Impaired endothelial function and increased carotid intima-media thickness in association with elevated von
13rd Department of Medicine, Institute for Internal Medicine, University of Debrecen, Medical and Health Science Center, Debrecen, Hungary.
Insights
Patients with primary antiphospholipid syndrome (APS) show impaired endothelial function and increased atherosclerosis markers. These findings suggest endothelial damage and support considering vasoprotective therapies for APS.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Rheumatology
Background:
- Primary antiphospholipid syndrome (APS) involves thrombotic events and pregnancy complications, linked to antiphospholipid antibodies.
- Antiphospholipid antibodies can activate endothelial cells and are associated with atherosclerosis.
- Endothelial dysfunction and early atherosclerosis are potential complications in primary APS.
Purpose of the Study:
- To assess endothelial impairment in primary APS patients.
- To evaluate early signs of atherosclerosis in primary APS.
- To compare vasodilation, von Willebrand factor, and carotid artery intima-media thickness (IMT) between primary APS patients and healthy controls.
Main Methods:
- Measured flow-mediated (endothelium-dependent) and nitrate-mediated (endothelium-independent) vasodilation.
- Assessed von Willebrand factor antigen levels.
- Determined carotid artery intima-media thickness (IMT).
Main Results:
- Significantly lower flow-mediated vasodilation in primary APS patients compared to controls (3.43% vs. 7.96%).
- Significantly higher von Willebrand factor antigen levels in primary APS patients (157.91% vs. 125.87%).
- Significantly larger carotid artery IMT in primary APS patients (0.714 mm vs. 0.58 mm).
Conclusions:
- Primary APS is associated with ongoing endothelial damage.
- Patients with primary APS exhibit accelerated atherosclerosis.
- Vasoprotective therapy may benefit patients with primary APS.
Abstract:
Primary antiphospholipid syndrome (APS) is characterized by venous or arterial thrombotic events and/or recurrent abortions, fetal death, preeclasmpsia, eclampsia in the presence of anticardiolipin antibodies or lupus anticoagulant, in the absence of accompanying diseases. Antiphospholipid antibodies can activate endothelial cells, and were recently implicated in atherosclerosis. To assess potential endothelial impairment and early signs of atherosclerosis, flow-mediated (endothelium-dependent) and nitrate-mediated (endothelium independent) vasodilation, as well as von Willebrand factor antigen level and carotid artery intima-media thickness (IMT) were measured in patients with primary antiphospholipid syndrome and in healthy controls. Flow-mediated vasodilation in patients with primary APS was significantly lower than that of controls (3.43 +/- 2.86% versus 7.96 +/- 3.57%; P < 0.0001). We also found significantly higher von Willebrand antigen levels in patients with primary APS than in the control group (157.91 +/- 52.45% versus 125.87 +/- 32.8%; P = 0.012). Moreover, carotid artery IMT was significantly larger in the primary APS group compared to controls (0.714 +/- 0.2 mm versus 0.58 +/- 0.085 mm; P = 0.0037). Our results reflect ongoing endothelial damage and accelerated atherosclerosis in patients with primary APS, and suggest that vasoprotective therapy may be beneficial in the treatment of these patients.
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