Fogacho como marcador de risco cardiovascular na pós-menopausa recente: efeitos de tratamentos não hormonais

Abstract

In this double-blind clinical trial, the effects of non-hormonal treatments for hot flushes on endothelial function, autonomic and blood pressure components of women's recent postmenopausal vascular function were investigated through the use of paroxetine at a dose of 7.5 mg / day and placebo. The effects of both on daytime sleepiness, sleep quality and perceived stress were also evaluated. A total of 142 patients (72 in the paroxetine group and 70 in the placebo group) were included. The endothelial function was evaluated through venous occlusion plethysmography, the autonomic component, through electrocardiography (ECG) of 10 minutes and blood pressure through 24-hour ambulatory blood pressure. Daytime sleepiness, sleep quality, and self perceived stress were assessed through Epworth Sleepiness Scale (ESS-BR), Pittsburgh Sleep Quality Index (PSQI-BR) and Perceived Stress Scale (PSS), respectively. The levels of estradiol (E2) and sex hormone-binding globulin (SHBG) were also evaluated. There was a significant reduction in hot flashes in both groups; however, lower levels of E2 (pre-treatment in the paroxetine group compared to the placebo group; post intervention in the two groups, more important in the placebo group, compared to the baseline assessment) were reflected in lower reactive hyperemia flows, despite the reduction of hot flushes in both groups. Also, the E2 delta presented a significant direct correlation with the absolute and relative deltas of the basal flow and with the deltas of the reactive hyperemia flow in the total sample. After adjusting for E2 levels, the inverse correlation of the hot flushes with the mean hyperemia reactive flow in the total sample did not maintain statistical significance and there was a loss of the direct correlation initially observed between the hot flashes subjective score and the mean sleep systolic blood pressure in the total sample. In the paroxetine group, the parasympathetic HF and pNN50 components increased so as endothelial-independent vasodilation did at plethysmography. There was a significant reduction of psychic subjective score symptoms and Kupperman-Blatt Index (IKB) in addition to improvement of PSQI-BR sleep quality in both groups, but a significant increase in sleep hours occurred only in the placebo group, at subjective evaluation. Significant increase in body mass index (BMI) occurred in the paroxetine group, however, it was not followed by an increase in waist circumference (WC). In relation to the other reported side effects, there were no significant differences between the groups. In conclusion, the reduction of hot flushes did not improve endothelial function, making it unlikely that the vasomotor symptom itself is directly responsible for endothelial dysfunction. The reduction of the hot flushes seemed to occur predominantly by effect on the central nervous system. E2 levels appeared to be responsible for endothelial function in this study. Unlike placebo, paroxetine appeared to modulate the autonomic nervous system by increasing parasympathetic tonus, which may bring some benefit beyond the mere reduction of symptoms in postmenopausal women.