Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection FractionстатьяЭлектронная публикация
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Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction
by Artem Ovchinnikov 1,2,*ORCID,Anastasiya Filatova 1,3ORCID,Alexandra Potekhina 1ORCID,Tatiana Arefieva 3ORCID,Anna Gvozdeva 1,Fail Ageev 4 andEvgeny Belyavskiy 5ORCID
1
Laboratory of Myocardial Fibrosis and Heart Failure with Preserved Ejection Fraction, Institute of Clinical Cardiology, National Medical Research Center of Cardiology Named after Academician E.I. Chazov, 121552 Moscow, Russia
2
Department of Clinical Functional Diagnostics, A.I. Yevdokimov Moscow State University of Medicine and Dentistry, 127473 Moscow, Russia
3
Laboratory of Cell Immunology, Institute of Experimental Cardiology, National Medical Research Center of Cardiology Named after Academician E.I. Chazov, 121552 Moscow, Russia
4
Out-Patient Department, Institute of Clinical Cardiology, National Medical Research Center of Cardiology Named after Academician E.I. Chazov, 121552 Moscow, Russia
5
MVZ des Deutschen Herzzentrums der Charité, 13353 Berlin, Germany
*
Author to whom correspondence should be addressed.
J. Cardiovasc. Dev. Dis. 2023, 10(7), 310; https://doi.org/10.3390/jcdd10070310
Submission received: 28 June 2023 / Revised: 17 July 2023 / Accepted: 18 July 2023 / Published: 20 July 2023
(This article belongs to the Special Issue Cardiovascular Imaging in Heart Failure with Preserved Ejection Fraction)
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Abstract
(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.