Inflammatory markers as related to disease severity in patients with chronic heart failure: Limited effects of exercise training

Abstract

Background. Chronic heart failure (CHF) is associated with increased inflammation, and exercise training has in some studies been shown to have anti-inflammatory effect, although controversies exist. We investigated the effects of exercise training in CHF patients on markers of inflammation, and further explored any association between inflammation and the severity and etiology of the disease. Methods. Eighty patients in stable CHF were randomized to 4 months of group-based high intensity exercise training or to a control group. Physical capacity was measured by 6-minute walk test and cycle ergometer test. Blood samples were drawn at baseline, after 4 months and after 12 months follow-up for analyses of a range of biomarkers. Results. Physical capacity was significantly inversely related to CRP, IL-6, VCAM-1 and TGF-β, and NT pro-BNP levels were significantly correlated to CRP, TNF-α, IL-6, VCAM-1, ICAM-1 and TGF-β (p < 0.05 for all). Patients with hypertension as etiology of CHF showed higher levels of CRP (p < 0.01), IL-6 (p = 0.05) and TNF-α (p = 0.02) as compared to other etiologies. No significant differences in changes between the exercise group and the control group were obtained in any of the measured variables, except in patients with idiopathic dilated cardiomyopathy (IDCM), where significant reductions in CRP, ICAM-1, TGF-β and TNF-α levels were observed (p < 0.05 for all). Conclusions. Measures of CHF severity were significantly correlated with several markers of inflammation. We could not demonstrate over-all anti-inflammatory effect of exercise in this population of CHF patients. However, the etiology of CHF affected the inflammatory profile and the effect of exercise training.

Key Words::

• Adhesion molecules
• cardiomyopathy
• cytokines
• heart failure
• inflammation
• physical training

Acknowledgements

We thank the physicians Svein Solheim, Haakon Kiil Grøgaard and Torstein Jensen, Department of Cardiology, for performance of the cycle ergometer testing of patients. We also thank the Department of Clinical Chemistry at Ulleval University Hospital for the NT pro-BNP analysis.

Funding

This work was supported by grants from the Eastern Norwegian Health Authority, Norway, The Norwegian Foundation for Health & Rehabilitation and Stein Erik Hagen Foundation for Clinical Heart Research, Oslo, Norway.

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the article.