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Immuno-haemostatic dysregulation in heart failure with preserved ejection fraction
Giorgia D'Italia1, Daniëlle M Coenen1,2, Titus P Lemmens1
1Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
ESC Heart Failure
|July 11, 2025
Summary
Heart failure with preserved ejection fraction (HFpEF) involves dysfunctional platelets, a procoagulant state, and neutrophil activation. These immuno-haemostatic changes, including aberrant platelet function, are intrinsic to HFpEF, independent of other conditions.
Area of Science:
- Cardiology
- Immunology
- Hematology
Background:
- Systemic inflammation is key in heart failure with preserved ejection fraction (HFpEF) pathophysiology.
- The roles of platelets, coagulation, and neutrophils in HFpEF are not fully understood.
Purpose of the Study:
- To investigate platelet function, coagulation, and neutrophil activation in HFpEF patients.
- To determine if these factors are associated with HFpEF independently of comorbidities or medications.
Main Methods:
- Assessed in vivo and ex vivo platelet activation, neutrophil activation, and coagulation markers in HFpEF patients (n=103) versus controls (n=40).
- Utilized flow cytometry and microfluidic assays for detailed analysis.
Main Results:
- HFpEF patients showed reduced platelet reactivity but increased in vivo platelet activation markers (β-TG, CXCL4).
- Elevated neutrophil activation markers (MPO, S100A8/A9) and a procoagulant state (elevated kallikrein, factors XI, IX, thrombin, D-dimer) were observed in HFpEF.
- Platelet dysfunction was independently associated with HFpEF.
Conclusions:
- HFpEF is characterized by dysfunctional platelets, a procoagulant state, and neutrophil activation.
- These immuno-haemostatic alterations, particularly platelet dysfunction, appear intrinsic to HFpEF.
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