Inflammatory markers in stable heart failure and their relationship with functional class☆
Received 12 April 2007; accepted 7 July 2007. published online 19 November 2007.
Abstract
Introduction and objectives
While it appears to be clear that an inflammatory process occurs in heart failure (HF), it is still to be defined whether inflammation depends to a greater extent on HF etiology, functional class (FC), or the extent of depression of ejection fraction (EF). Our objectives were to analyze differences in inflammatory marker levels as compared to a healthy population, to assess differences depending on HF etiology, and to relate values with FC and EF.
Patients and methods
Fifty-nine consecutive outpatients with stable HF (57+/−9 years, 89% males) and 59 controls (55+/−8 years, 85% males) were enrolled into the study. Causes of HF included ischemic heart disease (n=24), idiopathic dilated cardiomyopathy (n=24), and miscellaneous conditions (n=11). Patients with decompensation in the past 6 months were excluded from the study. Protein fibrinogen, sialic acid, C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-alpha) were measured. Echocardiography was performed in all study patients. FC was assessed using the NYHA classification.
Results
A comparison of inflammatory marker levels between the HF and control groups showed significant differences in all markers, except for TNF-alpha. Protein fibrinogen in controls: 253+/−54 mg/dl, protein fibrinogen in HF: 294+/−67 mg/dl; p<0.05. Sialic acid in controls: 53+/−1 mg/dl, sialic acid in HF: 61+/−12 mg/dl; p<0.05. CRP in controls: 1.3+/−0.7 mg/dl, CRP in HF: 7.8+/−1.2 mg/dl; p<0.05. TNF-alpha in controls: 183+/−51 ng/ml, TNF-alpha in HF: 203+/−13 ng/ml; p=0.2. No differences were found between the different etiologies of HF. A positive association was seen between FC and protein fibrinogen and TNF-alpha (p<0.05), but not with EF.
Conclusions
Increased inflammatory marker levels related to FC of the patient, but not to EF, are found in chronic HF.
ABSTRACT