Cardioautonomic control in healthy singleton and twin pregnancies

In conjunction with significant cardiovascular adaptation, changes in cardioautonomic balance, specifically greater sympathetic activation and vagal withdrawal, are considered normal adaptations to healthy singleton pregnancy. Cardiovascular adaptation to twin pregnancy is more profound than that of singleton pregnancies; however, the changes in cardioautonomic control during multifetal gestation are unknown. To address this gap, beat-by-beat blood pressure (photoplethysmography) and heart rate (lead II electrocardiogram) were measured continuously in 25 twin pregnancies and 25 singleton pregnancies (matched for age, pre-pregnancy BMI and gestational age) during 10-minutes of rest. Data extracted from a 3- to 5-minute period was used to analyze heart rate variability (HRV), blood pressure variability (BPV), cardiovagal baroreflex gain and cardiac intervals as indicators of cardioautonomic control. Independent t-tests were used to determine statistical differences between groups (α=0.05) and the false rate discovery was determined to adjust for multiple comparisons. Resting heart rate was greater in twin compared to singleton pregnancies (91±10 vs. 81±10 bpm; P=0.001), but blood pressure was not different. Individuals with twin pregnancies had lower HRV, evidenced by lower standard deviation of R-R intervals (32±11 vs. 47±18 ms; P=0.001), total power (1035±810 vs. 1945±1570 ms2; P=0.004) and high frequency power (224±262 vs. 810±806 ms2; P<0.001) compared to singleton pregnancies. There were no differences in cardiac intervals, BPV and cardiovagal baroreflex gain between groups. Our findings suggest that individuals with twin pregnancies have greater sympathetic and lower parasympathetic contributions to heart rate and that cardiac, but not vascular, autonomic control is impacted during twin compared to singleton pregnancy.

Related Products

Cat.No. Product Name Information
S7653 PND-1186 (VS-4718) PND-1186 (VS-4718, SR-2156) is a reversible and selective FAK inhibitor with IC50 of 1.5 nM. PND-1186 selectively promotes tumor cell apoptosis. Phase 1.

Related Targets

Apoptosis related FAK