Homocysteine Levels in Patients with Heart Failure with Preserved Ejection Fraction


Okuyan E., Uslu A., Cakar M. A. , Sahin I., Onur I., Enhos A. , ...More

CARDIOLOGY, vol.117, no.1, pp.21-27, 2010 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 117 Issue: 1
  • Publication Date: 2010
  • Doi Number: 10.1159/000320106
  • Title of Journal : CARDIOLOGY
  • Page Numbers: pp.21-27

Abstract

Objectives: Increased homocysteine (HCY) levels are associated with an increased risk of cardiovascular disease. Plasma HCY is increased in chronic heart failure (CHF) patients, and previous studies suggest that hyperhomocysteinemia causes adverse cardiac remodeling and affects pump function. We aimed to evaluate the HCY levels in patients with diastolic heart failure with preserved left ventricular ejection fraction (LVEF). Methods: We prospectively studied 68 patients (39 females and 29 males) who were hospitalized for symptomatic heart failure, as well as 40 age- and sex-matched healthy subjects who comprised the control group. CHF was diagnosed in all cases based on Framingham diagnostic criteria. CHF with preserved LVEF was defined as cases with CHF with an LVEF of 50% or more. Patients with regional left ventricular wall motion abnormalities, atrial fibrillation, and renal failure were excluded. Results: The mean age was 65.5 +/- 9.6 years in the heart failure group and 65.2 +/- 9.7 years in the control group. The mean LVEF was 59.8 +/- 5.3 in the heart failure group and 61.4 +/- 5.2 in the control group. The mean total fasting HCY concentrations were significantly higher in patients with heart failure (16.9 +/- 5.27 mu mol/l vs. 10.15 +/- 3.49 mu mol/l, respectively; p < 0.001). Multiple regression analysis indicated that NT-proBNP, hs-CRP, E/A ratio, and HbA1C were independently associated with hyperhomocysteinemia. Conclusions: Our results suggest that hyperhomocysteinemia is prevalent in heart failure with preserved ejection fraction. Larger scale studies are needed to clarify its pathogenic mechanisms and effects on the natural history of heart failure. Copyright (C) 2010 S. Karger AG, Basel