Inflammatory markers in stable heart failure and their relationship with functional class (original) (raw)

2008, International Journal of Cardiology

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 b 0.05. Sialic acid in controls: 53 +/− 1 mg/dl, sialic acid in HF: 61 +/− 12 mg/dl; p b 0.05. CRP in controls: 1.3 +/− 0.7 mg/dl, CRP in HF: 7.8 +/− 1.2 mg/dl; p b 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 b 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.