Utility of magnesium sulfate in the treatment of rapid atrial fibrillation in the emergency department: a systematic review and meta-analysis.

Atrial fibrillation with rapid ventricular response (Afib/RVR) is a frequent reason for emergency department (ED) visits and can be treated with a variety of pharmacological agents. Magnesium sulfate has been used to prevent and treat postoperative Afib/RVR. We performed a systematic review and meta-analysis to assess the effectiveness of magnesium for treatment of Afib/RVR in the ED. PubMed and Scopus databases were searched up to June 2021 to identify any relevant randomized trials or observational studies. We used Cochrane's Risk-of-Bias tools to assess study qualities and random-effects meta-analysis for the difference of heart rate (HR) before and after treatment. Our search identified 395 studies; after reviewing 11 full texts, we included five randomized trials in our analysis. There were 815 patients with Afib/RVR; 487 patients (60%) received magnesium treatment, whereas 328 (40%) patients received control treatment. Magnesium treatment was associated with significant reduction in HR [standardized mean difference (SMD), 0.34; 95% CI, 0.21-0.47; P < 0.001; I2 = 4%), but not associated with higher rates of sinus conversion (OR, 1.46; 95% CI, 0.726-2.94; P = 0.29), nor higher rates of hypotension and bradycardia (OR, 2.2; 95% CI, 0.62-8.09; P = 0.22). Meta-regressions demonstrated that higher maintenance dose (corr. coeff, 0.17; P = 0.01) was positively correlated with HR reductions, respectively. We observed that magnesium infusion can be an effective rate control treatment for patients who presented to the ED with Afib/RVR. Further studies with more standardized forms of control and magnesium dosages are necessary to assess the benefit/risk ratio of magnesium treatment, besides to confirm our observations.

Enhancement of placental inflammation by Dibutyl Phthalate.

Recent studies suggest that women with high exposures to dibutyl phthalate (DBP) are at increased risk for preterm birth, a condition associated with aberrant inflammation in the placenta often caused by subclinical infections. Placental inflammation is also a risk factor for neurodevelopmental disorders whose risk may also be enhanced by DBP. It is unclear, however, if DBP enhances placental inflammation. Therefore, we studied the effects of DBP on the production of biomarkers of placental inflammation and neurodevelopment under basal conditions and a setting of mild infection. Placental explant cultures established from women undergoing elective caesarean delivery were treated with DBP with and without co-stimulation by 107 CFU/mL heat-killed E. coli for 24 h at 37 °C. Conditioned medium was harvested and concentrations of IL-1ß, TNF-α, IL-10, HO-1 and BDNF, a biomarker for neurodevelopment, were quantified. DBP significantly enhanced IL-6 production in basal cultures but had no significant on the other biomarkers quantified. Both TNF-α and IL-1ß production was enhanced by DBP for cultures co-stimulated with E. coli. Although marginal enhancement of IL-6, and IL-10 were observed for bacteria co-treated cultures, results were either non-monotonic or only approached statistical significance. HO-1 production tended to be reduced at the highest concentration of DBP tested and BDNF production was reduced by DBP in a dose-dependent manner for bacteria-stimulated cultures. These results suggest that DBP enhances basal IL-6 production but has little or no effect on other biomarkers studied. However, DBP enhances IL-1ß and TNF-α production but reduces BDNF production by bacteria-stimulated cultures.