Background. Antiphospholipid syndrome (APS) is defined by the combination of thrombotic events and/or obstetrical morbidity associated with the presence of antiphospholipid antibodies. The pathogenesis of obstetrical APS remains poorly understood, but the role of the complement system and of endothelial cells, platelets, and monocytes seems important in the occurrence of placental thrombosis. Hydroxychloroquine is widely used in patients with various autoimmune diseases, particularly systemic lupus erythematosus. Antimalarials have many anti-inflammatory, anti-aggregant and immune-regulatory properties: they inhibit phospholipase activity, stabilize lysosomal membranes, block the production of several pro-inflammatory cytokines and, in addition, impair complement dependent antigen-antibody reactions. In one study plasma samples from APS patients revealed decreased nitric oxide (NO) availability. Reduced availability of NO leads to diminished angiogenesis, increased platelet aggregation, pro-inflammatory action and diminished ability of microvessels to dilate. The aim of our study was to compare vasodilator response of cutaneous microvasculature to local heating of APS patients without antimalarial treatment, APS patients treated with antimalarial drug chloroquine and healthy controls. Methods. We enrolled patients with APS and age and sex matched healthy controls. Participants were divided in three groups. In the first were 8 patients, receiving chloroquine; in the second were 15 patients without antimalarial treatment and in the third group were 23 healthy control subjects. All participants were 22 – 49 years old. Participants were asked to avoid coffee, tea or energy drinks on the day of the measurements. Laser Doppler (LD) flux of cutaneous microvessels was monitored on the ventral side of the forearm. After 30 minutes of acclimatisation we performed 6 minutes measurements at rest. Afterwards local warming (42°C) of skin on the forearm was used to assess heat-stimulated vasodilator response. Data were analysed using ANOVA followed by Dunnett’s test. The study was approved by the National Medical Ethics Committee; written informed consent was obtained from each subject. Results. LD flux at rest was in all three groups the same: 16.0 ± 2.8 PU in patients taking chloroquine, 17.6 ± 3.1 PU in patients without antimalarial therapy and 18.8 ± 3.1 PU in healthy controls. The APS patients without antimalarial drug had statistically significantly lower LD flux plateau during local warming in comparison to healthy subjects (41.6 ± 7.8 PU vs. 77.4 ± 11.9). APS patients treated with antimalarial (70.1 ± 22.4 PU) did not differ in vasodilation during local heating in comparison to healthy controls. Conclusions. Antimalarial drugs improve vasodilation capacity in patients with APS.