploratory subgroup estimates were heterogeneous and non-monotonic across several small strata; changes did not differ materially between remission/low and moderate/high RA activity groups. Conclusion Among patients with RA who developed ACS, CBC-derived inflammatory indices were higher than in a healthy comparison cohort before the event and increased further within the first 24 hours of ACS. The paired design quantifies change relative to each patient’s own pre-event value. Without a non-RA ACS comparator, however, the study cannot establish RA-specific inflammatory priming or a causal chronic-to-acute mechanism. Prospective studies with serial sampling and clinical outcomes are needed.
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Wang et al. (2026) studied this question.
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