Gonadotropin releasing hormone agonist (GnRH-a) serves as an alternative to human chorionic gonadotropin (hCG) to trigger final oocyte maturation, while significantly reduces the risk of ovarian hyperstimulation syndrome (OHSS), probably by attenuating vascular/endothelial activation.To compare the effect of different modes of final follicular maturation (hCG vs GnRH-a), following ovarian stimulation (OS) for in-vitro fertilization (IVF), on endothelial function.Prospective cohort study.Tertiary Medical Center.Patients age ≥37 years, undergoing OS for IVF, were allocated into two groups according to the type of final follicle maturation- hCG group (n=7) or GnRH-a group (n=8).Endothelial function was assessed by measurement of the peripheral arterial tonometry in reaction to temporary ischemia at three study points: day 3 of menstrual cycle (day- 0), day of hCG/GnRH-a administration (day-trigger) and day of oocyte pick-up (day-OPU). The ratio of arterial tonometry readings before and after ischemia is called reactive hyperemia index (RHI). Decreased RHI (<1.67) indicates endothelial dysfunction.Endothelial function at three study points during OS with different modes of triggering final follicular maturation.The mean RHI values at day-0 were within the normal range for all patients and comparable between both groups (hCG: 1.7±0.3 vs GnRH-a: 1.79±0.4, p=0.6). All patients presented a decrease in RHI values on day-trigger, which did not differ between the two groups (1.62±0.3 vs 1.4±0.2, respectively, p=0.2). However, the hCG group demonstrated a further decrease in RHI on day-OPU whereas patients who received GnRH-a restored normal endothelial function reflected by increased RHI values (1.4 ± 0.2 vs 1.75 ± 0.2, respectively, p=0.03).Triggering final follicular maturation with GnRH-a restored normal endothelial function, while hCG trigger resulted in a decrease in endothelial function.