Background: Immediately following percutaneous balloon mitral valvuloplasty
(PBMVP), patients have a 3% risk of systemic thromboembolism. Hypothesis:
We hypothesized that this may in part be due to an increase in hypercoagula
bility (as indicated by abnormal coagulation, platelet activation, and endo
thelial dysfunction) in such patients.
Methods: We measured indices of platelet activation [soluble P-selectin (sP
sel), ELISA], endothelial dysfunction [von Willebrand factor (vWf), ELISA],
and coagulation (fibrinogen, modified Clauss) in 16 patients (15 women, me
an age 59 +/- 10 years) with chronic atrial fibrillation admitted for PBMVP
, and 16 healthy age- and gender-matched controls. Blood samples were obtai
ned as follows: (1) peripheral venous samples prior to PBMVP, immediately f
ollowing PBMVP, and 24 h after PBMVP: and (2) arterial samples prior to and
immediately following PBMVP.
Results: Patients with mitral stenosis and chronic atrial fibrillation demo
nstrated significantly higher mean levels of vWf [148 (SD 24) vs. 102 (SD 3
7); t-test, p < 0.001] and plasma fibrinogen [4.2 (SD 0.8) vs. 3.3 (SD 0.8)
; p = 0.003] at baseline than matched healthy controls. There was a nonsign
ificant trend toward lower median sP-sel levels in patients with mitral ste
nosis [64 (inter quartile range 47-91) vs. 109 (46-128); Mann-Whitney test,
p = 0.08]. Following PBMVP, there was a significant increase in venous sP-
sel levels immediately post procedure (paired Wilcoxon test, p = 0.03) and
at 24 h after ward (p = 0.01). Arterial s-Psel levels correspondingly incre
ased immediately post procedure (p = 0.008). There was a significant increa
se in mean venous (at 24 h) but not arterial vWf levels post PBMVP. There w
ere no significant changes in mean venous or arterial plasma fibrinogen lev
els following PBMVP.
Conclusion: Patients with mitral stenosis and chronic atrial fibrillation h
ave increased plasma levels of vWf and fibrinogen levels compared with heal
thy controls, suggesting increased endothelial dysfunction and coagulation
at baseline in these patients. The increased levels of sP-sel immediately p
ost procedure and at 24 h, in association with increased vWf levels at 24 h
after PBMVP, are in keeping with an increase in platelet activation and en
dothelial dysfunction following PBMVP These changes may contribute to the i
ncreased risk of thromboembolism following PBMVP and suggest the need for a
dequate antithrombotic therapy following PBMVP.