@article{FreyErtlAngermannetal.2013,
  author    = {Frey, A. and Ertl, G. and Angermann, C. E. and Hofmann, U. and St{\"o}rk, S. and Frantz, S.},
  title     = {Complement C3c as a Biomarker in Heart Failure},
  series = {Mediators of Inflammation},
  volume    = {2013},
  journal   = {Mediators of Inflammation},
  number    = {Article ID 716902},
  doi       = {10.1155/2013/716902},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-129668},
  pages     = {7},
  year      = {2013},
  abstract  = {Experimental data indicates an important role of the innate immune system in cardiac remodeling and heart failure (HF). Complement is a central effector pathway of the innate immune system. Animals lacking parts of the complement system are protected from adverse remodeling. Based on these data, we hypothesized that peripheral complement levels could be a good marker for adverse remodeling and prognosis in patients with HF. Methods and Results. Since complement activation converges on the complement factor C3, we measured serum C3c, a stable C3-conversion product, in 197 patients with stable systolic HF. Subgroups with normal and elevated C3c levels were compared. C3c levels were elevated in 17\%of the cohort. Patients with elevated C3c levels exhibited a trend to better survival, slightly higher LVEF, and lower NTpro-BNP values in comparison to patients with normal C3c values. No differences were found regarding NYHA functional class. Significantly more patients with elevated C3c had preexisting diabetes. The prevalence of CAD, arterial hypertension, and atrial fibrillation was not increased in patients with elevated C3c. Conclusion. Elevated C3c levels are associated with less adverse remodeling and improved survival in patients with stable systolic heart failure.},
  language  = {en}
}