Association of ventricular–arterial coupling with biomarkers involved in heart failure pathophysiology – the STANISLAS cohort

医学 动脉硬化 内科学 心力衰竭 利钠肽 病理生理学 脉冲波速 心脏病学 队列 人口 肾上腺髓质素 内分泌学 血压 受体 环境卫生
作者
Hannes Holm,Martin Magnusson,Amra Jujić,Jérémy Lagrange,Erwan Bozec,Zohra Lamiral,Emmanuel Bresso,Olivier Huttin,Guillaume Baudry,Luca Monzo,Patrick Rossignol,F. Zannad,Nicolas Girerd
出处
期刊:European Journal of Heart Failure [Elsevier BV]
标识
DOI:10.1002/ejhf.3411
摘要

Aims Impaired left ventricular–arterial coupling (VAC) has been shown to correlate with worse prognosis in cardiac diseases and heart failure (HF). The extent of the relationship between VAC and circulating biomarkers associated with HF has been scarcely documented. We aimed to explore associations of VAC with proteins involved in HF pathophysiology within a large population‐based cohort of middle‐aged individuals. Methods and results In the forth visit of the STANISLAS family cohort, involving 1309 participants (mean age 48 ± 14 years; 48% male) from parent and children generations, we analysed the association of 32 HF‐related proteins with non‐invasively assessed VAC using pulse wave velocity (PWV)/global longitudinal strain (GLS) and arterial elastance (E a )/ventricular end‐systolic elastance (E es ). Among the 32 tested proteins, fatty acid‐binding protein adipocyte 4, interleukin‐6, growth differentiation factor 15, matrix metalloproteinase (MMP)‐1, and MMP‐9 and adrenomedullin were positively associated with PWV/GLS whereas transforming growth factor beta receptor type 3, MMP‐2 and N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) were negatively associated. In multivariable models, only MMP‐2 and NT‐proBNP were significantly and inversely associated with PWV/GLS in the whole population and in the parent generation. Higher levels of NT‐proBNP were also negatively associated with E a /E es in the whole cohort but this association did not persist in the parent subgroup. Conclusion Elevated MMP‐2 and NT‐proBNP levels correlate with better VAC (lower PWV/GLS), possibly indicating a compensatory cardiovascular response to regulate left ventricular pressure amidst cardiac remodelling and overload.
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