Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombosis and/or pregnancy morbidity in the persistent presence of antiphospholipid antibodies (aPL). Pathogenetic mechanisms of aPLs are not yet completely explained. Thrombosis may be linked to diminished production of nitric oxide (NO) in endothelium. Endothelium-derived NO normally exerts anti-thrombotic and vasodilator effects. We aimed to determine endothelium-dependent and endothelium-independent vasodilation in cutaneous microvasculature of APS patients and healthy controls.
In our measurement protocol electrocardiogram, arterial blood pressure and laser Doppler flux of cutaneous microvessels were monitored in patients with primary or secondary APS (all positive for at least two different aPL) and healthy controls. To assess endothelium-dependent vasodilation we used iontophoresis of acetylcholine, which stimulates NO production in endothelial cells. Iontophoresis of sodium nitroprusside, a direct NO donor, was used to assess endothelium-independent vasodilation. Data were analysed using independent samples t-test or repeated measures ANOVA followed by Dunnett’s test.
34 APS patients and 34 healthy age and sex-matched controls completed the study (24 female and 10 male in each group, age range 22-74). Participants were divided into three age groups, 22-38 years, 39-49 and ≥50. Endothelium-dependent vasodilator response was blunted in older patients (P<0.050 vs. healthy controls), but remained unaltered in younger participants. Endothelium-independent vasodilation was similar in all groups.
Our study shows that endothelium-dependent vasodilation in cutaneous microvasculature is diminished in older APS patients, indicating altered cutaneous microvasculature. This study supports reduced endothelial NO production in APS patients.