Endothelial function is impaired in patients with primary antiphospholipid syndrome
The aim of this study was to evaluate endothelial function in patients with primary antiphospholipid syndrome (PAPS). Flow mediated (FMD) and glyceryl trinitrate (GTN) induced dilation of the right brachial artery were studied in 25 patients with PAPS and 25 controls matched by age, sex and conventi...
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Published in | Thrombosis research Vol. 118; no. 4; pp. 455 - 461 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Ltd
2006
Elsevier Science |
Subjects | |
Online Access | Get full text |
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Summary: | The aim of this study was to evaluate endothelial function in patients with primary antiphospholipid syndrome (PAPS).
Flow mediated (FMD) and glyceryl trinitrate (GTN) induced dilation of the right brachial artery were studied in 25 patients with PAPS and 25 controls matched by age, sex and conventional risk factors for atherosclerosis. Fibrinogen, D-dimer, adhesion molecules, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) antigens and activities were measured.
Mean (SD) FMD was significantly lower in PAPS than in controls (8
±
5% vs. 15
±
6%,
P
<
0.001); GTN-induced dilation did not differ between the groups. There was a correlation between the baseline diameter of the brachial artery and duration of the disease (−
0.56,
P
<
0.05) and between GTN induced dilation and duration of the disease (0.51,
P
<
0.05). Concentrations of vascular cell adhesion molecule-1 (
P
<
0.001), intracellular adhesion molecule-1 (
P
<
0.001) and fibrinogen (
P
<
0.05) were higher in patients than in controls but no differences were observed for D-dimer, t-PA and PAI-1 antigens and activities. There was correlation between concentration of vascular cell adhesion molecule-1 and FMD (−
0.35,
P
<
0.05) and between intracellular adhesion molecule-1 and FMD (−
0.41,
P
<
0.05).
This study shows that endothelial function is impaired in patients with primary APS, possibly contributing to accelerated atherosclerosis and thromboembolic complications in these patients. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0049-3848 1879-2472 |
DOI: | 10.1016/j.thromres.2005.09.005 |