[Association between the polymorphism of GNB3C825T gene and vasovagal syncope in children]

Investigate the association between GNB3C825T gene polymorphism and pediatric vasovagal syncope.

Syncope group consisted of 54 cases of unexplained syncope in children, including 18 males and 36 females, at the age of 11.8 years; control group consisted of 54 healthy children over the same period, of whom 20 were male and 34 female, at the age of 11.2 years. The patients underwent head-up tilt test (HUTT). According to HUTT test results, HUTT-positive group and HUTT-negative group were further classified. For cases in HUTT-positive group, based on the changes in blood pressure and in heart rate during HUTT, vasodepressor, mixed and cardioinhibitory patterns were studied. DNA was extracted from peripheral blood in all the patients. A pair of primers was designed flanking 825 polymorphic loci. Products were recovered by using polymerase chain reaction (PCR). GNB3C825T polymorphism was detected by using gene-side GNB3C825T sequencing. Allele distribution between the various groups were studied.

Among fifty-four children with syncope, HUTT was positive in 30 cases, including vasodepressor pattern in 15 cases (50.0%), mixed pattern in 9 cases (30.0%) and cardioinhibitory pattern in 6 cases (20.0%). Whereas the subjects in control group had negative HUTT response. GNB3C825T allele C in the control and syncope groups was 81.5% and 65.7%, respectively. GNB3C825T allele T in the control and syncope groups was 18.5% and 34.3%, respectively (χ(2) = 6.888, P < 0.05). GNB3C825T allele C in HUTT-positive and negative groups was 61.7% and 81.3%, respectively. And GNB3C825T allele T in HUTT-positive and negative groups was 38.3% and 18.7%, respectively (χ(2) = 4.905, P < 0.05). GNB3C825T allele frequency did not show statistically significant difference among the 3 hemodynamic patterns of VVS (χ(2) = 0.658, P > 0.05).

Study on GNB3C825T allele frequency in children with vasovagal syncope is of significant value for a better understanding of the pathophysiology of VVS and provide a molecular biologic basis for its mechanisms.