PERINATAL AND HEREDITARY RISK FACTORS OF HEART RATE AND CONDUCTION DISORDERS IN CHILDREN WITH GASTROESOPHAGEAL REFLUX
Authors: Herasymova Oksana M. , Savvo Volodymyr M. 
Published: February 2022

Objective: to improve the early diagnosis of cardiac arrhythmias and conduction disorders in children with gastroesophageal reflux by evaluating hereditary and perinatal risk factors for this pathology.
Materials and Methods. The study involved 56 children aged 8 to 18 years, with an average age of 13.67 ± 2.67 years; 28 children with gastroesophageal reflux in combination with arrhythmias and cardiac conduction disorder comprised Group I (the main group), and 28 children with only gastroesophageal reflux without disorders of heart rhythm and conduction comprised Group II (the control group). Patients underwent clinical, anamnestic (with special attention paid to hereditary and perinatal history) and instrumental studies (electrocardiography, 24-hour Holter ECG monitoring, esophagogastroduodenoscopy).
Results. Genetic burden of cardiovascular disease was found in 57.1% of mothers and 42.9% of fathers of patients in the main group, which was significantly higher than that in the control group: by 3.2 times (17.9%; p ≤ 0.001) and 2 times (in 21.4%; p ≤ 0.05), respectively.
Apart from that, stratification of the parameter by the number of chronic diseases, namely ≤ 1 and ≥ 2, in both parents, showed that fewer (≤ 1) chronic diseases were characteristic of mothers and fathers of the control group children and were registered in 53.5% and 58,9% of them, respectively, while in the main group, the proportion of such parents was lower: by 5 times (10.7%; p ≤ 0.001) and 1.8 times (32.1%; p ≤ 0.05), respectively.
It was found that gravida 1 para 1 and gravida 2 para 2 mothers were significantly more common among those of patients in the control group (85.8% and 62.5%, respectively; p ≤ 0.05), while gravida 3 para 3 and more was typical for mothers of patients in the main group and were observed in 37.5% of them, while in the control group, this value was 2.6 times lower (14.2%; p ≤ 0.05).
As for the parity, the first childbirth was reported in 64.3% of mothers in the main group and in 28.6% of mothers (2.2 times less often) in the control group (p ≤ 0.05); while multipara mothers were characteristic of the control group children (71.4%), which was 2 times more often than in the main group (35.7%; p ≤ 0.05).
The risk factors of arrhythmias and cardiac conduction disorder were threatened miscarriage and toxemia in the first half of pregnancy. Thus, threatened miscarriage was reported in 46.4% of mothers of the main group children and was observed 2.2 times less often (21.4%; p ≤ 0.05) in the control group; toxemia in the first half of pregnancy was diagnosed in 50% of mothers of children in the main group and 2 times less often (in 25%; p ≤ 0.05) – in the control group.
Another predictor of the studied pathology was the physiological course of childbirth. Complicated childbirth was observed in 60.7% of mothers in the main group and 1.9 times less often (32.9%; p ≤ 0.05) – in the control group.
Relatively low (up to 3000 g) birthweight and fetal macrosomia (≥ 4000 g) also acted as risk factors. The proportion of patients with a bodyweight of up to 3000 g was 32.1% in the main group, and 3 times less (10.7%; p ≤ 0.05) – in the control group. The bodyweight of ≥ 4000 g (large fetus) was a specific feature of patients in the main group, as it was reported exclusively among them (17.9%) and was not observed in the control group (0%, p ≤ 0.001).
Conclusions. It was revealed that the maternal and paternal genetic burden of cardiovascular diseases and the number of chronic diseases in parents were statistically significant hereditary risk factors for the development of arrhythmias and conduction disorders in children.
It was found that statistically significant perinatal predictors of arrhythmias and conduction disorders in children with GER included threatened miscarriage; toxemia; multigravida and multipara status; complicated delivery; relatively low (up to 3000 g) birthweight and fetal macrosomia (≥ 4000 g).