Key result
SGLT2 inhibitors are linked to reduced fibrinogen in chronic heart failure, but not CRP or ESR.
Why the study?
Systemic inflammation drives chronic heart failure progression, prompting evaluation of whether SGLT2 inhibitors exert a potential anti-inflammatory effect when added to standard heart failure medications.
Do sodium-glucose co-transporter 2 inhibitors reduce inflammatory markers (CRP, ESR, or fibrinogen) in patients with chronic heart failure?
Cohort (n=220)
No
Do sodium-glucose co-transporter 2 inhibitors reduce inflammatory markers (CRP, ESR, or fibrinogen) in patients with chronic heart failure?
p-value: p=0.017
SGLT2 inhibitors demonstrate real-world anti-inflammatory properties in patients with chronic heart failure by significantly reducing fibrinogen levels, regardless of ejection fraction phenotype.
Fibrinogen reduction with SGLT2i in chronic HF is hypothesis-generating; requires RCTs before informing practice or biomarker monitoring.
Inflammation plays a major role in the etiology of chronic heart failure and in inducing the progression to end-stage heart failure. This chronic inflammation, which accompanies heart failure, is not only local but also systemic and is usually in a state of low-grade but constant activation. Because there is an interrelation between systemic inflammation and neurohormonal activation, almost all anti-remodeling classes of medication have been evaluated for a potential and hidden anti-inflammatory effect. This study aimed to evaluate the effect of sodium-glucose co-trans-porter 2 inhibitors (SGLT2i) (Dapagliflozin or Empagliflozin) on inflammation measured by C-reactive protein levels, erythrocyte sedimentation rate (ESR) and fibrinogen in patients with chronic heart failure when administered together with other standard heart failure medications. We retrospectively enrolled 220 patients with chronic heart failure admitted to our hospital from January 2021 until March 2023. The study included two visits, T0 (the initial visit) and T1 (after six months), to assess if SGLT2i initiation after the first visit (T0) had an effect on the levels of inflammatory biomarkers. SGLT2i showed a reduction in fibrinogen levels, an effect that was present both in heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) phenotypes. This was opposite to the dynamics of inflammatory markers in patients who did not receive SGLT2i, where the fibrinogen levels increased in HFrEF and HFpEF subgroups. SGLT2i proved an anti-inflammatory effect, showing a statistically significant reduction in fibrinogen levels in chronic heart failure, irrespective of the phenotype.
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Arvunescu et al. (2025) conducted a cohort in Chronic heart failure (n=220). SGLT2 inhibitors (Dapagliflozin or Empagliflozin) vs. Guideline-directed medical treatment without SGLT2 inhibitors was evaluated on Reduction in at least one inflammatory marker (CRP, ESR, fibrinogen) from baseline (T0) to 6 months (T1) (p=0.017). SGLT2 inhibitors significantly reduced fibrinogen levels (interaction p=0.017) over 6 months in patients with chronic heart failure, whereas no significant effects were seen for CRP or ESR.
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