Effects of congestive heart failure on plasma von Willebrand factor and soluble P-selectin concentrations in patients with non-valvar atrial fibrillation.
OBJECTIVE
To examine further the relations of plasma von Willebrand factor (vWf, an index of endothelial damage and dysfunction) and soluble P-selectin (sP-sel, an index of platelet activation) concentrations to the presence and onset of clinical congestive heart failure (CHF) and the degree of left ventricular (LV) dysfunction in patients taking part in the SPAF (stroke prevention in atrial fibrillation) study.


METHODS
Plasma concentrations of vWf and sP-sel were measured by enzyme linked immunosorbent assay (ELISA) in 1321 participants in the SPAF III study and related to the presence and onset of clinical CHF, as well as echocardiographic findings. Of the 1321 patients with atrial fibrillation (AF), 331 (25%) had a documented history of clinical heart failure, of which 168 cases were related to a new or recurrent episode of acute decompensated heart failure occurring within the preceding three months.


RESULTS
Mean plasma vWf was higher among patients with AF and CHF (154 (29) v 144 (31) IU/dl, p < 0.001), particularly those with acute or recent decompensated symptoms. Patients with severe LV dysfunction on two dimensional echocardiography and low fractional shortening also had significantly higher vWf concentrations than those with no LV dysfunction. CHF patients with clinical features--with (156 (28) IU/dl) and without (152 (31) IU/dl) LV dysfunction--also had higher mean vWf concentrations than patients with asymptomatic LV dysfunction (146 (31) IU/dl, p < 0.001). The presence of mitral regurgitation in CHF was associated with lower vWf concentrations. Plasma sP-sel concentrations were not affected by presence, onset, or severity of heart failure.


CONCLUSIONS
CHF may contribute to hypercoagulability and thrombotic risk in AF through increased endothelial damage and dysfunction. Patients with acute or recent decompensated features have the highest degree of endothelial damage and dysfunction. The presence of CHF clinical features was an important determinant of plasma vWf concentrations.
Lip
G Y H
GY
Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK. g.y.h.lip@bham.ac.uk
Pearce
L A
LA
Chin
B S P
BS
Conway
D S G
DS
Hart
R G
RG
D000368:Aged; D000925:Anticoagulants / Q000008:administration & dosage; D001241:Aspirin / Q000008:administration & dosage; D001281:Atrial Fibrillation / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy; D006801:Humans; D008297:Male; D019007:P-Selectin / Q000032:analysis*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000517:prevention & control; D018487:Ventricular Dysfunction, Left / Q000097:blood; D014859:Warfarin / Q000008:administration & dosage; D014841:von Willebrand Factor / Q000032:analysis*
D000925:Anticoagulants; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D014841:von Willebrand Factor; D014859:Warfarin; D001241:Aspirin