Wannamethee S Goya, Whincup Peter H, Papacosta Olia, Lennon Lucy, Lowe Gordon D
Department of Primary Care and Population Health, University College London, UK.
Population Health Research Centre, Division of Population Health Sciences and Education, St George's, University of London, UK.
Int J Cardiol. 2017 Mar 1;230:567-571. doi: 10.1016/j.ijcard.2016.12.056. Epub 2016 Dec 20.
Chronic heart failure (HF) is associated with activation of blood coagulation but there is a lack of prospective studies on the association between coagulation markers and incident HF in general populations. We have examined the association between the coagulation markers fibrinogen, von Willebrand Factor (VWF), Factors VII, VIII and IX, D-dimer, activated protein C (APC) and activated partial thromboplastin time (aPPT) with NT-proBNP and incident HF.
Prospective study of 3366 men aged 60-79years with no prevalent HF, myocardial infarction or venous thrombosis and who were not on warfarin, followed up for a mean period of 13years, in whom there were 203 incident HF cases. D-dimer and vWF were significantly and positively associated with NT-proBNP (a marker of neurohormonal activation and left ventricular wall stress) even after adjustment for age, lifestyle characteristics, renal dysfunction, atrial fibrillation (AF) and inflammation (C-reactive protein). By contrast Factor VII related inversely to AF and NT-proBNP even after adjustment. No association was seen however between the coagulation markers VWF, Factor VII, Factor VIII, Factor IX, D-dimer, APC resistance or aPPT with incident HF in age-adjusted analyses. Fibrinogen was associated with incident HF but this was abolished after adjustment for HF risk factors.
Coagulation activity is not associated with the development of HF. However D-dimer and vWF were significantly associated with NT-proBNP, suggesting that increased coagulation activity is related to cardiac stress; and the increased coagulation seen in HF patients may in part be a consequence of neurohormonal activation.
慢性心力衰竭(HF)与凝血激活有关,但缺乏关于一般人群中凝血标志物与新发HF之间关联的前瞻性研究。我们研究了凝血标志物纤维蛋白原、血管性血友病因子(VWF)、凝血因子VII、VIII和IX、D-二聚体、活化蛋白C(APC)以及活化部分凝血活酶时间(aPPT)与N末端脑钠肽前体(NT-proBNP)和新发HF之间的关联。
对3366名年龄在60 - 79岁、无HF、心肌梗死或静脉血栓病史且未服用华法林的男性进行前瞻性研究,平均随访13年,其中有203例新发HF病例。即使在调整年龄、生活方式特征、肾功能不全、心房颤动(AF)和炎症(C反应蛋白)后,D-二聚体和vWF仍与NT-proBNP(神经激素激活和左心室壁应力的标志物)显著正相关。相比之下,即使在调整后,凝血因子VII与AF和NT-proBNP呈负相关。然而,在年龄调整分析中,凝血标志物VWF、凝血因子VII、VIII、IX、D-二聚体、APC抵抗或aPPT与新发HF之间未发现关联。纤维蛋白原与新发HF有关,但在调整HF危险因素后这种关联消失。
凝血活性与HF的发生无关。然而,D-二聚体和vWF与NT-proBNP显著相关,表明凝血活性增加与心脏应激有关;HF患者中凝血增加可能部分是神经激素激活的结果。