Значение инфекции в развитии фетальных нарушений сердечного ритма

Abstract

Objective. To assess the impact of infection on the development of fetal arrhythmias. Patients and methods. The study included 84 pregnant women who were divided into two groups: the study group, which consisted of 44 patients aged 20–42 years (Me 31 ± 0.93 years) with fetal arrhythmia and/or minor heart defects at 21–41 weeks’ gestation (Me 37.41 ± 0.58 weeks), and the comparison group, which enrolled 40 pregnant women without fetal heart defects and with normal fetal heart rate to determine the significance of serological markers of myocarditis. Results. Significant titers of non-specific anti-myocardial antibodies to vascular smooth muscle and endothelium were detected in 14 (31.8%) and 7 (15.9%) fetuses, respectively. “Conditionally positive” titers for anti-smooth muscle antibodies were detected in 3 (6.8%) fetuses and for anti-endothelial cell antibodies in 4 (9%) fetuses. There was no significant increase in specific anti-heart antibody titers in both groups. Conclusion. Hypoxia should be considered as a trigger for fetal arrhythmias. The infectious and inflammatory processes are one of the links in the pathogenesis of fetal arrhythmias. Key words: fetal arrhythmia, intrauterine infection, minor heart defects