Neutrophils and Circulating Inflammatory Biomarkers in Diabetes Mellitus and Heart Failure With Preserved Ejection Fraction

Chaar, Diana; Dumont, Benjamin; Vulesevic, Branka; Neagoe, Paul‐Eduard; Räkel, Agnès; White, Michel; Sirois, Martin G.

doi:10.1016/j.amjcard.2022.05.026

Cited by 5 publications

(1 citation statement)

References 31 publications

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“…From a pathophysiological point of view, T2DM exacerbates the course of HFpEF via several mechanisms: toxic intermediates and reactive oxygen species, accumulated due to insulin resistance [5], a reduction in nitric oxide bioavailability [52], and the secretion of proinflammatory cytokines by the myocardium and epicardium with the sub-sequent involvement of monocytes [53]. All these mechanisms worsen LVDD thorough increased myocardial extracellular matrix accumulation and the presence of stiffer cardiomyocytes [54][55][56].…”

Section: Discussionmentioning

confidence: 99%

Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction

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et al. 2023

JCDD

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(1) Background: Chronic inflammation and fibrosis are key players in cardiac remodeling associated with left ventricular hypertrophy (LVH) and heart failure with a preserved ejection fraction (HFpEF). Monocytes and T-helpers (Th) are involved in both pro-inflammatory and fibrotic processes, while regulatory T-cells (Treg) could be considered to suppress chronic inflammation in the hypertrophied myocardium. We aimed to estimate the relationship between the frequencies of circulating CD4+ T-cell and monocyte subpopulations and the variables of left ventricular (LV) diastolic function in patients with LVH depending on the presence of HFpEF. (2) Methods: We enrolled 57 patients with asymptomatic hypertensive LVH (n = 21), or LVH associated with HFpEF (n = 36). A clinical assessment and echocardiographs were analyzed. CD4+ Treg, activated Th (Th-act), and monocyte (classical, intermediate, and non-classical) subpopulations were evaluated via direct immunofluorescence and flow cytometry. (3) Results: Patients with HFpEF had a lower Treg/Th-act ratio (p = 0.001). Though asymptomatic patients and patients with HFpEF were comparable in terms of both the total monocyte number and monocyte subsets, there were moderate correlations between intermediate monocyte count and conventional and novel echocardiographic variables of LV diastolic dysfunction in patients with HFpEF. (4) Conclusions: In patients with LVH, the clinical deterioration (transition to HFpEF) and progression of LV diastolic dysfunction are probably associated with T-cell disbalance and an increase in intermediate monocyte counts.

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