Bielecka-Dabrowa Agata, Sakowicz Agata, Misztal Małgorzata, von Haehling Stephan, Ahmed Ali, Pietrucha Tadeusz, Rysz Jacek, Banach Maciej
Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland.
Department of Medical Biotechnology, Medical University of Lodz, Poland.
Int J Cardiol. 2016 Oct 15;221:1073-80. doi: 10.1016/j.ijcard.2016.07.150. Epub 2016 Jul 12.
BACKGROUND/OBJECTIVES: To evaluate whether biomarkers reflecting pathophysiological pathways and selected single nucleotide polymorphisms differ between patients (pts) with heart failure (HF).
110 pts with were involved, including HF pts with preserved ejection fraction (HFpEF, n=51) with hypertensive origin, HF pts with reduced ejection fraction (HFrEF) with ischemic aetiology (ICM) (n=32) and HFrEF with dilated cardiomyopathy (DCM) (n=27). We assessed selected HF biomarkers, echocardiographic examinations and functional polymorphisms selected from six candidate genes: CYP27B1, NOS3, IL-6, TGF beta, TNF alpha, and PPAR gamma.
Higher concentrations of TNF alpha were observed in pts with hypertensive HFpEF compared to pts with DCM (p=0.008). Pts with HFpEF had higher concentrations of TGF beta 1 compared to DCM and ICM (p=0.0001 and p=0.0003, respectively). For the NOS3 -786 C/T rs2070744 polymorphism in DCM there were significantly more CT heterozygotes than in ICM and HFpEF. In multivariate analysis TGF beta 1 (p=0.001) and syndecan 4 (p=0.001) were the only factors distinguishing HFrEF pts with DCM vs HFpEF and also TGF beta 1 (p=0.001) and syndecan 4 (p=0.023) were the only factors distinguishing HFrEF pts with ICM vs HFpEF pts.
Inflammation mediated through TNF alpha and TGF beta 1 may represent an important component of an inflammatory response that partially drives the pathophysiology of HFpEF. NOS3 -786 C/T rs2070744 polymorphism in DCM may serve as a marker for more rapid progression of heart failure. The only biomarkers independently distinguishing HFpEF and HFrEF are syndecan 4 and TGF beta 1.
背景/目的:评估反映病理生理途径的生物标志物和选定的单核苷酸多态性在心力衰竭(HF)患者之间是否存在差异。
纳入110例患者,包括高血压性射血分数保留的HF患者(HFpEF,n = 51)、缺血性病因(ICM)的射血分数降低的HF患者(HFrEF)(n = 32)和扩张型心肌病(DCM)的HFrEF患者(n = 27)。我们评估了选定的HF生物标志物、超声心动图检查以及从六个候选基因(CYP27B1、NOS3、IL - 6、TGFβ、TNFα和PPARγ)中选择的功能多态性。
与DCM患者相比,高血压性HFpEF患者中观察到更高浓度的TNFα(p = 0.008)。与DCM和ICM患者相比,HFpEF患者具有更高浓度的TGFβ1(分别为p = 0.0001和p = 0.0003)。对于DCM中NOS3 - 786 C/T rs2070744多态性,CT杂合子明显多于ICM和HFpEF患者。在多变量分析中,TGFβ1(p = 0.001)和Syndecan 4(p = 0.001)是区分DCM与HFpEF的HFrEF患者的唯一因素,并且TGFβ1(p = 0.001)和Syndecan 4(p = 0.023)也是区分ICM与HFpEF患者的HFrEF患者的唯一因素。
通过TNFα和TGFβ1介导的炎症可能是炎症反应的重要组成部分,部分驱动了HFpEF的病理生理学。DCM中NOS3 - 786 C/T rs2070744多态性可能作为心力衰竭更快速进展的标志物。独立区分HFpEF和HFrEF的唯一生物标志物是Syndecan 4和TGFβ1。