Abstract
Background. Despite significant progress in diagnosis and treatment, early prediction and effective prevention of preeclampsia remain pressing challenges in modern obstetric practice. Primiparous women are at increased risk of developing preeclampsia due to the specifics of uteroplacental adaptation and greater vulnerability of the endothelial system. Aim: to evaluate the impact of prophylactic therapy on cerebrovascular reactivity and uterine artery hemodynamics in primiparous women at high risk of preeclampsia and to investigate the relationship between parameters of these systems. Materials and methods. A prospective study was conducted involving 98 primiparous women. The main group (n = 68) included patients at high risk for developing preeclampsia. Depending on the type of pharmacological prophylaxis, the main group was divided into two subgroups: Subgroup Ia (n = 36) received comprehensive preeclampsia prevention, including acetylsalicylic acid (ASA) (150 mg/day from 11–13 to 35 weeks of gestation), L-arginine (3 g/day until 35 weeks if vascular disturbances persisted), and vaginal micronized progesterone (400 mg/day until 33 weeks). Subgroup Ib (n = 32) included women who received only ASA (150 mg/day from 11–13 to 35 weeks). The control group (n = 30) consisted of low-risk pregnant women who did not receive pharmacological prophylaxis. Cerebrovascular reactivity was assessed using ophthalmic artery Doppler in the second trimester (20–22 weeks), determining the first (PSV1) and second (PSV2) peak systolic velocities, pulsatility index (PI), and the PSV2/PSV1 ratio. For comparison, uterine artery hemodynamic parameters (PI UtA) were measured in the second and third trimesters. Statistical analysis was performed using methods of variation statistics; results were considered significant at p<0.05. Results. In Ia subgroup PI UtA decreased 1.46-fold – from 1.45 ± 0.06 in the second trimester to 0.99 ± 0.09 in the third trimester – approaching the reference level of the control group, which indicates normalization of the uteroplacental blood flow under the influence of comprehensive prophylaxis. In Ib subgroup, the PI UtA decreased from 1.52 ± 0.07 to 1.04 ± 0.09; however, it remained 9.5% higher than in the control group (ANOVA p < 0.001). Doppler parameters of the ophthalmic artery in the second trimester showed that PSV1 did not differ significantly between groups (p = 0.455), indicating a baseline level of central hemodynamics. PSV2 in Ib subgroup (30.64 ± 1.24 cm/s) exceeded the values of the control group (28.42 ± 1.15 cm/s) by 7.8% and those of Ia subgroup (29.08 ± 1.36 cm/s) by 5.3% (p < 0.001). A similar trend was observed in the PSV2/PSV1 ratio: the lowest values were in the control group (0.846 ± 0.016), intermediate in Ia subgroup (0.874 ± 0.019), and the highest in Ib subgroup (0.911 ± 0.020) (p < 0.001). Conclusion. The proposed comprehensive preeclampsia prophylaxis (ASA + L-arginine + vaginal micronized progesterone) in primiparous women promotes stabilization and gradual normalization of uteroplacental blood flow throughout the second and third trimesters and maintains balanced cerebrovascular perfusion according to ophthalmic artery Doppler. Ophthalmic artery Doppler parameters (PSV2, PSV2/PSV1, PI OA) reflect cerebrovascular reactivity and correlate with high-resistance uterine artery blood flow, allowing assessment of subclinical endothelial dysfunction. The results support the use of ophthalmic artery Doppler as a tool for monitoring the effectiveness of prophylactic therapy and early prediction of preeclampsia