Complement C3c as a biomarker in heart failure.
BACKGROUND
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.


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.


CONCLUSIONS
Elevated C3c levels are associated with less adverse remodeling and improved survival in patients with stable systolic heart failure.
Department of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany ; Comprehensive Heart Failure Center, University of Würzburg, Straubmühlweg 2a, Haus A9, 97078 Würzburg, Germany.
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Frey
Department of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany ; Comprehensive Heart Failure Center, University of Würzburg, Straubmühlweg 2a, Haus A9, 97078 Würzburg, Germany.
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Ertl
Department of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany ; Comprehensive Heart Failure Center, University of Würzburg, Straubmühlweg 2a, Haus A9, 97078 Würzburg, Germany.
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Angermann
Department of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany ; Comprehensive Heart Failure Center, University of Würzburg, Straubmühlweg 2a, Haus A9, 97078 Würzburg, Germany.
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Hofmann
Department of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany ; Comprehensive Heart Failure Center, University of Würzburg, Straubmühlweg 2a, Haus A9, 97078 Würzburg, Germany.
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Störk
Department of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany ; Comprehensive Heart Failure Center, University of Würzburg, Straubmühlweg 2a, Haus A9, 97078 Würzburg, Germany.
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Frantz
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D015932:Complement C3c / Q000378:metabolism*; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000097:blood* / Q000401:mortality; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism; D013599:Systole; D016896:Treatment Outcome; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
D015415:Biomarkers; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D015932:Complement C3c; D002097:C-Reactive Protein