Abstract
Chronic heart failure (HF) is a syndrome of heterogeneous etiology associated with multiple co-morbidities. Inflammation is increasingly recognized as a key contributor to the pathophysiology of HF. Heterogeneity and lack of data on the immune mechanism(s) contributing to HF may partially underlie the failure of clinical trials targeting inflammatory mediators. We studied the Immunome in HF cohort using mass cytometry and used data-driven systems immunology approach to discover and characterize modulated immune cell subsets from peripheral blood. We showed cytotoxic and inflammatory innate lymphoid and myeloid cells were expanded in HF patients compared to healthy controls. Network analysis showed highly modular and centralized immune cell architecture in healthy control immune cell network. In contrast, the HF immune cell network showed greater inter-cellular communication and less modular structure. Furthermore, we found, as an immune mechanism specific to HF with preserved ejection fraction (HFpEF), an increase in inflammatory MAIT and CD4 T cell subsets.
Highlights
Chronic heart failure (HF) is a clinical syndrome characterized by typical symptoms reflecting raised intracardiac pressures and/or insufficient cardiac output to meet systemic requirements at rest or on exertion [1, 2]
The accumulating evidence for the role of inflammation and immune mechanism in HF has led to clinical trials targeting inflammatory cytokines
A systems immunology analysis approach could enhance the development of precision medicine for HF
Summary
Chronic HF is a clinical syndrome characterized by typical symptoms reflecting raised intracardiac pressures and/or insufficient cardiac output to meet systemic requirements at rest or on exertion [1, 2]. The global prevalence of HF is increasing and among adverse cardiovascular events, acute HF is a leading cause of hospitalization [3]. Left Ventricular (LV) Ejection Fraction (EF) has emerged as a useful clinical marker for categorizing HF patients. LVEF shows a bimodal distribution among patients with HF [4]. The European Society of Cardiology (ESC) guideline [5] categorizes HF patients into three categories, HF with reduced EF (HFrEF; EF ≤ 40%), HF with preserved EF (HFpEF ≥ 50%), and HF with mildly reduced EF (HFmrEF; EF 41-49%) EF. HFpEF and HFrEF show similar bedside clinical phenotypes, the underlying pathogenesis is distinct [4, 6]
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