Associations between blood coagulation markers, NT-proBNP and risk of incident heart failure in older men: The British Regional Heart Study.
- Publisher: Elsevier
International Journal of Cardiology,
(issn: 0167-5273, eissn: 1874-1754)
Heart failure | D-dimer | Cardiology and Cardiovascular Medicine | Coagulation, D-dimer, Heart failure, NT-proBNP | Coagulation | Article | NT-proBNP
Aims: \ud \ud 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.\ud \ud Methods and results: \ud \ud Prospective study of 3366 men aged 60–79 years with no prevalent HF, myocardial infarction or venous thrombosis and who were not on warfarin, followed up for a mean period of 13 years, 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.\ud \ud Conclusion: \ud \ud 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.