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Prenatal depression and preeclampsia (PE) are well-known risk factors of maternal and fetal mortality and morbidity. In recent years, there are emerging evidence suggesting that prenatal depression and PE could be environmental risk factors for several neurodevelopment disorders of offspring. Prenatal depression and PE were also found to be risk factors of each other. At present, the mechanism (s) of how prenatal depression and PE affect one another and their roles in the development of maternal and fetal adverse outcomes are uncertain. In this review, we outline the most recent clinical studies on the effects of prenatal depression and PE on the neurodevelopmental outcomes of offspring, as well as the plausible mechanism(s) of how these two maternal conditions affect each other and their roles in the neurodevelopment of offspring, including inflammation, oxidative stress, and maternal immune activation. We postulate that the overproduction of pro-inflammatory cytokines and increased cortisol levels in maternal depression can alter fetal neurodevelopment, and the autonomic nervous system dysfunction caused by maternal depression may accelerate heart rate and elevate blood pressure in mothers. Similarly, in PE, the elevated inflammation and exaggerated oxidative stress in the mothers, placenta, and fetus could negatively affect maternal depression on and impair the neurodevelopment of offspring. Further studies are needed to examine the combined effects of prenatal depression and PE on the health outcomes of mothers and offspring, to explore the mechanism of maternal depression in the development of PE and to investigate their roles in the neurodevelopment of offspring.

Aim: The aim of this study is to evaluate the association between serum sodium concentrations at hospital admission and all-cause mortality within 365 days post-discharge in patients with atrial fibrillation (AF) without heart failure (HF). Methods: The prospective cohort study enrolled 1,446 patients with AF without HF between November 2018 and October 2020. A follow-up was performed 30, 90, 180, and 365 days after enrollment through outpatient visits or telephone interviews. All-cause mortality was estimated in three groups according to serum sodium concentrations: hyponatremia ( < 135 mmol/L), normonatremia (135 – 145 mmol/L), and hypernatremia ( > 145 mmol/L). We estimated the risk of all-cause mortalities using univariable and multivariable Cox proportional hazards models with normonatremia as the reference. Results: The all-cause mortalities of hyponatremia, normonatremia, and hypernatremia were 20.6, 9.4, and 33.3 % within 365 days post-discharge, respectively. In the univariable analysis, hyponatremia (HR: 2.19, CI 1.5 – 3.2) and hypernatremia (HR: 4.03, CI 2.32 – 7.02) increased the risk of all-cause mortality. The HRs for hyponatremia and hypernatremia were 1.55 (CI 1.05 – 2.28) and 2.55 (CI 1.45 – 4.46) after adjustment for age, diabetes mellitus, loop diuretics, antisterone, antiplatelet drugs, and anticoagulants in the patients with AF without HF. The association between serum sodium concentrations and the HRs of all-cause mortality was U-shaped. Conclusion: Dysnatremia at hospital admission was an independent factor for all-cause mortality in patients with AF without HF within 365 days post-discharge.

Background: Low-dose rivaroxaban and low-intensity warfarin are widely used in Asia for patients with atrial fibrillation (AF). However, in Asians, it is unclear whether low-dose rivaroxaban and low-intensity warfarin can improve the prognosis of AF. In this study, we investigate the survival benefits of low-dose rivaroxaban and low-intensity warfarin in Asian patients with AF in clinical practice. Methods: This cohort study used medical records in a single tertiary hospital in China, between 2019 and 2020, to identify patients with AF who used rivaroxaban or warfarin, or had no anticoagulant therapy. Follow-ups were performed through telephone contact or medical record review. Cox proportional hazards models were used to compare the risk of mortality of patients in the anticoagulant-untreated group vs. warfarin-treated groups and rivaroxaban-treated groups. Results: A total of 1727 AF patients, discharged between 2019 and 2020, were enrolled in this cohort, of which 873 patients did not use any anticoagulant, 457 patients received warfarin and 397 patients used rivaroxaban. Multivariable analysis showed that, of all the warfarin groups, patients with an international normalized ratio (INR) below 2, good INR control, or poor INR control had a significantly lower risk of mortality compared with that of patients without anticoagulants (HR 0.309, p = 0.0001; HR 0.387, p = 0.0238; HR 0.363, p < 0.0001). Multivariable Cox proportional hazard analyses also demonstrated that, compared with the no anticoagulant group, all rivaroxaban dosage groups (≤ 10 mg, HR 0.456, p = 0.0129; 15 mg, HR 0.246, p = 0.0003; 20 mg, HR 0.264, p = 0.0237) were significantly associated with a lower risk of mortality. Conclusion: Despite effects being smaller than observed with recommended optimal anticoagulation, the use of warfarin with an INR below 2, poor INR control and the use of low-dose rivaroxaban may still provide survival benefits, suggesting viable alternatives that enable physicians