Key result
Patients with HFpEF and diabetes mellitus demonstrated a heightened pro-inflammatory state, with neutrophils releasing significantly more IL-6 (3.7-fold; p≤0.001) than healthy controls.
Why the study?
HFpEF is characterized by low-grade chronic inflammation, which could be exacerbated by type 2 diabetes mellitus, and it was hypothesized that neutrophils contribute to this inflammation via pro-inflammatory cytokine release.
Observational (n=71)
p-value: p=≤0.001
Patients with HFpEF and diabetes exhibit heightened systemic inflammation and neutrophil-derived pro-inflammatory cytokine release, which may contribute to their worse clinical outcomes.
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May link diabetes to worse HFpEF outcomes via neutrophil IL-6; hypothesis-generating, requires prospective validation before clinical consideration.
Chaar et al. (2022) conducted an observational in Heart Failure with Preserved Ejection Fraction and Diabetes Mellitus (n=71). Diabetes mellitus and/or HFpEF vs. Healthy controls was evaluated on Circulating cytokines and in vitro cytokines released by isolated neutrophils (p=≤0.001). Patients with HFpEF and diabetes mellitus demonstrated a heightened pro-inflammatory state, with neutrophils releasing significantly more IL-6 (3.7-fold; p≤0.001) than healthy controls.
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